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  • 1.
    Apró, William
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Wang, Li
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Pontén, Marjan
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Blomstrand, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Endurance Exercise Does Not Impair mTOR Signalling After Resistance Exercise: D-58 Thematic Poster - Skeletal Muscle Cell Signaling: JUNE 2, 2011 3:15 PM - 5:15 PM: ROOM: 3042011In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 43, no 5, p. 52-Article in journal (Other academic)
    Abstract [en]

    Resistance exercise is known to stimulate muscle hypertrophy and this effect is mainly mediated by the mammalian target of rapamycin (mTOR) pathway. In contrast, endurance exercise results in a divergent phenotypic response which to a large extent is mediated by adenosine monophosphate-activated protein kinase (AMPK). Research indicates that molecular interference may exist, possibly through an inhibitory effect on mTOR signalling by AMPK, when these two modes of exercise are combined.

    PURPOSE: To investigate the impact of subsequent endurance exercise on resistance exercise induced mTOR signalling.

    METHODS: In a randomized and cross-over fashion, ten male subjects performed either heavy resistance exercise (R) or heavy resistance exercise followed by endurance exercise (RE) on two separate occasions. The R protocol consisted of thirteen sets of leg press exercise with 3 minutes of recovery allowed between each set. In the RE session, resistance exercise was followed by 15 minutes recovery after which 30 min of cycling was initiated at an intensity equal to 70 % of the subjects' maximal oxygen consumption. Muscle biopsies were collected before, 1 and 3 hours after resistance exercise in both trials. Samples were analyzed for several signalling proteins in the mTOR pathway using western blot technique.

    RESULTS: Phosphorylation of mTOR increased approx. twofold at 1 h post resistance exercise and remained elevated at the 3 h time point (p< 0.01) with no difference between the two trials. Phosphorylation of p70S6k, a downstream target of mTOR, was increased about 6-and18-fold at 1 h and 3 h post resistance exercise (p< 0.01). There was no difference in p70S6k phosphorylation at any time point between the two trials. Phosphorylation of the eukaryotic elongation factor eEF2 was decreased 3- to 4-fold at both time points post resistance exercise (p< 0.01) with no difference between trials. Phosphorylation of AMPK was unchanged at the 1 h time point but decreased approximately 30 % from pre-exercise values in both trials at 3 h post resistance exercise (p< 0.01).

    CONCLUSIONS: The signalling response following heavy resistance exercise is not blunted by subsequent endurance exercise. Supported by the Swedish National Centre for Research in Sports.

  • 2.
    Apró, William
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Wang, Li
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Pontén, Marjan
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Blomstrand, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Resistance exercise induced mTORC1 signaling is not impaired by subsequent endurance exercise in human skeletal muscle.2013In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 305, no 1, p. E22-32Article in journal (Refereed)
    Abstract [en]

    The current dogma is that the muscle adaptation to resistance exercise is blunted when combined with endurance exercise. The suggested mechanism (based on rodent experiments) is that activation of adenosine monophosphate-activated protein kinase (AMPK) during endurance exercise impairs muscle growth through inhibition of the mechanistic target of rapamycin complex 1 (mTORC1). The purpose of this study was to investigate potential interference of endurance training on the signaling pathway of resistance training [mTORC1 phosphorylation of ribosomal protein S6 kinase 1 (S6K1)] in human muscle. Ten healthy and moderately trained male subjects performed on two separate occasions either acute high-intensity and high-volume resistance exercise (leg press, R) or R followed by 30 min of cycling (RE). Muscle biopsies were collected before and 1 and 3 h post resistance exercise. Phosphorylation of mTOR (Ser(2448)) increased 2-fold (P < 0.05) and that of S6K1 (Thr(389)) 14-fold (P < 0.05), with no difference between R and RE. Phosphorylation of eukaryotic elongation factor 2 (eEF2, Thr(56)) was reduced ∼70% during recovery in both trials (P < 0.05). An interesting finding was that phosphorylation of AMPK (Thr(172)) and acetyl-CoA carboxylase (ACC, Ser(79)) decreased ∼30% and ∼50%, respectively, 3 h postexercise (P < 0.05). Proliferator-activated receptor-γ coactivator-1 (PGC-1α) mRNA increased more after RE (6.5-fold) than after R (4-fold) (RE vs. R: P < 0.01) and was the only gene expressed differently between trials. These data show that the signaling of muscle growth through the mTORC1-S6K1 axis after heavy resistance exercise is not inhibited by subsequent endurance exercise. It is also suggested that prior activation of mTORC1 signaling may repress subsequent phosphorylation of AMPK.

  • 3. Bakkman, Linda
    et al.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Holmberg, H-C
    Tonkonogi, Michail
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Quantitative and qualitative adaptation of human skeletal muscle mitochondria to hypoxic compared with normoxic training at the same relative work rate.2007In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 190, no 3, p. 243-51Article in journal (Refereed)
    Abstract [en]

    AIM: To investigate if training during hypoxia (H) improves the adaptation of muscle oxidative function compared with normoxic (N) training performed at the same relative intensity. METHOD: Eight untrained volunteers performed one-legged cycle training during 4 weeks in a low-pressure chamber. One leg was trained under N conditions and the other leg under hypobaric hypoxia (526 mmHg) at the same relative intensity as during N (65% of maximal power output, W(max)). Muscle biopsies were taken from vastus lateralis before and after the training period. Muscle samples were analysed for the activities of oxidative enzymes [citrate synthase (CS) and cytochrome c oxidase (COX)] and mitochondrial respiratory function. RESULTS: W(max) increased with more than 30% over the training period during both N and H. CS activity increased significantly after training during N conditions (+20.8%, P < 0.05) but remained unchanged after H training (+4.5%, ns) with a significant difference between conditions (P < 0.05 H vs. N). COX activity was not significantly changed by training and was not different between exercise conditions [+14.6 (N) vs. -2.3% (H), ns]. Maximal ADP stimulated respiration (state 3) expressed per weight of muscle tended to increase after N (+31.2%, P < 0.08) but not after H training (+3.2%, ns). No changes were found in state four respiration, respiratory control index, P/O ratio, mitochondrial Ca(2+) resistance and apparent Km for oxygen. CONCLUSION: The training-induced increase in muscle oxidative function observed during N was abolished during H. Altitude training may thus be disadvantageous for adaptation of muscle oxidative function.

  • 4.
    Berthelson, Per
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Katz, Abram
    Institutionen för Fysiologi och Farmakologi, Karolinska Instititutet.
    Andersson, Eva
    Swedish School of Sport and Health Sciences, GIH.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Acute exercise and starvation induced insulin resistance2012In: Medicine & Science In Sports & Exercise, 2012, S498 Vol. 44 No. 5 Supplement. 2661., 2012, p. 2661-Conference paper (Other academic)
    Abstract [en]

    It is well known that starvation causes insulin resistance. The mechanism is unclear but may relate disturbances in lipid metabolism i.e. incomplete mitochondrial FA oxidation and/or accumulation of lipid intermediates. Exercise results in increased substrate oxidation and may thus remove interfering lipid metabolites and reverse starvation-induced insulin resistance. However, the effect of acute exercise and starvation on insulin sensitivity is not known.

    Purpose: The aim of this study was to investigate the effect of exercise on starvation-induced insulin resistance and to elucidate potential mechanisms.

    Methods: Nine healthy lean subjects underwent 84h starvation on two occasions separated by at least 2 weeks. The starvation period was followed by either exercise (EX; 5x10 min intervals with 2-4 min rest, starting at 70 %VO2 max) or an equal period of rest (NE). Before and after the starvation period (3h after exercise/rest) subjects were investigated with muscle biopsies, bloo samples and an intravenous glucose tolerance test. Muscle samples were used for measurement of mitochondrial respiration in permeabilized muscle fibers (Oroboros oxygraph), glycogen content and activation of signaling proteins.

    Results: Insulin sensitivity was significantly higher in the EX group compared to the NE group (p<0.05). After starvation mitochondrial respiration was lower in both groups with complex I substrates whereas respiration with complex I+II substrates was higher in EX (p<0.05 vs. basal and NE). Muscle glycogen was decreased to 73% (NE) and 31% (EX) of the basal values. The EX group had a significant increased activation of AS160. Plasma FA increased 3-4 fold to 1.39±0.32(NE) and 1.80±0.49 (EX) (mmol/l) after starvation and plasma beta-hydroxybutyrate increased about 50-fold to 6.43±2.01(NE) and 7.12±1.59 (EX)(mmol/l).

    Conclusion: Acute exercise reverses starvation-induced insulin resistance. Plasma FA and BOH were increased to similar extent after NE and EX and cannot explain the changes in insulin sensitivity. However, an increased substrate oxidation together with the observed increased capacity for mitochondrial FA oxidation after EX may be involved in the activation of AS160 and the reversal of starvation-induced insulin resistance.

  • 5. Bishop, David J
    et al.
    Thomas, Claire
    Moore-Morris, Tom
    Tonkonogi, Michail
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Mercier, Jacques
    Sodium bicarbonate ingestion prior to training improves mitochondrial adaptations in rats.2010In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 299, no 2, p. E225-33Article in journal (Refereed)
    Abstract [en]

    We tested the hypothesis that reducing hydrogen ion accumulation during training would result in greater improvements in muscle oxidative capacity and time to exhaustion (TTE). Male Wistar rats were randomly assigned to one of three groups (CON, PLA, and BIC). CON served as a sedentary control, whereas PLA ingested water and BIC ingested sodium bicarbonate 30 min prior to every training session. Training consisted of seven to twelve 2-min intervals performed five times/wk for 5 wk. Following training, TTE was significantly greater in BIC (81.2 +/- 24.7 min) compared with PLA (53.5 +/- 30.4 min), and TTE for both groups was greater than CON (6.5 +/- 2.5 min). Fiber respiration was determined in the soleus (SOL) and extensor digitorum longus (EDL), with either pyruvate (Pyr) or palmitoyl carnitine (PC) as substrates. Compared with CON (14.3 +/- 2.6 nmol O(2).min(-1).mg dry wt(-1)), there was a significantly greater SOL-Pyr state 3 respiration in both PLA (19.6 +/- 3.0 nmol O(2).min(-1).mg dry wt(-1)) and BIC (24.4 +/- 2.8 nmol O(2).min(-1).mg dry wt(-1)), with a significantly greater value in BIC. However, state 3 respiration was significantly lower in the EDL from both trained groups compared with CON. These differences remained significant in the SOL, but not the EDL, when respiration was corrected for citrate synthase activity (an indicator of mitochondrial mass). These novel findings suggest that reducing muscle hydrogen ion accumulation during running training is associated with greater improvements in both mitochondrial mass and mitochondrial respiration in the soleus.

  • 6.
    Björkman, Frida
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Edin, Fredrik
    University of Gothenburg.
    Mattsson, C Mikael
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Larsen, Filip
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Regular moist snuff dipping does not affect endurance exercise performance.2017In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 7, article id e0181228Article in journal (Refereed)
    Abstract [en]

    Physiological and medical effects of snuff have previously been obtained either in cross-sectional studies or after snuff administration to non-tobacco users. The effects of snuff cessation after several years of daily use are unknown. 24 participants with >2 years of daily snuff-use were tested before and after >6 weeks snuff cessation (SCG). A control group (CO) of 11 snuff users kept their normal habits. Resting heart rate (HR) and blood pressure (BP) were significantly lower in SCG after snuff cessation, and body mass was increased by 1.4 ± 1.7 kg. Total cholesterol increased from 4.12 ± 0.54 (95% CI 3.89-4.35) to 4.46 ± 0.70 (95% CI 4.16-4.75) mM L-1 in SCG, due to increased LDL, and this change was significantly different from CO. Resting values of HDL, C-reactive protein, and free fatty acids (FFA) remained unchanged in both groups. In SCG group, both HR and BP were reduced during a four-stage incremental cycling test (from 50 to 80% of VO2max) and a prolonged cycling test (60 min at 50% of VO2max). Oxygen uptake (VO2), respiratory exchange ratio, blood lactate (bLa) and blood glucose (bGlu) concentration, and rate of perceived exertion (RPE) were unchanged. In CO group, all measurements were unchanged. During the prolonged cycling test, FFA was reduced, but with no significant difference between groups. During the maximal treadmill running test peak values of VO2, pulmonary ventilation (VE), time to exhaustion and bLa were unchanged in both groups. In conclusion, endurance exercise performance (VO2max and maximal endurance time) does not seem to be affected by prolonged snuff use, while effects on cardiovascular risk factors are contradictory. HR and BP during rest and submaximal exercise are reduced after cessation of regular use of snuff. Evidently, the long-time adrenergic stress on circulation is reversible.

  • 7.
    Boushel, Robert
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Lundby, Carsten
    Qvortrup, Klaus
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Mitochondrial plasticity with exercise training and extreme environments.2014In: Exercise and sport sciences reviews, ISSN 0091-6331, E-ISSN 1538-3008, Vol. 42, no 4, p. 169-74Article in journal (Refereed)
    Abstract [en]

    Mitochondria form a reticulum in skeletal muscle. Exercise training stimulates mitochondrial biogenesis, yet an emerging hypothesis is that training also induces qualitative regulatory changes. Substrate oxidation, oxygen affinity, and biochemical coupling efficiency may be regulated differentially with training and exposure to extreme environments. Threshold training doses inducing mitochondrial upregulation remain to be elucidated considering fitness level.

  • 8.
    Cardinale, Daniele A.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Exercise training strategies to optimize muscle oxygen uptake, muscle oxidative capacity and performance in humans2015Conference paper (Other academic)
    Abstract [en]

    My research area focuses on studying the entire O2 cascade in humans from lungs to mitochondria with an integrative approach.

    The overall aim of the PhD project is to examine in detail 1) the differences in convective O2 delivery (Fick method) and mitochondrial function (high resolution respirometry technique) between individuals with low and high VO2 max, 2) to quantify the effect of aerobic interval training with elevated O2 delivery on circulatory, muscle mitochondrial components on VO2 max in highly trained individuals, as well as, 3) to quantify the effect of elevated O2 delivery on circulatory and metabolic responses (blood flow and muscle VO2) to exercise engaging small and large muscle groups. A specific focus of the PhD project is to examine and quantify how differences in a) mitochondrial OXPHOS capacity and b) mitochondrial O2 affinity (p50) define differences in muscle O2 extraction and muscle VO2 between individuals of low fitness and those with high aerobic endurance capacity. Although a vast body of literature supports a strong link between muscle oxidative capacity and peak VO2 during exercise, almost all studies are correlative, and the dependence and contribution of mitochondrial capacity to muscle VO2 has yet to be quantified. To this end, experiments are designed to control for O2 transport during exercise as the independent variable between groups with high and low aerobic capacities. The effect of aerobic interval training with elevated O2 delivery on central (circulatory) and peripheral (muscle oxidative) mechanisms for elevating peak VO2 and endurance performance are explored in endurance-trained individuals. Hyperoxic air increases O2 dissolved in the blood, elevates arterial O2 saturation, and increases arterial O2 concentration, resulting in a higher O2 delivery to the working muscle independently from blood flow. Since mitochondria have an excess oxidative capacity in relation to O2 delivery during whole body exercise in normoxia, we hypothesize that mitochondrial volume, function and O2 affinity as well as endurance performance are largely improved following endurance interval training with elevated O2 delivery compared to normoxia.

    Our preliminary data show that OXPHOS and performance are significantly enhanced following six weeks of periodized aerobic interval training. Significantly differences in performance but not in OXPHOS are found when training is conducted in hyperoxia compared to normoxia.

  • 9.
    Cardinale, Daniele A.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Skeletal muscle V̇O2max and mitochondrial p50 measured in-vivo and ex-vivo: effect of hyperoxia in exercise with small and large muscle mass in well-trained individuals2016Conference paper (Other academic)
    Abstract [en]

    In healthy individuals maximal oxygen uptake is limited by cardiac output when exercising with large musclemass, e.g. 2-legged cycling (BIKE), whereas during one-leg knee extension (KE) exercise there is a closermatch between the amounts of O2 delivered to O2 demand. However hyperoxia has been shown to increaseO2 uptake in both work modalities. This study examined the extent to which hyperoxia affects leg oxygentransport, muscle diffusion capacity, mitochondrial oxygen affinity (p50mito) in vivo and ex vivo, and muscleO2 uptake during exercise engaging a large and small muscle mass in well-trained individuals. In this studywe show that light hyperoxia increases O2 uptake at peak incremental exercise (~10%, p< 0.05) in bothBIKE and KE due to an increased O2 delivery (~ 10%, p< 0.05), which in turn is mainly caused by anincreased arterial O2 content (~5%, p< 0.05), and a non-significant increased leg blood flow (~ 5%). Hencehyperoxia decreases mitochondrial O2 affinity as indicated by the higher calculated in vivo mitochondrialp50. Inspired O2 enhanced maximal work rate in BIKE (~6.5%) and in KE (~4.5%).Our data show that in vivo mitop50 is lower than the ex vivo measure in BIKE, whereas in vivo mitop50 issimilar to ex vivo measure in KE. These indicates that mitochondrial OXPHOS capacity was in excess inBIKE, whereas in KE was almost fully utilized in vivo. This study indicated that both during whole body peakexercise as well as during exercise with smaller muscle mass, V̇O2 may not limit O2 diffusion capacity.

  • 10.
    Cardinale, Daniele A.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Syrgas – så påverkas prestationen2016In: Idrottsforskning, ISSN 2002-3944, article id 31 marsArticle in journal (Other (popular science, discussion, etc.))
    Abstract [sv]

    Vältränade idrottare som andas syrgas ökar omedelbart prestationen. Trots det är metoden inte dopningsklassad. En genomgång av aktuell forskning visar att syrgasandning skulle ha en signifikant effekt under tävlingar, men hur det fungerar som träningsmetod är mer osäkert. Vanlig luft kan vara minst lika bra.

  • 11.
    Cardinale, Daniele A.
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Cardinale, Marco
    Aspire Academy, Doha, Qatar.
    Nilsson, Johnny E.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, The Laboratory of Applied Sports Science (LTIV). University of Dalarna, Falun.
    Comparison between single and combined data collection methods in loaded squat jump power output2017In: Gazzetta Medica Italiana, ISSN 0393-3660, E-ISSN 1827-1812, Vol. 176, no 6, p. 315-321Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The aim of this study was to compare linear position transducer force plate-based methods and more complex combinations of those for calculation of power output in loaded squat jump.

    METHODS: Eight methods were used simultaneously in data collection: vertical ground reaction force (VGRF), ground reaction forces (GRF), 1 linear position transducer (1LPT), 1LPT and VGRF (1LPT+VGRF), 2 linear position transducers (2LPTs), 2LPTs and VGRF (2LPTs+VGRF), 5 linear position transducers (5LPTs), 5LPTs and GRF (5LPTs+GRF). Power output was calculated for each lift according to the sensor or sensors used and the results were compared.

    RESULTS: Power output calculated separately with LPTs and GRF method did not differ significantly from combined methods such as 1LPT+VGRF, 2LPTs+VGRF. No significant differences were found when comparing power output between 5LPTs+GRF and combined methods such as 2LPTs+VGRF.

    CONCLUSIONS: This study indicates that test methodology with a simple single linear position transducer setup and or force platform suffice when recording vertical jump such as loaded squat jump.

  • 12.
    Cardinale, Daniele A
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll. Elite Performance Centre, Bosön.
    Gejl, Kasper D
    University of Southern Denmark.
    Ørtenblad, Niels
    University of Southern Denmark.
    Ekblom, Bjorn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Blomstrand, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Eva Blomstrand's research group.
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Reliability of maximal mitochondrial oxidative phosphorylation in permeabilized fibers from the vastus lateralis employing high-resolution respirometry.2018In: Physiological Reports, E-ISSN 2051-817X, Vol. 6, no 4, article id e13611Article in journal (Refereed)
    Abstract [en]

    The purpose was to assess the impact of various factors on methodological errors associated with measurement of maximal oxidative phosphorylation (OXPHOS) in human skeletal muscle determined by high-resolution respirometry in saponin-permeabilized fibers. Biopsies were collected from 25 men to assess differences in OXPHOS between two muscle bundles and to assess the correlation between OXPHOS and the wet weight of the muscle bundle. Biopsies from left and right thighs of another five subjects were collected on two occasions to compare limbs and time-points. A single muscle specimen was used to assess effects of the anesthetic carbocaine and the influence of technician. The difference in OXPHOS between two fiber-bundles from the same biopsy exhibited a standard error of measurement (SEM) of 10.5 pmol · s-1  · mg-1 and a coefficient of variation (CV) of 15.2%. The differences between left and right thighs and between two different time-points had SEMs of 9.4 and 15.2 pmol · s-1  · mg-1 and CVs of 23.9% and 33.1%, respectively. The average (±SD) values obtained by two technicians monitoring different bundles of fibers from the same biopsy were 31.3 ± 7.1 and 26.3 ± 8.1 pmol · s-1  · mg-1 . The time that elapsed after collection of the biopsy (up to a least 5 h in preservation medium), wet weight of the bundle (from 0.5 to 4.5 mg) and presence of an anesthetic did not influence OXPHOS. The major source of variation in OXPHOS measurements is the sample preparation. The thigh involved, time-point of collection, size of fiber bundles, and time that elapsed after biopsy had minor or no effect.

  • 13.
    Cardinale, Daniele A.
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Jensen-Urstad, M
    Karolinska institutet.
    Rullman, E
    Karolinska institutet.
    Søndergaard, H
    Rigshospitalet, Köpenhamn, Danmark.
    Morales-Alamo, D
    University of Las Palmas de Gran Canaria, Spanien.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Calbet, J A L
    University of Las Palmas de Gran Canaria, Spanien.
    Boushel, Robert
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology. University of British Columbia, Vancouver, British Columbia, Canada.
    Muscle mass and inspired oxygen influence oxygen extraction at maximal exercise: role of mitochondrial oxygen affinity.2018In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, article id e13110Article in journal (Refereed)
    Abstract [en]

    AIM:We examined the Fick components together with mitochondrial O2 affinity (p50mito ) in defining O2 extraction and O2 uptake during exercise with large and small muscle mass during normoxia (NORM) and hyperoxia (HYPER).

    METHODS:Seven individuals performed two incremental exercise tests to exhaustion on a bicycle ergometer (BIKE) and two on a one-legged knee extension ergometer (KE) in NORM or HYPER. Leg blood flow and VO2 were determined by thermodilution and the Fick method. Maximal ADP-stimulated mitochondrial respiration (OXPHOS) and p50mito were measured ex vivo in isolated mitochondria. Mitochondrial excess capacity in the leg was determined from OXPHOS in permeabilized fibers and muscle mass measured with magnetic resonance imaging in relation to peak leg O2 delivery.

    RESULTS:The ex vivo p50mito increased from 0.06±0.02 to 0.17±0.04 kPa with varying substrate supply and O2 flux rates from 9.84±2.91 to 16.34±4.07 pmol O2 ·s-1 ·μg-1 respectively. O2 extraction decreased from 83% in BIKE to 67% in KE as a function of a higher O2 delivery, and lower mitochondrial excess capacity. There was a significant relationship between O2 extraction and mitochondrial excess capacity and p50mito that was unrelated to blood flow and mean transit time.

    CONCLUSION:O2 extraction varies with mitochondrial respiration rate, p50mito and O2 delivery. Mitochondrial excess capacity maintains a low p50mito which enhances O2 diffusion from microvessels to mitochondria during exercise. This article is protected by copyright. All rights reserved.

  • 14.
    Cardinale, Daniele A.
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Schiffer, Tomas A
    Karolinska Institute.
    Morales-Alamo, David
    University of Las Palmas de Gran Canaria.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Calbet, Jose A L
    University of Las Palmas de Gran Canaria.
    Holmberg, Hans-Christer
    Mid Sweden University, Östersund, The University of British Columbia, Vancouver, BC, Canada..
    Boushel, Robert
    The University of British Columbia, Vancouver, BC, Canada..
    Superior Intrinsic Mitochondrial Respiration in Women Than in Men.2018In: Frontiers in Physiology, ISSN 1664-042X, E-ISSN 1664-042X, Vol. 9, article id 1133Article in journal (Refereed)
    Abstract [en]

    Sexual dimorphism is apparent in humans, however, to date no studies have investigated mitochondrial function focusing on intrinsic mitochondrial respiration (i.e., mitochondrial respiration for a given amount of mitochondrial protein) and mitochondrial oxygen affinity (p50mito) in relation to biological sex in human. A skeletal muscle biopsy was donated by nine active women, and ten men matched for maximal oxygen consumption (VO2max) and by nine endurance trained men. Intrinsic mitochondrial respiration, assessed in isolated mitochondria, was higher in women compared to men when activating complex I (CIP) and complex I+II (CI+IIP) (p < 0.05), and was similar to trained men (CIP, p = 0.053; CI+IIP, p = 0.066). Proton leak and p50mito were higher in women compared to men independent of VO2max. In conclusion, significant novel differences in mitochondrial oxidative function, intrinsic mitochondrial respiration and p50mito exist between women and men. These findings may represent an adaptation in the oxygen cascade in women to optimize muscle oxygen uptake to compensate for a lower oxygen delivery during exercise.

  • 15.
    Cardinale, Daniele A.
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll. Elite Performance Centre, Bosön.
    Lilja, Mats
    Karolinska institutet.
    Mandic, Mirko
    Karolinska institutet.
    Gustafsson, Thomas
    Karolinska institutet.
    Larsen, Filip J.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Lundberg, Tommy R.
    Karolinska institutet.
    Resistance Training with Co-ingestion of Anti-inflammatory Drugs Attenuates Mitochondrial Function2017In: Frontiers in Physiology, ISSN 1664-042X, E-ISSN 1664-042X, Vol. 8, article id 1074Article in journal (Refereed)
    Abstract [en]

    Aim: The current study aimed to examine the effects of resistance exercise with concomitant consumption of high versus low daily doses of non-steroidal anti-inflammatory drugs (NSAIDs) on mitochondrial oxidative phosphorylation in skeletal muscle. As a secondary aim, we compared the effects of eccentric-overload with conventional training. Methods: Twenty participants were randomized to either a group taking high doses (3 x 400 mg/day) of ibuprofen (IBU; 27±5 yr; n=11) or a group ingesting a low dose (1 x 75 mg/day) of acetylsalicylic acid (ASA; 26±4 yr; n=9) during 8 weeks of supervised knee extensor resistance training. Each of the subject’s legs were randomized to complete the training program using either a flywheel (FW) device emphasizing eccentric-overload, or a traditional weight stack machine (WS). Maximal mitochondrial oxidative phosphorylation (CI+IIP) from permeabilized skeletal muscle bundles was assessed using high-resolution respirometry. Citrate synthase (CS) activity was assessed using spectrophotometric techniques and mitochondrial protein content using western blotting. Results: After training, CI+IIP decreased (P<0.05) in both IBU (23%) and ASA (29%) with no difference across medical treatments. Although CI+IIP decreased in both legs, the decrease was greater (interaction p = 0.015) in WS (33%, p = 0.001) compared with FW (19%, p = 0.078). CS activity increased (p = 0.027) with resistance training, with no interactions with medical treatment or training modality. Protein expression of ULK1 increased with training in both groups (p < 0.001). The increase in quadriceps muscle volume was not correlated with changes in CI+IIP (R=0.16). Conclusion: These results suggest that 8 weeks of resistance training with co-ingestion of anti-inflammatory drugs reduces mitochondrial function but increases mitochondrial content. The observed changes were not affected by higher doses of NSAIDs consumption, suggesting that the resistance training intervention was the prime mediator of the decreased mitochondrial phosphorylation. Finally, we noted that flywheel resistance training, emphasizing eccentric overload, rescued some of the reduction in mitochondrial function seen with conventional resistance training.

  • 16.
    Cardinale, Daniele A.
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Nilsson, Johnny
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control. Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, The Laboratory of Applied Sports Science (LTIV).
    Cardinale, Marco
    Comparative multiple sensor approach for power calculation in loaded squat jump and power clean2013In: Comparative multiple sensor approach for power calculation in loaded squat jump and power clean, 2013Conference paper (Refereed)
    Abstract [en]

    Introduction

    Power output is a critical component of athletic performance (McGuigan et al., 2012); therefore, strength and conditioning specialists are nowadays employed to help athletes increase the power-generating capacity in specific motor tasks. Due to the widespread need to assess power output in common strength training exercises, the development and validation of various assessment approaches has led to studies aimed at identifying the external optimal load (OL) to maximize power output (Cormie et al., 2007). The aim of this study was to compare conventionally used linear position transducer and force plate based methods with a new methodology for calculation of peak power (PP) and average power (AP) output in conjunction with the load-power relationship.

    Methods

    Nineteen male elite athletes performed loaded squat jump (LSJ) and power clean (PC) with different external loads to determine the load/power relationship. Nine methods were used simultaneously in data collection: vertical ground reaction force (VGRF), ground reaction force (GRF) i.e. vertical, anterio-posterior and medio-lateral reaction force components, 1 linear encoder (1Encoder), 1 linear position transducer (1LPT), 1LPT and VGRF (1LPT+VGRF), 2 linear position transducers (2LPTs), 2LPTs and VGRF (2LPTs+VGRF), 5 linear position transducers (5LPTs), 5LPTs and GRF (5LPTs+GRF; novel method). Power output was calculated for each lift according to the sensor or sensors simultaneously used and the results were compared.

    Results

    Power output calculated separately with LPTs and GRF method differed significantly from combined methods such as 1LPT+VGRF, 2LPTs+VGRF, and 5LPTs+GRF (novel method). The optimal load in LSJ and PC with respect to PP output was identified at loads between 30 and 50% of their body mass (bm), respectively; and with respect to AP output equal to loads between 85 and 75% of bm, respectively.

    Discussion

    This study indicates that test methodology influences the results of the power output and the load–power relationship in LSJ and PC exercises. The results of this study suggest the possibility that the combined methods provide a better representation of muscle power generation during dynamic movements involving the non-linear trajectories of the barbell than kinematic or kinetic methods alone.

    References

    Cormie, P., McBride, J. M., & McCaulley, G. O. (2007). J Appl Biomech, 23(2), 103-118. McGuigan. (2012). Strength and Power Assessment Protocols. Physiological Tests for Elite Athletes (2nd ed., pp. 207-230). Stanningley Leeds, United Kingdom: Human Kinetics.

  • 17.
    Cardinale, Daniele
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Boushel, Robert
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Ekblom-Bak, Elin
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, The Research Unit for Movement, Health and Environment.
    Is the Ekblom-Bak Test a valid screening tool for Vo2peak in highly active individuals?2015Conference paper (Refereed)
    Abstract [en]

    Introduction

    Maximal oxygen consumption testing is suggested to be regularly included between training blocks of athletes in order to monitor changes in fitness throughout the season. However, despite the good reliability and validity of this physiological test, an expensive metabolic chart, and expert personnel are needed. Further, the maximal effort needed by the athlete makes this test difficult to be performed routinely. Therefore, it is important to develop valid tools that are also feasible for the estimation of the maximal oxygen consumption. The aim of this study was to validate the Ekblom-Bak test (EBT) (Ekblom-Bak et al., 2014) against an incremental test measuring peak VO2 by gas exchange on a cycle ergometer in well-trained individuals.

    Methods

    33 highly active individuals aged 34.5±6.6yrs (mean ± standard deviation (SD)) body mass 74.5±12kg, and height; 178± 9.3m) participated in the study. The EBT test was performed prior to the incremental exercise test to peak effort on a cycle ergometer for VO2peak assessment. Oxygen uptake was determined by an automated measuring system for oxygen uptake with a mixing chamber (OxygenPro, Jaeger GmbH, Germany) validated against the Douglas bag method resulting in a typical error of 2%. The mean difference and standard deviation of the differences between the EBT and measured VO2peak was calculated with Bland-Altman analysis.

    Results

    The measured mean and SD VO2peak was 4.1±0.8 L•min-1 for the whole group (male 4.4±0.6 L•min-1 and female 2.9±0.5 L•min-1). The mean differences between measured and estimated (EBT) VO2peak was 0.05 L•min-1 (95% CI; -0.15 to 0.25). CV was 13.2% in the whole group with no significant differences between sexes. For individuals with a VO2peak within the valid range of the EBT (VO2max 1.56 to 4.49 L•min-1, n=23), the mean differences between measured and estimate VO2peak was -0.22 L•min-1 (95% CI; -0.36 to -0.08), resulting in a CV of 8.2%. For individuals above the valid limit (n=10), the mean difference was 0.68L•min-1(95% CI; 0.47 to 0.98) with a CV of 6.9%. Discussion The Ekblom-Bak test is an easily applied and inexpensive screening tool for a population of highly active individuals within the current validity range, and may be used routinely in monitoring fitness.

    References

    Ekblom-Bak E, Björkman F, Hellenius ML, Ekblom B (2014). Scand J Med Sci Sports, 24(2), 319-326

  • 18.
    Cardinale, Daniele
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Lilja, Mats
    Karolinska Institutet, Stockholm, Sweden..
    Mandic, Mirko
    Karolinska Institutet, Stockholm, Sweden..
    Gustafsson, Thomas
    Karolinska Institutet, Stockholm, Sweden..
    Larsen, Filip J.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Lundberg, Tommy R.
    Karolinska Institutet Stockholm, Sweden..
    Resistance Exercise Attenuates Mitochondrial Function: Effects Of NSAID Intake And Eccentric-Overload Training2017In: Medicine & Science in Sports & Exercise. 49(5S):329, MAY 2017, 2017, Vol. 49, no 5, p. 329-329Conference paper (Refereed)
    Abstract [en]

    Although nonsteroidal antiinflammatorydrugs (NSAIDs) have been shown to modulate skeletal muscle adaptations and protein metabolism in response toresistance exercise, little is known about the effects of NSAIDs on mitochondrial function. Thus, the current study aimed to examine the effects of resistanceexercise with concomitant NSAID consumption on mitochondrial oxidative phosphorylation in skeletal muscle. Twenty participants were randomized in asingleblindedfashion to either an experimental group receiving ibuprofen (IBU: 27±5 yr; n=11; 1200 mg/d) or a control group receiving a lowdoseacetylsalicylic acid (CON: 26±4 yr; n=9; 75 mg/d) During this period, subjects performed 8 weeks of supervised resistance exercise involving the kneeextensors muscles. Each of the subject’s legs were randomized to complete the training program using either a flywheel (FW) device emphasizing eccentricoverload,or a traditional weight stack machine (WS). Maximal mitochondrial oxidative phosphorylation (OXPHOS) from permeabilized skeletal muscle bundleswas assessed using high resolution respirometry before and after the training intervention. Citrate synthase activity was assessed using spectrophotometrictechniques. After training, OXPHOS decreased (P<0.05) in both IBU (23%) and CON (29%) with no difference across medical treatments. Although OXPHOSdecreased in both legs, the decrease was greater (interaction P= 0.015) in WS (33%, P= 0.015) than in FW (19%, P= 0.078). Citrate synthase (CS) did notchange after the intervention. The increase in quadriceps muscle volume was not significantly correlated with the change in OXPHOS (R=0.15). These resultssuggest that 1) eight weeks of resistance training reduces mitochondrial function but not mitochondrial content, 2) The decreased mitochondrial function withresistance exercise was not affected by ibuprofen consumption, 3) flywheel resistance training, emphasizing eccentric overload, rescues some of thereduction in mitochondrial function seen with conventional resistance training.

  • 19.
    Fernström, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Hög aerob uthållighet förenat med låg risk för hjärt-kärlsjukdom hos svenska unga vuxna2018In: BestPracticeArticle in journal (Other academic)
  • 20.
    Fernström, Maria
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Bakkman, Linda
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Tonkonogi, Michail
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Shabalina, Irina
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Rozhdestvenskaya, Z
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Mattsson, C. Mikael
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Enqvist, Jonas K
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Reduced efficiency, but increased fat oxidation, in mitochondria from human skeletal muscle after 24-h ultraendurance exercise.2007In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 102, no 5, p. 1844-1849Article in journal (Refereed)
    Abstract [en]

    The hypothesis that ultraendurance exercise influences muscle mitochondrial function has been investigated. Athletes in ultraendurance performance performed running, kayaking, and cycling at 60% of their peak O(2) consumption for 24 h. Muscle biopsies were taken preexercise (Pre-Ex), postexercise (Post-Ex), and after 28 h of recovery (Rec). Respiration was analyzed in isolated mitochondria during state 3 (coupled to ATP synthesis) and state 4 (noncoupled respiration), with fatty acids alone [palmitoyl carnitine (PC)] or together with pyruvate (Pyr). Electron transport chain activity was measured with NADH in permeabilized mitochondria. State 3 respiration with PC increased Post-Ex by 39 and 41% (P < 0.05) when related to mitochondrial protein and to electron transport chain activity, respectively. State 3 respiration with Pyr was not changed (P > 0.05). State 4 respiration with PC increased Post-Ex but was lower than Pre-Ex at Rec (P < 0.05 vs. Pre-Ex). Mitochondrial efficiency [amount of added ADP divided by oxygen consumed during state 3 (P/O ratio)] decreased Post-Ex by 9 and 6% (P < 0.05) with PC and PC + Pyr, respectively. P/O ratio remained reduced at Rec. Muscle uncoupling protein 3, measured with Western blotting, was not changed Post-Ex but tended to decrease at Rec (P = 0.07 vs. Pre-Ex). In conclusion, extreme endurance exercise decreases mitochondrial efficiency. This will increase oxygen demand and may partly explain the observed elevation in whole body oxygen consumption during standardized exercise (+13%). The increased mitochondrial capacity for PC oxidation indicates plasticity in substrate oxidation at the mitochondrial level, which may be of advantage during prolonged exercise.

  • 21.
    Fernström, Maria
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Mogensen, M
    Bagger, M
    Pedersen, PK
    The potential for mitochondrial fat oxidation in human skeletal muscle influences whole body fat oxidation during low-intensity exercise2007In: American journal of physiology. Endocrinology and metabolism, ISSN 0193-1849, Vol. 292, no 1, p. E223-30Article in journal (Refereed)
    Abstract [en]

    The purpose of this study was to investigate fatty acid (FA) oxidation in isolated mitochondrial vesicles (mit) and its relation to training status, fiber type composition, and whole body FA oxidation. Trained (Vo(2 peak) 60.7 +/- 1.6, n = 8) and untrained subjects (39.5 +/- 2.0 ml.min(-1).kg(-1), n = 5) cycled at 40, 80, and 120 W, and whole body relative FA oxidation was assessed from respiratory exchange ratio (RER). Mit were isolated from muscle biopsies, and maximal ADP stimulated respiration was measured with carbohydrate-derived substrate [pyruvate + malate (Pyr)] and FA-derived substrate [palmitoyl-l-carnitine + malate (PC)]. Fiber type composition was determined from analysis of myosin heavy-chain (MHC) composition. The rate of mit oxidation was lower with PC than with Pyr, and the ratio between PC and Pyr oxidation (MFO) varied greatly between subjects (49-93%). MFO was significantly correlated to muscle fiber type distribution, i.e., %MHC I (r = 0.62, P = 0.03), but was not different between trained (62 +/- 5%) and untrained subjects (72 +/- 2%). MFO was correlated to RER during submaximal exercise at 80 (r = -0.62, P = 0.02) and 120 W (r = -0.71, P = 0.007) and interpolated 35% Vo(2 peak) (r = -0.74, P = 0.004). ADP sensitivity of mit respiration was significantly higher with PC than with Pyr. It is concluded that MFO is influenced by fiber type composition but not by training status. The inverse correlation between RER and MFO implies that intrinsic mit characteristics are of importance for whole body FA oxidation during low-intensity exercise. The higher ADP sensitivity with PC than that with Pyr may influence fuel utilization at low rate of respiration.

  • 22.
    Fernström, Maria
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Shabalina, Irina
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Bakkman, Linda
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Tonkonogi, Michail
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Mattsson, C. Mikael
    Swedish School of Sport and Health Sciences, GIH.
    Enqvist, Jonas
    Swedish School of Sport and Health Sciences, GIH.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Skeletal muscle mitochondrial function and ROS production in response to extreme endurance exercise in athletes.2006In: 14 European bioenergetic conference, Moscow, Russia, 22-27 July, 2006, 2006Conference paper (Other academic)
    Abstract [en]

    Although it is well known that endurance exercise induces oxidative stress (1) there is no evidence of deteriorated mitochondrial function after 1-2 hours intensive exercise (2). However, the effects of extreme endurance exercise on mitochondrial function and mitochondrial ROS production have not been investigated previously. Nine healthy well-trained men (age 27.1 ± 0.87 (mean ± SE), BMI 24.2 ± 0.64 and VO2 peak 62.5 ± 1.78 ml/kg. min) performed 24 hours exercise, consisting of equal parts running, cycling and paddling. Muscle biopsies were taken from vastus lateralis pre-exercise (PreEx), immediately post-exercise (PostEx) and after 28 hours of recovery (PostEx-28). Mitochondria were isolated and mitochondrial respiration was analyzed with palmitoyl-carnitine (PC) and pyruvate (Pyr). Mitochondrial H2O2 release was measured with the Amplex Red-horseradish peroxide method. The reaction was initiated by addition of succinate with following addition of antimycin A (reversed electron flow). UCP3 protein expression, evaluated with western blot technique, was not changed by exercise. Both state 3 (Pyr and PC) and state 4 (PC) rates of oxygen consumption (estimated per maximal ETC-activity) were increased PostEx (+29%, +11% and +18%). State 3 remained elevated PostEx-28, whereas state 4 (Pyr) decreased below that at PreEx (-18%). Mitochondrial efficiency (P/O) decreased PostEx (Pyr -8.9%, PC -6.1%) and remained reduced PostEx-28. The relative substrate oxidation (state 3 PC/Pyr) increased after exercise PreEx: (0.71 ± 0.06 vs. PostEx (0.90 ±0.04) and (0.77 ±0.06) PostEx-28. Mitochondrial H2O2 release (succinate) increased dramatically after exercise (+189 ± 64%). Treatment with Antimycin A resulted in a twofold-increased rate of mitochondrial H2O2 release PreEx but a decreased rate in PostEx samples. The exercise-induced changes in mitochondrial ROS production was totally abolished PostEx-28. In conclusion extreme endurance exercise decreases mitochondrial efficiency and increases mitochondrial ROS production. Both of these changes would increase the oxygen demand during exercise. Relative fatty acid oxidation as measured in isolated mitochondria increased after exercise indicating that the capacity to oxidize fat is improved during prolonged exercise.

    1. Mastaloudis, A., S.W. Leonard, and M.G. Traber, Oxidative stress in athletes during extreme endurance exercise. Free Radic Biol Med, 2001. 31(7): p. 911-22.

    2. Tonkonogi, M., et al., Mitochondrial function and antioxidative defence in human muscle: effects of endurance training and oxidative stress. J Physiol, 2000. 528 Pt 2: p. 379-88.

  • 23.
    Fernström, Maria
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Tonkonogi, Michail
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Effects of acute and chronic endurance exercise on mitochondrial uncoupling in human skeletal muscle.2004In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 554, p. 755-763Article in journal (Refereed)
    Abstract [en]

    Mitochondrial proteins such as uncoupling protein 3 (UCP3) and adenine nucleotide translocase (ANT) may mediate back-leakage of protons and serve as uncouplers of oxidative phosphorylation. We hypothesized that UCP3 and ANT increase after prolonged exercise and/or endurance training, resulting in increased uncoupled respiration (UCR). Subjects were investigated with muscle biopsies before and after acute exercise (75 min of cycling at 70% of .VO2peak) or 6 weeks endurance training. Mitochondria were isolated and respiration measured in the absence (UCR or state 4) and presence of ADP (coupled respiration or state 3). Protein expression of UCP3 and ANT was measured with Western blotting. After endurance training, .VO2peak, citrate synthase activity (CS), state 3 respiration and ANT increased by 24, 47, 40 and 95%, respectively (all P < 0.05), whereas UCP3 remained unchanged. When expressed per unit of CS (a marker of mitochondrial volume) UCP3 and UCR decreased by 54% and 18%(P < 0.05). CS increased by 43% after acute exercise and remained elevated after 3 h of recovery (P < 0.05), whereas the other muscle parameters remained unchanged. An intriguing finding was that acute exercise reversibly enhanced the capacity of mitochondria to accumulate Ca2+(P < 0.05) before opening of permeability transition pores. In conclusion, UCP3 protein and UCR decrease after endurance training when related to mitochondrial volume. These changes may prevent excessive basal thermogenesis. Acute exercise enhances mitochondrial resistance to Ca2+ overload but does not influence UCR or protein expression of UCP3 and ANT. The increased Ca2+ resistance may prevent mitochondrial degradation and the mechanism needs to be further explored.

  • 24.
    Frank, Per
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll. Karolinska institutet, Inst för fysiologi och farmakologi.
    Exercise strategies to improve aerobic capacity, insulin sensitivity and mitochondrial biogenesis2014Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Regular exercise plays a key role in the maintenance of health and physical capabilities. Extensive research shows that exercise is an efficient method to prevent diabetes. Both resistance and aerobic exercise training are well known countermeasures for insulin resistance. However, depending on factors like purpose, capability and accessibility, different exercise modes need to be evaluated on both applied and molecular levels. In addition, exercise is the means to improve performance. New training strategies have emerged, like training with low glycogen stores or combining strength with endurance training, and guidelines based on empirical data are needed. Although knowledge of exercise physiology has advanced, much more needs to be learned before we can exploit the full potential of exercise with regard to health and performance. Therefore, the overall aim of this thesis is to provide knowledge of how different exercise strategies improve performance and insulin sensitivity. The mitochondria represent a central part of this thesis considering their key role in both health and performance. Study I was an acute crossover investigation of the effect of exercise with low glycogen levels on markers of mitochondrial biogenesis. Study II investigated the effect of concurrent resistance and endurance training on mitochondrial density and endurance performance. Study III investigated the acute effect of exercise on starvation-induced insulin resistance. In Study IV, the effect of resistance exercise training on health and performance in the elderly was investigated. The main findings were:

    • Training with low glycogen levels enhanced the response in markers of mitochondrial biogenesis.
    • Adding resistance training to endurance training did not improve mitochondrial density or endurance performance in trained individuals. 
    • Resistance training for only eight weeks is an efficient strategy to improve strength, heart rate (HR) during submaximal cycling and glucose tolerance in elderly. It also improves muscular quality by increasing mitochondrial and hypertrophy signaling proteins. 
    • Starvation-induced insulin resistance is attenuated by exercise. Mitochondrial respiration and reactive oxygen species (ROS) production is reduced during starvation. Exercise during starvation reduced glycogen stores and resulted in the activation of enzymes involved in glucose metabolism.
    • When exercise was performed during starvation there was an increase in markers for mitochondrial lipid oxidation.

    
In conclusion, training with low glycogen stores seems to be a promising strategy to increase mitochondrial density. In contrast to our previous acute findings, concurrent training had no effect on mitochondrial biogenesis or endurance performance. Exercise can reverse yet another mode of insulin resistance (starvation) which strengthens its role in the treatment for other states of insulin resistance, e.g. Type 2 diabetes (T2D). Resistance exercise training is an efficient and safe strategy for the elderly to improve health and performance.

  • 25.
    Frank, Per
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Andersson, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Pontén, Marjan
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's and Mats Börjesson's research group.
    Ekblom, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Strength training improves muscle aerobic capacity and glucose tolerance in elderly2016In: Scandinavian Journal of Medicine and Science in Sports, ISSN 0905-7188, E-ISSN 1600-0838, Vol. 26, no 7, p. 764-773Article in journal (Refereed)
    Abstract [en]

    The primary aim of this study was to investigate the effect of short-term resistance training (RET) on mitochondrial protein content and glucose tolerance in elderly. Elderly women and men (age 71 ± 1, mean ± SEM) were assigned to a group performing 8 weeks of resistance training (RET, n = 12) or no training (CON, n = 9). The RET group increased in (i) knee extensor strength (concentric +11 ± 3%, eccentric +8 ± 3% and static +12 ± 3%), (ii) initial (0-30 ms) rate of force development (+52 ± 26%) and (iii) contents of proteins related to signaling of muscle protein synthesis (Akt +69 ± 20 and mammalian target of rapamycin +69 ± 32%). Muscle fiber type composition changed to a more oxidative profile in RET with increased amount of type IIa fibers (+26.9 ± 6.8%) and a trend for decreased amount of type IIx fibers (-16.4 ± 18.2%, P = 0.068). Mitochondrial proteins (OXPHOS complex II, IV, and citrate synthase) increased in RET by +30 ± 11%, +99 ± 31% and +29 ± 8%, respectively. RET resulted in improved oral glucose tolerance measured as reduced area under curve for glucose (-21 ± 26%) and reduced plasma glucose 2 h post-glucose intake (-14 ± 5%). In CON parameters were unchanged or impaired. In conclusion, short-term resistance training in elderly not only improves muscular strength, but results in robust increases in several parameters related to muscle aerobic capacity.

  • 26.
    Frank, Per
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Katz, Abram
    Institutionen för Fysiologi och Farmakologi, Karolinska Institutet.
    Andersson, Eva
    Swedish School of Sport and Health Sciences, GIH.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Acute exercise during starvation improves insulin sensitivity and increases mitochondrial FA oxidation2012Conference paper (Other academic)
    Abstract [en]

    Aim: To investigate if exercise can reverse starvation-induced insulin resistance and to elucidate the mechanism. Methods: Nine subjects underwent 87 h of starvation with (EX) or without (NE) one exercise session at the end. Before and after starvation (3 h post-exercise) subjects underwent an intravenous glucose tolerance test and muscle biopsy. Results: Insulin sensitivity decreased after starvation (NE) but increased after exercise (EX). Glycogen stores were reduced and plasma FA and β-Hydroxybutyrate increased in both conditions. Mitochondrial respiration with FA substrate increased in EX but was unchanged in NE. RCR and mitochondrial ROS production decreased in both conditions. Phosphorylation of Acetyl-CoA carboxylase (ACC) and Akt substrate of 160 kDA (AS160) proteins increased in EX. Conclusion: Exercise improves starvation induced insulin resistance, probably by increased mitochondrial FA oxidation, reduced glycogen stores and alterations in signaling proteins involved in glucose uptake and FA metabolism.

  • 27.
    Frank, Per
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Katz, Abram
    Karolinska Institutet.
    Andersson, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Acute exercise reverses starvation-mediated insulin resistance in humans.2013In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 304, no 4, p. E436-43Article in journal (Refereed)
    Abstract [en]

    Within 2-3 days of starvation, pronounced insulin resistance develops, possibly mediated by increased lipid load. Here, we show that one exercise bout increases mitochondrial fatty acid (FA) oxidation and reverses starvation-induced insulin resistance. Nine healthy subjects underwent 75-h starvation on two occasions: with no exercise (NE) or with one exercise session at the end of the starvation period (EX). Muscle biopsies were analyzed for mitochondrial function, contents of glycogen, and phosphorylation of regulatory proteins. Glucose tolerance and insulin sensitivity, measured with an intravenous glucose tolerance test (IVGTT), were impaired after starvation, but in EX the response was attenuated or abolished. Glycogen stores were reduced, and plasma FA was increased in both conditions, with a more pronounced effect in EX. After starvation, mitochondrial respiration decreased with complex I substrate (NE and EX), but in EX there was an increased respiration with complex I + II substrate. EX altered regulatory proteins associated with increases in glucose disposal (decreased phosphorylation of glycogen synthase), glucose transport (increased phosphorylation of Akt substrate of 160 kDa), and FA oxidation (increased phosphorylation of acetyl-CoA carboxylase). In conclusion, exercise reversed starvation-induced insulin resistance and was accompanied by reduced glycogen stores, increased lipid oxidation capacity, and activation of signaling proteins involved in glucose transport and FA metabolism.

  • 28.
    Gejl, Kasper Degn
    et al.
    University of Southern Denmark.
    Thams, Line
    University of Southern Denmark.
    Hansen, Mette
    Aarhus University, Aarhus, Denmark.
    Rokkedal-Lausch, Torben
    Aalborg University, Aalborg, Denmark.
    Plomgaard, Peter
    Rigshospitalet, Copenhagen, Denmark.
    Nybo, Lars
    University of Copenhagen, Copenhagen Denmark.
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll. Karolinska Institute.
    Cardinale, Daniele A
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Jensen, Kurt
    University of Southern Denmark.
    Holmberg, Hans-Christer
    Mid Sweden University, Östersund, Sweden.
    Vissing, Kristian
    Aarhus University, Aarhus, Denmark.
    Ørtenblad, Niels
    University of Southern Denmark.
    No Superior Adaptations to Carbohydrate Periodization in Elite Endurance Athletes.2017In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 49, no 12, p. 2486-2497Article in journal (Refereed)
    Abstract [en]

    PURPOSE: The present study investigated the effects of periodic CHO restriction on endurance performance and metabolic markers in elite endurance athletes.

    METHODS: Twenty-six male elite endurance athletes (VO2max: 65.0 ml O2[BULLET OPERATOR]kg[BULLET OPERATOR]min) completed 4 weeks of regular endurance training, while matched and randomized into two groups training with (Low) or without (High) carbohydrate (CHO) manipulation three days a week. The CHO manipulation days consisted of a 1-hr high intensity bike session in the morning, recovery for 7 hrs while consuming isocaloric diets containing either high CHO (414±2.4 g) or low CHO (79.5±1.0 g), and a 2-hr moderate bike session in the afternoon with or without CHO. VO2max, maximal fat oxidation and power output during a 30-min time trial (TT) were determined before and after the training period. The TT was undertaken after 90 mins of intermittent exercise with CHO provision before the training period and both CHO and placebo after the training period. Muscle biopsies were analyzed for glycogen, citrate synthase (CS) and β-hydroxyacyl-coenzyme A dehydrogenase (HAD) activity, carnitine palmitoyltransferase (CPT1b) and phosphorylated acetyl-CoA carboxylase (pACC).

    RESULTS: The training effects were similar in both groups for all parameters. On average, VO2max and power output during the 30-min TT increased by 5 ± 1% (P<0.05) and TT performance was similar after CHO and placebo during the preload phase. Training promoted overall increases in glycogen content (18 ± 5%), CS activity (11 ± 5%) and pACC (38 ± 19%) (P<0.05) with no differences between groups. HAD activity and CPT1b protein content remained unchanged.

    CONCLUSION: Superimposing periodic CHO restriction to 4 weeks of regular endurance training had no superior effects on performance and muscle adaptations in elite endurance athletes.

  • 29. Gejl, Kasper
    et al.
    Hvid, Lars G
    Frandsen, Ulrik
    Jensen, Kurt
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Ortenblad, Niels
    Muscle Glycogen Content Modifies SR Ca2 + Release Rate in Elite Endurance Athletes.2014In: Medicine & Science in Sports & Exercise, ISSN 0195-9131, E-ISSN 1530-0315, Vol. 46, no 3, p. 496-505Article in journal (Refereed)
    Abstract [en]

    PURPOSE: The aim of the present study was to investigate the influence of muscle glycogen content on sarcoplasmic reticulum (SR) function and peak power output (Wpeak) in elite endurance athletes.

    METHODS: Fourteen highly trained male triathletes (VO2max 66.5 ± 1.3 ml O2 kg min), performed 4h of glycogen depleting cycling exercise (HRmean 73 ± 1% of maximum). During the first 4h recovery, athletes received either water (H2O) or carbohydrate (CHO), separating alterations in muscle glycogen content from acute changes affecting SR function and performance. Thereafter, all subjects received CHO enriched food for the remaining 20h recovery.

    RESULTS: Immediately following exercise, muscle glycogen content and SR Ca release rate was reduced to 32 ± 4% (225 ± 28 mmol kg dw) and 86 ± 2% of initial levels, respectively (P < 0.01). Glycogen markedly recovered after 4h recovery with CHO (61 ± 2% of pre) and SR Ca release rate returned to pre-exercise level. However, in the absence of CHO during the first 4h recovery, glycogen and SR Ca release rate remained depressed, with normalization of both parameters at the end of the 24h recovery after receiving a CHO enriched diet. Linear regression demonstrated a significant correlation between SR Ca release rate and muscle glycogen content (P < 0.01, r = 0.30). The 4h cycling exercise reduced Wpeak by 5.5-8.9% at different cadences (P < 0.05) and Wpeak was normalized after 4h recovery with CHO whereas Wpeak remained depressed (P < 0.05) following water provision. Wpeak was fully recovered after 24h in both the H2O and the CHO group.

    CONCLUSION: In conclusion, the present results suggest that low muscle glycogen depresses muscle SR Ca release rate, which may contribute to fatigue and delayed recovery of Wpeak 4 hours post exercise.

  • 30. Gullstrand, Lennart
    et al.
    Lindberg, Thomas
    Cardinale, Daniele
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Tarassova, Olga
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Bjerkefors, Anna
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Validation of a kayak ergometer power output2013Conference paper (Refereed)
    Abstract [en]

    Introduction

    It is of a significant interest that ergometers used for evaluating elite athletes are valid and reliable. In this study the aim was to investigate how well displayed power output on a widely used kayak ergometer, DS, (Dansprint ApS, DK) related to a validation setup. Previously Gore et al. (2013) described the accuracy of 12 of the same ergometer using a motor driven calibration rig simulating power between 50 up to 450 W. They found that the ergometers underestimated true mean power with 21-23%. The reference rig simulated a 1 dimensional (1D) movement; this study however, is based on 3D analysis, which was hypothesized to better describe real paddling movement’s and allow more precise power calculations.

    Methods

    Two male national team kayakers took part in the study performing workloads from 70 up to 500 W (+30 W/stage) two times with 3 days between the measurement sessions. They were instructed to target the desired workloads displayed during 35 s bouts. The reference method included a ProReflex optoelectronic system (Qualisys AB, Gothenburg, Sweden) and force transducers (LCM 200, Futek Inc, Ca, US). The force transducers were connected with the rope from ergometer flywheel close to each end of the ergometer paddle to continuously measure force during the bouts of work. The kinematic set-up included eight cameras placed around the ergometer and two reflective markers were attached close to each force transducer.

    Results

    The reference method used here showed that the validated ergometer underestimated power with 37.7 % over the whole measured range compared to the reference method. The difference was systematic (r2=0.989) and the linear regression model could be applied (DS power = -2.362+0.628*x). When applying a 1D analysis of the collected data, it coincided with the results from Gore et al. (2013).

    Discussion

    The data suggest that 1. The measurement solution and/or calculation for describing power output in the DS have limitations. 2. The testing rig referred to in the Introduction (Gore et al. 2013) do not fully estimate true power and 3. The reference method used here is suggested to more exactly represent true paddling power as it includes a 3D movement analysis and close to original paddling simulation set-up. Both reference methods (1D and 3D analysis) show linear differences vs. the DS ergometer, giving an option to adjust the displayed power to a true power produced by elite-athletes.

  • 31. Hey-Mogensen, M
    et al.
    Højlund, K
    Vind, B F
    Wang, Li
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Dela, F
    Beck-Nielsen, H
    Fernström, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Effect of physical training on mitochondrial respiration and reactive oxygen species release in skeletal muscle in patients with obesity and type 2 diabetes.2010In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 53, no 9, p. 1976-85Article in journal (Refereed)
    Abstract [en]

    AIM/HYPOTHESIS: Studies have suggested a link between insulin resistance and mitochondrial dysfunction in skeletal muscles. Our primary aim was to investigate the effect of aerobic training on mitochondrial respiration and mitochondrial reactive oxygen species (ROS) release in skeletal muscle of obese participants with and without type 2 diabetes. METHODS: Type 2 diabetic men (n = 13) and control (n = 14) participants matched for age, BMI and physical activity completed 10 weeks of aerobic training. Pre- and post-training muscle biopsies were obtained before a euglycaemic-hyperinsulinaemic clamp and used for measurement of respiratory function and ROS release in isolated mitochondria. RESULTS: Training significantly increased insulin sensitivity, maximal oxygen consumption and muscle mitochondrial respiration with no difference between groups. When expressed in relation to a marker of mitochondrial density (intrinsic mitochondrial respiration), training resulted in increased mitochondrial ADP-stimulated respiration (with NADH-generating substrates) and decreased respiration without ADP. Intrinsic mitochondrial respiration was not different between groups despite lower insulin sensitivity in type 2 diabetic participants. Mitochondrial ROS release tended to be higher in participants with type 2 diabetes. CONCLUSIONS/INTERPRETATION: Aerobic training improves muscle respiration and intrinsic mitochondrial respiration in untrained obese participants with and without type 2 diabetes. These adaptations demonstrate an increased metabolic fitness, but do not seem to be directly related to training-induced changes in insulin sensitivity.

  • 32. Iaia, F Marcello
    et al.
    Hellsten, Ylva
    Nielsen, Jens Jung
    Fernström, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Bangsbo, Jens
    Four weeks of speed endurance training reduces energy expenditure during exercise and maintains muscle oxidative capacity despite a reduction in training volume.2009In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 106, no 1, p. 73-80Article in journal (Refereed)
    Abstract [en]

    We studied the effect of an alteration from regular endurance to speed endurance training on muscle oxidative capacity, capillarization, as well as energy expenditure during submaximal exercise and its relationship to mitochondrial uncoupling protein 3 (UCP3) in humans. Seventeen endurance-trained runners were assigned to either a speed endurance training (SET; n = 9) or a control (Con; n = 8) group. For a 4-wk intervention (IT) period, SET replaced the ordinary training ( approximately 45 km/wk) with frequent high-intensity sessions each consisting of 8-12 30-s sprint runs separated by 3 min of rest (5.7 +/- 0.1 km/wk) with additional 9.9 +/- 0.3 km/wk at low running speed, whereas Con continued the endurance training. After the IT period, oxygen uptake was 6.6, 7.6, 5.7, and 6.4% lower (P < 0.05) at running speeds of 11, 13, 14.5, and 16 km/h, respectively, in SET, whereas remained the same in Con. No changes in blood lactate during submaximal running were observed. After the IT period, the protein expression of skeletal muscle UCP3 tended to be higher in SET (34 +/- 6 vs. 47 +/- 7 arbitrary units; P = 0.06). Activity of muscle citrate synthase and 3-hydroxyacyl-CoA dehydrogenase, as well as maximal oxygen uptake and 10-km performance time, remained unaltered in both groups. In SET, the capillary-to-fiber ratio was the same before and after the IT period. The present study showed that speed endurance training reduces energy expenditure during submaximal exercise, which is not mediated by lowered mitochondrial UCP3 expression. Furthermore, speed endurance training can maintain muscle oxidative capacity, capillarization, and endurance performance in already trained individuals despite significant reduction in the amount of training.

  • 33. Jensen, Line
    et al.
    Gejl, Kasper D
    Ørtenblad, Niels
    Nielsen, Jakob L
    Bech, Rune D
    Nygaard, Tobias
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Frandsen, Ulrik
    Carbohydrate restricted recovery from long term endurance exercise does not affect gene responses involved in mitochondrial biogenesis in highly trained athletes.2015In: Physiological Reports, E-ISSN 2051-817X, Vol. 3, no 2Article in journal (Refereed)
    Abstract [en]

    The aim was to determine if the metabolic adaptations, particularly PGC-1α and downstream metabolic genes were affected by restricting CHO following an endurance exercise bout in trained endurance athletes. A second aim was to compare baseline expression level of these genes to untrained. Elite endurance athletes (VO2max 66 ± 2 mL·kg(-1)·min(-1), n = 15) completed 4 h cycling at ~56% VO2max. During the first 4 h recovery subjects were provided with either CHO or only H2O and thereafter both groups received CHO. Muscle biopsies were collected before, after, and 4 and 24 h after exercise. Also, resting biopsies were collected from untrained subjects (n = 8). Exercise decreased glycogen by 67.7 ± 4.0% (from 699 ± 26.1 to 239 ± 29.5 mmol·kg(-1)·dw(-1)) with no difference between groups. Whereas 4 h of recovery with CHO partly replenished glycogen, the H2O group remained at post exercise level; nevertheless, the gene expression was not different between groups. Glycogen and most gene expression levels returned to baseline by 24 h in both CHO and H2O. Baseline mRNA expression of NRF-1, COX-IV, GLUT4 and PPAR-α gene targets were higher in trained compared to untrained. Additionally, the proportion of type I muscle fibers positively correlated with baseline mRNA for PGC-1α, TFAM, NRF-1, COX-IV, PPAR-α, and GLUT4 for both trained and untrained. CHO restriction during recovery from glycogen depleting exercise does not improve the mRNA response of markers of mitochondrial biogenesis. Further, baseline gene expression of key metabolic pathways is higher in trained than untrained.

  • 34. Jeppesen, Jacob
    et al.
    Mogensen, Martin
    Prats, Clara
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Madsen, Klavs
    Kiens, Bente
    Copenhagen University.
    FAT/CD36 is localized in sarcolemma and in vesicle-like structures in subsarcolemma regions but not in mitochondria.2010In: Journal of Lipid Research, ISSN 0022-2275, E-ISSN 1539-7262, Vol. 51, no 6, p. 1504-12Article in journal (Refereed)
    Abstract [en]

    The primary aim of the present study was to investigate in which cellular compartments fatty acid trans-locase CD36 (FAT/CD36) is localized. Intact and fully functional skeletal muscle mitochondria were isolated from lean and obese female Zucker rats and from 10 healthy male individuals. FAT/CD36 could not be detected in the isolated mitochondria, whereas the mitochondrial marker F(1)ATPase-beta was clearly detected using immunoblotting. Lack of markers for other membrane structures indicated that the mitochondria were not contaminated with membranes known to contain FAT/CD36. In addition, fluorescence immunocytochemistry was performed on single muscle fibers dissected from soleus muscle of lean and obese Zucker rats and from the vastus lateralis muscle from humans. Costaining against FAT/CD36 and MitoNEET clearly show that FAT/CD36 is highly present in sarcolemma and it also associates with some vesicle-like intracellular compartments. However, FAT/CD36 protein was not detected in mitochondrial membranes, supporting the biochemical findings. Based on the presented data, FAT/CD36 seems to be abundantly expressed in sarcolemma and in vesicle-like structures throughout the muscle cell. However, FAT/CD36 is not present in mitochondria in rat or human skeletal muscle. Thus, the functional role of FAT/CD36 in lipid transport seems primarily to be allocated to the plasma membrane in skeletal muscle.

  • 35.
    Larsen, Filip
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Mitochondrial oxygen affinity predicts basal metabolic rate in humans2011In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 25, no 8, p. 2843-52Article in journal (Refereed)
    Abstract [en]

    The basal metabolic rate (BMR) is referred to as the minimal rate of metabolism required to support basic body functions. It is well known that individual BMR varies greatly, even when correcting for body weight, fat content, and thyroid hormone levels, but the mechanistic determinants of this phenomenon remain unknown. Here, we show in humans that mass-related BMR correlates strongly to the mitochondrial oxygen affinity (p50(mito); R(2)=0.66, P=0.0004) measured in isolated skeletal muscle mitochondria. A similar relationship was found for oxygen affinity and efficiency during constant-load submaximal exercise (R(2)=0.46, P=0.007). In contrast, BMR did not correlate to overall mitochondrial density or to proton leak. Mechanistically, part of the p50(mito) seems to be controlled by the excess of cytochrome c oxidase (COX) protein and activity relative to other mitochondrial proteins. This is illustrated by the 5-fold increase in p50(mito) after partial cyanide inhibition of COX at doses that do not affect maximal mitochondrial electron flux through the ETS. These data suggest that the interindividual variation in BMR in humans is primarily explained by differences in mitochondrial oxygen affinity. The implications of these findings are discussed in terms of a trade-off between aerobic efficiency and power.

  • 36.
    Larsen, Filip J
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Schiffer, Tomas A
    Ørtenblad, Niels
    Zinner, Christoph
    Morales-Alamo, David
    Willis, Sarah J
    Calbet, Jose A
    Holmberg, Hans-Christer
    Boushel, Robert
    High-intensity sprint training inhibits mitochondrial respiration through aconitase inactivation.2016In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 30, no 1, p. 417-427Article in journal (Refereed)
    Abstract [en]

    Intense exercise training is a powerful stimulus that activates mitochondrial biogenesis pathways and thus increases mitochondrial density and oxidative capacity. Moderate levels of reactive oxygen species (ROS) during exercise are considered vital in the adaptive response, but high ROS production is a serious threat to cellular homeostasis. Although biochemical markers of the transition from adaptive to maladaptive ROS stress are lacking, it is likely mediated by redox sensitive enzymes involved in oxidative metabolism. One potential enzyme mediating such redox sensitivity is the citric acid cycle enzyme aconitase. In this study, we examined biopsy specimens of vastus lateralis and triceps brachii in healthy volunteers, together with primary human myotubes. An intense exercise regimen inactivated aconitase by 55-72%, resulting in inhibition of mitochondrial respiration by 50-65%. In the vastus, the mitochondrial dysfunction was compensated for by a 15-72% increase in mitochondrial proteins, whereas H2O2 emission was unchanged. In parallel with the inactivation of aconitase, the intermediary metabolite citrate accumulated and played an integral part in cellular protection against oxidative stress. In contrast, the triceps failed to increase mitochondrial density, and citrate did not accumulate. Instead, mitochondrial H2O2 emission was decreased to 40% of the pretraining levels, together with a 6-fold increase in protein abundance of catalase. In this study, a novel mitochondrial stress response was highlighted where accumulation of citrate acted to preserve the redox status of the cell during periods of intense exercise.-Larsen, F. J., Schiffer, T. A., Ørtenblad, N., Zinner, C., Morales-Alamo, D., Willis, S. J., Calbet, J. A., Holmberg, H.-C., Boushel, R. High-intensity sprint training inhibits mitochondrial respiration through aconitase inactivation.

  • 37.
    Larsen, Filip
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Schiffer, TA
    Borniquel, S
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Lundberg, JO
    Weitzberg, E
    Dietary inorganic nitrate improves mitochondrial efficiency in humans.2011In: Cell Metabolism, ISSN 1550-4131, Vol. 13, no 2, p. 149-159Article in journal (Refereed)
    Abstract [en]

    Nitrate, an inorganic anion abundant in vegetables, is converted in vivo to bioactive nitrogen oxides including NO. We recently demonstrated that dietary nitrate reduces oxygen cost during physical exercise, but the mechanism remains unknown. In a double-blind crossover trial we studied the effects of a dietary intervention with inorganic nitrate on basal mitochondrial function and whole-body oxygen consumption in healthy volunteers. Skeletal muscle mitochondria harvested after nitrate supplementation displayed an improvement in oxidative phosphorylation efficiency (P/O ratio) and a decrease in state 4 respiration with and without atractyloside and respiration without adenylates. The improved mitochondrial P/O ratio correlated to the reduction in oxygen cost during exercise. Mechanistically, nitrate reduced the expression of ATP/ADP translocase, a protein involved in proton conductance. We conclude that dietary nitrate has profound effects on basal mitochondrial function. These findings may have implications for exercise physiology- and lifestyle-related disorders that involve dysfunctional mitochondria.

  • 38.
    Manselin, Tom A
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Södergård, Olof
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Lindholm, Peter
    Karolinska institutet.
    Aerobic efficiency is associated with the improvement in maximal power output during acute hyperoxia.2017In: Physiological Reports, E-ISSN 2051-817X, Vol. 5, no 2, article id e13119Article in journal (Refereed)
    Abstract [en]

    This study investigated the relationship between aerobic efficiency during cycling exercise and the increase in physical performance with acute hyperoxic exposure (FiO2 ~31%) (HOX) and also tested the hypothesis that fat oxidation could be increased by acute hyperoxia. Fourteen males and four females were recruited for two sessions, where they exercised for 2 × 10 min at 100 W to determine efficiency. HOX and normoxia (NOX) were administered randomly on both occasions to account for differences in nitrogen exchange. Thereafter, a progressive ramp test was performed to determine VO2max and maximal power output (Wmax). After 30 min rest, workload was set to 80% of maximal power output (Wmax) for a time to exhaustion test (TTE). At 100W gross efficiency was reduced from 19.4% during NOX to 18.9% during HOX (P ≤ 0.0001). HOX increased fat oxidation at 100 W by 52% from 3.41 kcal min(-1) to 5.17 kcal min(-1) (P ≤ 0.0001) with a corresponding reduction in carbohydrate oxidation. Wmax increased by 2.4% from 388.8 (±82.1) during NOX to 397.8 (±83.5) during HOX (P ≤ 0.0001). SaO2 was higher in HOX both at the end of the maximal exercise test and TTE. Subjects with a high level of efficiency in NOX had a larger improvement in Wmax with HOX, in agreement with the hypothesis that an optimum level of efficiency exists that maximizes power production. No association between mitochondrial excess capacity and endurance performance was found; increases in oxygen supply seemed to increase maximal aerobic power production and maintain/increase endurance capacity at the same relative workload.

  • 39.
    Mattsson, C. Mikael
    et al.
    Swedish School of Sport and Health Sciences, GIH.
    Enqvist, Jonas
    Swedish School of Sport and Health Sciences, GIH.
    Brink-Elfegoun, Thibault
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Johansson, Patrik
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Bakkman, Linda
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Unexpected cardiovascular response during ultra-endurance exercise.2008In: 13th Annual Congress of the European College of Sport Science (ECSS), Estoril, Lissabon, Portugal.: Sport Science by the sea, 2008, p. 142-Conference paper (Other academic)
    Abstract [en]

    During prolonged exercise at fixed work rate heart rate (HR) increases slowly with concomitant decrease in stroke volume (SV) in order to maintain cardiac output. Simultaneously, an increased oxygen uptake (VO2) occurs. In this paper we report an unexpected and previously not observed cardiovascular response to ultra-endurance exercise. Nine well-trained male athletes performed 24-h exercise in a controlled laboratory setting, with altering blocks of kayaking, running and cycling. Each block consisted of 110 min of exercise and 10 min of rest. Measurements (HR, VO2 and blood samples) were conducted during cycling at fixed work rate every 6th hour. The average work intensity was approximately 55 % of respective VO2peak. HR was increased at 6 h with 15 beats/min (13 %) compared to pre-exercise (Pre-Ex), but thereafter unexpectedly returned towards initial values. VO2 on the other hand was increased with 0.22 l/min (10 %) at 6 h and 0.37 l/min (17 %) at 12 h compared to Pre-Ex, and thereafter remained stable. This implies an increased oxygen pulse (VO2/HR) with approximately 10 % compared to Pre-Ex at the later half of the exercise. The cardiovascular drift did not progress continuously, but instead changed drastically when duration exceeded 6 hours. The changes in HR and VO2 might have different and complex explanations. HR drift might be explained mainly by central circulatory adaptation (e.g. desensitisation of cardiac adrenergic receptors) whereas drift in VO2 may depend upon peripheral changes (e.g. decreased mitochondrial efficiency). Consequently, using solely HR for determining exercise intensity and energy expenditure becomes invalid during ultra-endurance exercise, if the cardiovascular drift is not measured and taken into account.

     

  • 40.
    Mijwel, Sara
    et al.
    Karolinska Institutet.
    Cardinale, Daniele A.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Norrbom, Jessica
    Karolinska Institutet.
    Chapman, Mark
    Karolinska Institutet.
    Ivarsson, Niklas
    Karolinska Institutet.
    Wengström, Yvonne
    Karolinska Institutet.
    Sundberg, Carl Johan
    Karolinska Institutet.
    Rundqvist, Helene
    Karolinska Institutet.
    Exercise training during chemotherapy preserves skeletal muscle fiber area, capillarization, and mitochondrial content in patients with breast cancer.2018In: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 32, no 10, p. 5495-5505, article id fj201700968RArticle in journal (Refereed)
    Abstract [en]

    Exercise has been suggested to ameliorate the detrimental effects of chemotherapy on skeletal muscle. The aim of this study was to compare the effects of different exercise regimens with usual care on skeletal muscle morphology and mitochondrial markers in patients being treated with chemotherapy for breast cancer. Specifically, we compared moderate-intensity aerobic training combined with high-intensity interval training (AT-HIIT) and resistance training combined with high-intensity interval training (RT-HIIT) with usual care (UC). Resting skeletal muscle biopsies were obtained pre- and postintervention from 23 randomly selected women from the OptiTrain breast cancer trial who underwent RT-HIIT, AT-HIIT, or UC for 16 wk. Over the intervention, citrate synthase activity, muscle fiber cross-sectional area, capillaries per fiber, and myosin heavy chain isoform type I were reduced in UC, whereas RT-HIIT and AT-HIIT were able to counteract these declines. AT-HIIT promoted up-regulation of the electron transport chain protein levels vs. UC. RT-HIIT favored satellite cell count vs. UC and AT-HIIT. There was a significant association between change in citrate synthase activity and self-reported fatigue. AT-HIIT and RT-HIIT maintained or improved markers of skeletal muscle function compared with the declines found in the UC group, indicating a sustained trainability in addition to the preservation of skeletal muscle structural and metabolic characteristics during chemotherapy. These findings highlight the importance of supervised exercise programs for patients with breast cancer during chemotherapy.-Mijwel, S., Cardinale, D. A., Norrbom, J., Chapman, M., Ivarsson, N., Wengström, Y., Sundberg, C. J., Rundqvist, H. Exercise training during chemotherapy preserves skeletal muscle fiber area, capillarization, and mitochondrial content in patients with breast cancer.

  • 41. Mijwel, Sara
    et al.
    Cardinale, Daniele
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Ekblom-Bak, Elin
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Sundberg, Carl Johan
    Wengström, Yvonne
    Rundqvist, Helene
    Validation of 2 Submaximal Cardiorespiratory Fitness Tests in Patients With Breast Cancer Undergoing Chemotherapy.2016In: Rehabilitation oncology (American Physical Therapy Association. Oncology Section), ISSN 2168-3808, Vol. 34, no 4, p. 137-143Article in journal (Refereed)
    Abstract [en]

    Patients with breast cancer have an impaired cardiorespiratory fitness, in part, due to the toxic effects of anticancer therapy. Physical exercise as a means of rehabilitation for patients with cancer is an emerging area of research and treatment, emphasizing the need for accurate and feasible physical capacity measurements. The purpose of this study was to evaluate the validity of peak oxygen consumption (o2peak) predicted by the Ekblom-Bak test (E-B) and the Åstrand-Rhyming prediction model (A-R).

    METHODS: Eight patients with breast cancer undergoing chemotherapy participated in the study. Submaximal exercise tests were performed at 2 different submaximal workloads. Estimated o2peak values were obtained by inserting the heart rate (HR) from the 2 workloads into the E-B prediction model and the HR of only the higher workload into the Åstrand nomogram. A 20-W incremental cycle test-to-peak effort was performed to obtain o2peak values.

    RESULTS: Results from A-R overestimated o2peak by 6% (coefficient of variation = 7%), whereas results from E-B overestimated o2peak with 42% (coefficient of variation = 21%) compared with measured o2peak. Pearson's correlation coefficient revealed a significant strong relationship between the estimated o2peak from A-R and the measured o2peak (r = 0.86; P < .05), whereas the relationship between the estimated o2peak from E-B and the measured o2peak resulted in a nonsignificant weak correlation (r = 0.21).

    CONCLUSION: In a situation where maximal exercise testing is not practical or undesirable from a patient safety perspective, submaximal exercise testing provides an alternative way of estimating o2peak. The A-R prediction model appears to be a valid submaximal exercise test for determining cardiorespiratory fitness in this population.

  • 42.
    Moberg, Marcus
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Hendo, Gina
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Jakobsson, Madelene
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Mattsson, C Mikael
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Ekblom-Bak, Elin
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Flockhart, Mikael
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Pontén, Marjan
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Söderlund, Karin
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Increased autophagy signaling but not proteasome activity in human skeletal muscle after prolonged low-intensity exercise with negative energy balance2017In: Physiological Reports, E-ISSN 2051-817X, Vol. 5, no 23, article id e13518Article in journal (Refereed)
    Abstract [en]

    Little is known about the molecular regulation of skeletal muscle protein turnover during exercise in field conditions where energy is intake inadequate. Here, 17 male and 7 female soldiers performed an 8 day long field based military operation. Vastus lateralis muscle biopsies, in which autophagy, the ubiquitin-proteasome system and the mTORC1 signaling pathway where studied, were collected before and after the operation. The 187 h long operation resulted in a 15% and 29% negative energy balance as well as a 4.1% and 4.6% loss of body mass in women and men respectively. After the operation protein levels of ULK1 as well as the phosphorylation of ULK1Ser317 and ULK1Ser555 had increased by 11%, 39% and 13%, respectively, and this was supported by a 17% increased phosphorylation of AMPKThr172 (P<0.05). The LC3b-I/II ratio was 3-fold higher after compared to before the operation (P<0.05), whereas protein levels of p62/SQSTM1 were unchanged. The β1, β2, and β5 activity of the proteasome and protein levels of MAFbx did not change, while levels of MuRF-1 were slightly reduced (6%, P<0.05). Protein levels and phosphorylation status of key components in the mTORC1 signaling pathway remained at basal levels after the operation. Muscle levels of glycogen decreased from 269±12 to 181±9 mmol ∙ kg dry muscle-1 after the exercise period (P<0.05). In conclusion, the 8 days of field based exercise resulted in induction of autophagy without any increase in proteasome activity or protein ubiquitination. Simultaneously, the regulation of protein synthesis through the mTORC1 signaling pathway was maintained.

  • 43. Mogensen, M
    et al.
    Vind, B F
    Højlund, K
    Beck-Nielsen, H
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Maximal lipid oxidation in patients with type 2 diabetes is normal and shows an adequate increase in response to aerobic training.2009In: Diabetes, obesity and metabolism, ISSN 1462-8902, E-ISSN 1463-1326, Vol. 11, no 9, p. 874-83Article in journal (Refereed)
    Abstract [en]

    AIM: Insulin resistance in subjects with type 2 diabetes (T2D) and obesity is associated with an imbalance between the availability and the oxidation of lipids. We hypothesized that maximal whole-body lipid oxidation during exercise (FATmax) is reduced and that training-induced metabolic adaptation is attenuated in T2D. METHODS: Obese T2D (n = 12) and control (n = 11) subjects matched for age, sex, physical activity and body mass index completed 10 weeks of aerobic training. Subjects were investigated before and after training with maximal and submaximal exercise tests and euglycaemic-hyperinsulinaemic clamps combined with muscle biopsies. RESULTS: Training increased maximal oxygen consumption (VO(2max)) and muscle citrate synthase activity and decreased blood lactate concentrations during submaximal exercise in both groups (all p < 0.01). FATmax increased markedly (40-50%) in both T2D and control subjects after training (all p < 0.001). There were no significant differences in these variables and lactate threshold (%VO(2max)) between groups before or after training. Insulin-stimulated glucose disappearance rate (Rd) was lower in T2D vs. control subjects both before and after training. Rd increased in response to training in both groups (all p < 0.01). There was no correlation between Rd and measures of oxidative capacity or lipid oxidation during exercise or the training-induced changes in these parameters. CONCLUSIONS: FATmax was not reduced in T2D, and muscle oxidative capacity increased adequately in response to aerobic training in obese subjects with and without T2D. These metabolic adaptations to training seem to be unrelated to changes in insulin sensitivity and indicate that an impaired capacity for lipid oxidation is not a major cause of insulin resistance in T2D.

  • 44. Mogensen, Martin
    et al.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Mitochondrial efficiency in rat skeletal muscle: influence of respiration rate, substrate and muscle type.2006In: Acta Physiologica Scandinavica, ISSN 0001-6772, E-ISSN 1365-201X, Vol. 185, p. 229-236Article in journal (Refereed)
    Abstract [en]

    Aim: To investigate the hypothesis that mitochondrial efficiency (i.e. P/O ratio) is higher in type I than in type II fibres during submaximal rates of respiration.

    Methods: Mitochondria were isolated from rat soleus and extensor digitorum longus (EDL) muscles, representing type I and type II fibres, respectively. Mitochondrial efficiency (P/O ratio) was determined with pyruvate (Pyr) or palmitoyl-L-carnitine (PC) during submaximal (constant rate of ADP infusion) and maximal (Vmax, state 3) rates of respiration and fitted to monoexponential functions.

    Results: There was no difference in Vmax between PC and Pyr in soleus but in EDL Vmax with PC was only 58% of that with Pyr. The activity of 3-hydroxyacyl-CoA dehydrogenase (HAD) was 3-fold higher in soleus than in EDL. P/O ratio at Vmax was 8-9% lower with PC (2.33±0.02 (soleus) and 2.30±0.02 (EDL)) than with Pyr (2.52±0.03 (soleus) and 2.54±0.03 (EDL)) but not different between the two muscles (P>0.05). P/O ratio was low at low rates of respiration and increased exponentially when the rate of respiration increased. The asymptotes of the curves were similar to P/O ratio at Vmax. P/O ratio at submaximal respirations was not different between soleus and EDL neither with Pyr nor with PC.

    Conclusion: Mitochondrial efficiency, as determined in vitro, was not significantly different in the two fibre types neither at Vmax nor at submaximal rates of respiration. The low Vmax for PC oxidation in EDL may relate to low activity of β-oxidation.

  • 45.
    Mogensen, Martin
    et al.
    University of Southern Denmark, Odense, Denmark.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll. University of Southern Denmark, Odense, Denmark.
    Fernström, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology. Karolinska institutet.
    Glintborg, Dorte
    Odense University Hospital, Odense, Denmark.
    Vind, Birgitte F
    Odense University Hospital, Odense, Denmark.
    Beck-Nielsen, Henning
    Odense University Hospital, Odense, Denmark.
    Højlund, Kurt
    Odense University Hospital, Odense, Denmark.
    Mitochondrial respiration is decreased in skeletal muscle of patients with type 2 diabetes.2007In: Diabetes, ISSN 0012-1797, E-ISSN 1939-327X, Vol. 56, no 6, p. 1592-9Article in journal (Refereed)
    Abstract [en]

    We tested the hypothesis of a lower respiratory capacity per mitochondrion in skeletal muscle of type 2 diabetic patients compared with obese subjects. Muscle biopsies obtained from 10 obese type 2 diabetic and 8 obese nondiabetic male subjects were used for assessment of 3-hydroxy-Acyl-CoA-dehydrogenase (HAD) and citrate synthase activity, uncoupling protein (UCP)3 content, oxidative stress measured as 4-hydroxy-2-nonenal (HNE), fiber type distribution, and respiration in isolated mitochondria. Respiration was normalized to citrate synthase activity (mitochondrial content) in isolated mitochondria. Maximal ADP-stimulated respiration (state 3) with pyruvate plus malate and respiration through the electron transport chain (ETC) were reduced in type 2 diabetic patients, and the proportion of type 2X fibers were higher in type 2 diabetic patients compared with obese subjects (all P < 0.05). There were no differences in respiration with palmitoyl-l-carnitine plus malate, citrate synthase activity, HAD activity, UCP3 content, or oxidative stress measured as HNE between the groups. In the whole group, state 3 respiration with pyruvate plus malate and respiration through ETC were negatively associated with A1C, and the proportion of type 2X fibers correlated with markers of insulin resistance (P < 0.05). In conclusion, we provide evidence for a functional impairment in mitochondrial respiration and increased amount of type 2X fibers in muscle of type 2 diabetic patients. These alterations may contribute to the development of type 2 diabetes in humans with obesity.

  • 46. Montenegro, Marcelo F
    et al.
    Sundqvist, Michaela L
    Larsen, Filip J
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Zhuge, Zhengbing
    Carlström, Mattias
    Weitzberg, Eddie
    Lundberg, Jon O
    Blood Pressure-Lowering Effect of Orally Ingested Nitrite Is Abolished by a Proton Pump Inhibitor.2017In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 69, no 1, p. 23-31Article in journal (Refereed)
    Abstract [en]

    Inorganic nitrate and nitrite from dietary and endogenous sources are metabolized to NO and other bioactive nitrogen oxides that affect blood pressure. The mechanisms for nitrite bioactivation are unclear, but recent studies in rodents suggest that gastric acidity may influence the systemic effects of this anion. In a randomized, double-blind, placebo-controlled crossover study, we tested the effects of a proton pump inhibitor on the acute cardiovascular effects of nitrite. Fifteen healthy nonsmoking, normotensive subjects, aged 19 to 39 years, were pretreated with placebo or esomeprazole (3×40 mg) before ingesting sodium nitrite (0.3 mg kg(-1)), followed by blood pressure monitoring. Nitrite reduced systolic blood pressure by a maximum of 6±1.3 mm Hg when taken after placebo, whereas pretreatment with esomeprazole blunted this effect. Peak plasma nitrite, nitrate, and nitroso species levels after nitrite ingestion were similar in both interventions. In 8 healthy volunteers, we then infused increasing doses of sodium nitrite (1, 10, and 30 nmol kg(-1) min(-1)) intravenously. Interestingly, although plasma nitrite peaked at similar levels as with orally ingested nitrite (≈1.8 µmol/L), no changes in blood pressure were observed. In rodents, esomeprazole did not affect the blood pressure response to the NO donor, DEA NONOate, or vascular relaxation to nitroprusside and acetylcholine, demonstrating an intact downstream NO-signaling pathway. We conclude that the acute blood pressure-lowering effect of nitrite requires an acidic gastric environment. Future studies will reveal if the cardiovascular complications associated with the use of proton pump inhibitors are linked to interference with the nitrate-nitrite-NO pathway.

  • 47. Nielsen, Joachim
    et al.
    Mogensen, Martin
    Vind, Birgitte F
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Højlund, Kurt
    Schrøder, Henrik D
    Ortenblad, Niels
    Increased subsarcolemmal lipids in type 2 diabetes: effect of training on localization of lipids, mitochondria, and glycogen in sedentary human skeletal muscle.2010In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 298, no 3, p. E706-13Article in journal (Refereed)
    Abstract [en]

    The purpose of the study was to investigate the effect of aerobic training and type 2 diabetes on intramyocellular localization of lipids, mitochondria, and glycogen. Obese type 2 diabetic patients (n = 12) and matched obese controls (n = 12) participated in aerobic cycling training for 10 wk. Endurance-trained athletes (n = 15) were included for comparison. Insulin action was determined by euglycemic-hyperinsulinemic clamp. Intramyocellular contents of lipids, mitochondria, and glycogen at different subcellular compartments were assessed by transmission electron microscopy in biopsies obtained from vastus lateralis muscle. Type 2 diabetic patients were more insulin resistant than obese controls and had threefold higher volume of subsarcolemmal (SS) lipids compared with obese controls and endurance-trained subjects. No difference was found in intermyofibrillar lipids. Importantly, following aerobic training, this excess SS lipid volume was lowered by approximately 50%, approaching the levels observed in the nondiabetic subjects. A strong inverse association between insulin sensitivity and SS lipid volume was found (r(2)=0.62, P = 0.002). The volume density and localization of mitochondria and glycogen were the same in type 2 diabetic patients and control subjects, and showed in parallel with improved insulin sensitivity a similar increase in response to training, however, with a more pronounced increase in SS mitochondria and SS glycogen than in other localizations. In conclusion, this study, estimating intramyocellular localization of lipids, mitochondria, and glycogen, indicates that type 2 diabetic patients may be exposed to increased levels of SS lipids. Thus consideration of cell compartmentation may advance the understanding of the role of lipids in muscle function and type 2 diabetes.

  • 48. Ortenblad, Niels
    et al.
    Macdonald, Will A
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Glycolysis in contracting rat skeletal muscle is controlled by factors related to energy state.2009In: Biochemical Journal, ISSN 0264-6021, E-ISSN 1470-8728, Vol. 420, no 2, p. 161-8Article in journal (Refereed)
    Abstract [en]

    The control of glycolysis in contracting muscle is not fully understood. The aim of the present study was to examine whether activation of glycolysis is mediated by factors related to the energy state or by a direct effect of Ca2+ on the regulating enzymes. Extensor digitorum longus muscles from rat were isolated, treated with cyanide to inhibit aerobic ATP production and stimulated (0.2 s trains every 4 s) until force was reduced to 70% of initial force (control muscle, referred to as Con). Muscles treated with BTS (N-benzyl-p-toluene sulfonamide), an inhibitor of cross-bridge cycling without affecting Ca2+ transients, were stimulated for an equal time period as Con. Energy utilization by the contractile apparatus (estimated from the observed relation between ATP utilization and force-time integral) was 60% of total. In BTS, the force-time integral and ATP utilization were only 38 and 58% of those in Con respectively. Glycolytic rate in BTS was only 51% of that in Con but the relative contribution of ATP derived from PCr (phosphocreatine) and glycolysis and the relation between muscle contents of PCr and Lac (lactate) were not different. Prolonged cyanide incubation of quiescent muscle (low Ca2+) did not change the relation between PCr and Lac. The reduced glycolytic rate in BTS despite maintained Ca2+ transients, and the unchanged PCr/Lac relation in the absence of Ca2+ transients, demonstrates that Ca2+ is not the main trigger of glycogenolysis. Instead the preserved relative contribution of energy delivered from PCr and glycolysis during both conditions suggests that the glycolytic rate is controlled by factors related to energy state.

  • 49.
    Psilander, Niklas
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll. Karolinska institutet, Inst för fysiologi och farmakologi / Dept of Physiology and Pharmacology .
    The effect of different exercise regimens on mitochondrial biogenesis and performance2014Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Endurance training is a powerful tool to improve both health and performance. Physical activity is now recognized as an effective treatment and prevention therapy for a wide range of diseases. One of the most profound adaptations to endurance training is increased mitochondrial function and content within the exercising muscles. Mitochondrial quality and quantity are closely related to several of the positive health effects reported after training. High mitochondrial content strongly correlates with muscle oxidative capacity and endurance performance. Even though it is well known that endurance training increases mitochondrial content, it is unclear which type of training is the most efficient to promote mitochondrial biogenesis. Therefore, the basis for current exercise recommendations relative to mitochondrial biogenesis is poor or absent. Thus, the main objective of this thesis was to evaluate the effect of different training strategies on mitochondrial biogenesis.

    Recent developments in molecular methods have made it possible to study the initial adaptations to training through measurement of mRNA gene expression of exercise induced genes. One such gene is transcriptional coactivator peroxisome proliferator–activated receptor-γ coactivator-1α (PGC-1α). PGC-1α is a key regulator of mitochondrial biogenesis and the expression of PGC-1α can therefore be used as a marker of this process.

    The first four studies presented in this thesis are acute exercise studies where two different exercise models were compared using a cross-over design. Muscle biopsies were obtained pre and post exercise and analysed for gene expression and glycogen, apart from study II. The final study was a long-term training study where muscle biopsies were obtained before and after the training period and analysed for mitochondrial enzyme activities and protein content.

    Study I: The expression of PGC-1α and related genes were examined after 90 min of continuous and interval exercise in untrained subjects. The exercise protocols influenced the expression of genes involved in mitochondrial biogenesis and oxidative metabolism in a similar manner. Both interval and continuous exercise were potent training strategies for relatively sedentary individuals.

    Study II: The expression of PGC-1α and related genes were examined after low-volume sprint interval (SIT) and high-volume interval (IE) exercise in highly trained cyclists. SIT induced a similar increase in PGC-1α expression as IE despite a much lower time commitment and work completed. Sprint interval exercise might, therefore, be a time efficient training strategy for highly trained individuals.

    Study III: The expression of PGC-1α and related genes, as well as the activity of upstream proteins, were examined after concurrent (ER: cycling + leg press) and single-mode (E: cycling only) exercise in untrained subjects. PGC-1α expression doubled after ER compared with E. It was concluded that concurrent training might be beneficial for mitochondrial biogenesis in untrained individuals.

    Study IV: The expression of PGC-1α and related genes were examined after exercise performed with low (LG) and normal (NG) muscle glycogen in well-trained cyclists. PGC-1α expression increased approximately three times more after LG compared with NG. This finding suggested that low glycogen exercise is a potent inducer of mitochondrial biogenesis in well-trained individuals.

    Study V: Mitochondrial enzyme activity, protein content and endurance performance were examined after eight weeks of concurrent (ES: cycling + leg press) or single-mode (E: cycling only) training in cyclists. ES did not affect enzyme activity, protein content or endurance performance differently than E. The beneficial effect previously observed in untrained subjects did not translate to higher numbers of mitochondria in trained individuals.

    In three of the studies, I, III, and IV, both glycogen and PGC-1α expression were measured after exercise. These data were then pooled and examined. The highest PGC-1α mRNA expression levels were identified when glycogen levels were low, and vice versa. This suggests that low glycogen might play an important role in the regulation of mitochondrial biogenesis also during interval and concurrent strength and endurance exercise.

    In conclusion, key markers of mitochondrial biogenesis can be effectively up-regulated by interval, concurrent and low glycogen exercise. A possible explanation for this might be that though the exercise protocols are quite divergent in nature, they all have a pronounced effect on muscle glycogen and/or perturbation in energetic stress.

  • 50.
    Psilander, Niklas
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Frank, Per
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Flockhart, Mikael
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Research group for Mitokondriell funktion och metabolisk kontroll.
    Adding strength to endurance training does not enhance aerobic capacity in cyclists2015In: Scandinavian Journal of Medicine and Science in Sports, ISSN 0905-7188, E-ISSN 1600-0838, Vol. 25, no 4, p. e353-e359Article in journal (Refereed)
    Abstract [en]

    The molecular signaling of mitochondrial biogenesis is enhanced when resistance exercise is added to a bout of endurance exercise. The purpose of the present study was to examine if this mode of concurrent training translates into increased mitochondrial content and improved endurance performance. Moderately trained cyclists performed 8 weeks (two sessions per week) of endurance training only (E, n = 10; 60-min cycling) or endurance training followed by strength training (ES, n = 9; 60-min cycling + leg press). Muscle biopsies were obtained before and after the training period and analyzed for enzyme activities and protein content. Only the ES group increased in leg strength (+19%, P < 0.01), sprint peak power (+5%, P < 0.05), and short-term endurance (+9%, P < 0.01). In contrast, only the E group increased in muscle citrate synthase activity (+11%, P = 0.06), lactate threshold intensity (+3%, P < 0.05), and long-term endurance performance (+4%, P < 0.05). Content of mitochondrial proteins and cycling economy was not affected by training. Contrary to our hypothesis, the results demonstrate that concurrent training does not enhance muscle aerobic capacity and endurance performance in cyclists.

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