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  • 1. Brink-Elfegoun, Tibault
    et al.
    Kaijser, L
    Gustafsson, T
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Maximal oxygen uptake is not limited by a central nervous system governor.2007In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 102, no 2, p. 781-6Article in journal (Refereed)
    Abstract [en]

    We tested the hypothesis that the work of the heart was not a limiting factor in the attainment of maximal oxygen uptake (VO2 max). We measured cardiac output (Q) and blood pressures (BP) during exercise at two different rates of maximal work to estimate the work of the heart through calculation of the rate-pressure product, as a part of the ongoing discussion regarding factors limiting VO2 max. Eight well-trained men (age 24.4 +/- 2.8 yr, weight 81.3 +/- 7.8 kg, and VO2 max 59.1 +/- 2.0 ml x min(-1) x kg(-1)) performed two maximal combined arm and leg exercises, differing 10% in watts, with average duration of time to exhaustion of 4 min 50 s and 3 min 40 s, respectively. There were no differences between work rates in measured VO2 max, maximal Q, and peak heart rate between work rates (0.02 l/min, 0.3 l/min, and 0.8 beats/min, respectively), but the systolic, diastolic, and calculated mean BP were significantly higher (19, 5, and 10 mmHg, respectively) in the higher than in the lower maximal work rate. The products of heart rate times systolic or mean BP and Q times systolic or mean BP were significantly higher (3,715, 1,780, 569, and 1,780, respectively) during the higher than the lower work rate. Differences in these four products indicate a higher mechanical work of the heart on higher than lower maximal work rate. Therefore, this study does not support the theory, which states that the work of the heart, and consequently VO2 max, during maximal exercise is hindered by a command from the central nervous system aiming at protecting the heart from being ischemic.

  • 2. Calbet, Jose A L
    et al.
    Boushel, Robert C
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Assessment of cardiac output with transpulmonary thermodilution during exercise in humans.2015In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 118, no 1, p. 1-10Article in journal (Refereed)
    Abstract [en]

    The accuracy and reproducibility of transpulmonary thermodilution (TPTd) to assess cardiac output (Q) in exercising men was determined using indocyanine green (ICG) dilution as a reference method. TPTd has been utilized for the assessment of Q and preload indices of global end-diastolic volume (GEDV) and intrathoracic blood volume (ITBV), as well as extravascular lung water (EVLW) in resting humans. It remains unknown if this technique is also accurate and reproducible during exercise. Sixteen healthy men underwent catheterization of the right femoral vein (for iced saline injection), an antecubital vein (ICG injection) and femoral artery (thermistor) to determine their Q by TPTd and [ICG] during incremental 1 and 2-legged pedaling on a cycle ergometer, and combined arm cranking with leg pedaling to exhaustion. There was a close relationship between Td-Q and ICG-Q (r=0.95, n=151, SEE: 1.452 L/min, P<0.001; mean difference of 0.06 L/min; limits of agreement -2.98 to 2.86 L/min), and TPTd-Q and ICG-Q increased linearly with VO2 with similar intercepts and slopes. Both methods had mean coefficients of variation (CV) close to 5% for Q, GEDV and ITBV. The mean CV of EVLW, assessed with both indicators (ICG and thermal) was 17%, and was sensitive enough as to detect a reduction in EVLW of 107 ml when changing from resting supine to upright exercise. In summary, transpulmonary thermodilution with bolus injection into the femoral vein is an accurate and reproducible method to assess cardiac output during exercise in humans.

  • 3.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Comments on Point: Counterpoint "Positive effects of intermittent hypoxia (live high:train low) on exercise performance are/are not mediated primarily by augmented red cell volume2005In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 99, no 6, p. 2462-Article in journal (Other academic)
  • 4.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Counterpoint: maximal oxygen uptake is not limited by a central nervous system governor.2009In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 106, no 1, p. 339-41; discussion 341Article in journal (Refereed)
  • 5.
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    "In health and in a normoxic environment, VO2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow".: Comment2006In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 100, no 4, p. 1416-Article in journal (Other academic)
  • 6.
    Ekblom, Björn T
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Last word on point: counterpoint : Maximal oxygen uptake is/is not limited by a central nervous system governor : Letter to the editor2009In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 106, no 1, p. 348-Article in journal (Other academic)
  • 7.
    Fernström, Maria
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    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.

  • 8.
    Hamrin, Kerstin
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Rosdahl, Hans
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Ungerstedt, Urban
    Henriksson, Jan
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Microdialysis in human skeletal muscle: effects of adding a colloid to the perfusate.2002In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 92, no 1, p. 385-93Article in journal (Refereed)
    Abstract [en]

    Microdialysis catheters (CMA-60 with a polyamide dialysis membrane; 20,000-molecular wt cutoff) were either immersed in an external medium or were inserted in the quadriceps femoris muscle of healthy subjects, using perfusate with or without dextran 70. Varying the position of the outflow tubing induced changes in hydrostatic pressure. The sample volumes were significantly smaller in catheters perfused without a colloid compared with those perfused with a colloid [11-50% (in vitro) and 8-59% (in vivo) lower than in colloid-perfused catheters with the same position of the outflow tubing]. The sample volumes were also significantly smaller when the dialysis membrane was influenced by maximal hydrostatic pressure (above position) compared with minimal hydrostatic pressure (below position) [7-38% (in vitro) and 3-46% (in vivo) lower than in catheters in the below position with the same perfusion fluid]. In vivo, glucose concentration at a perfusion flow rate of 0.33 microl/min was higher when the catheters were perfused without a colloid [18-28% higher than in colloid-perfused catheters with the same position of the outflow tubing (P < 0.001)] than with a colloid. A corresponding difference also tended to occur with lactate, glycerol, and urea. At 0.16 microl/min, the glucose concentration was the same irrespective of whether fluid loss had been counteracted by colloid inclusion or by lowering of outlet tubing. The mechanism behind the observed concentration difference is thought to be a higher effective perfusion flow rate when fluid loss is prevented at low-perfusion flows. This study shows that fluid imbalances can have important implications for microdialysis results at low-perfusion flow rates.

  • 9. 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.
    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.

  • 10. Marklund, Peter
    et al.
    Mattsson, C. Mikael
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Wåhlin-Larsson, Britta
    Ponsot, Elodie
    Lindvall, Björn
    Lindvall, Lisbeth
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Kadi, Fawzi
    Extensive inflammatory cell infiltration in human skeletal muscle in response to an ultra-endurance exercise bout in experienced athletes.2013In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 114, no 1, p. 66-72Article in journal (Refereed)
    Abstract [en]

    The impact of a 24h ultra-endurance exercise bout on systemic and local muscle inflammatory reactions was investigated in nine experienced athletes. Blood and muscle biopsies were collected before (PRE), immediately after the exercise (POST) and after 28h of recovery (POST28). Circulating blood levels of leukocytes, CK, CRP and selected inflammatory cytokines were assessed together with the evaluation of the occurrence of inflammatory cells (CD3(+), CD8(+), CD68(+)) and the expression of major histocompatibility complex class-I (MHC class-I) in skeletal muscle. An extensive inflammatory cell infiltration occurred in all athletes and the number of CD3(+), CD8(+) and CD 68(+) cells were 2-3 fold higher at POST28 compared to PRE (P<0.05). The inflammatory cell infiltration was associated with a significant increase in the expression of MHC class-I in muscle fibers. There was a significant increase in blood leukocyte count, IL-6, IL-8, CRP and CK at POST. At POST28 total leukocytes, IL-6 and CK had declined, whereas IL-8 and CRP continued to increase. Increases in IL-1β and TNF-α were not significant. There were no significant associations between the magnitude of the systemic and local muscle inflammatory reactions. Signs of muscle degenerative and regenerative events were observed in all athletes with various degrees of severity and were not affected by the ultra-endurance exercise bout. In conclusion, a low-intensity but very prolonged single endurance exercise bout can generate a strong inflammatory cell infiltration in skeletal muscle of well-trained experienced ultra-endurance athletes, and the amplitude of the local reaction is not proportional to the systemic inflammatory response.

  • 11.
    Nordlund Ekblom, Maria M
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Improvements in dynamic plantar flexor strength after resistance training are associated with increased voluntary activation and V: M ratio.2010In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 109, no 1, p. 19-26Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to investigate if, and via what mechanisms, resistance training of the plantar flexor muscles affects voluntary activation during maximal voluntary eccentric and concentric muscle actions. Twenty healthy subjects were randomized into a resistance training group (N = 9) or a passive control group (N = 11). Training consisted of 15 sessions of unilateral mainly eccentric plantar flexor exercise over a 5-week period. During pre- and post-training testing, dynamic plantar flexor strength was measured and voluntary activation was calculated using the twitch interpolation technique. The Soleus H-reflex was used to assess motoneurone excitability and presynaptic inhibition of Ia-afferents whereas the Soleus V-wave to test for both changes in presynaptic inhibition of Ia-afferents and changes in supraspinal inputs to the motoneurone pool. H-reflexes, V-waves, supramaximal M-waves and twitches were evoked as the foot was moved at 5 degrees (.)s(-1) through an angle of 90 degrees during passive ankle rotations (passive H and M) and during maximal voluntary concentric and eccentric plantar flexion (MVC H, M and V-wave). Training induced significant improvements in plantar flexor strength and voluntary activation during both concentric and eccentric maximal voluntary actions. Soleus passive and MVC H:M ratios remained unchanged after training, whereas the Soleus V:M ratio was increased during both concentric and eccentric contractions after training. No change was seen in the control group for any of the parameters. The enhanced voluntary strength could be attributed partly to an increase in voluntary activation induced by eccentric training. Since the passive and MVC H:M ratios remained unchanged, the increase in activation is probably not due to decreased presynaptic inhibition. The increased V:M ratio for both action types indicate, that increased voluntary drive from supraspinal centers and/or modulation in afferents other than Ia:s, may have contributed to such an increase in voluntary activation.

  • 12.
    Nordlund Ekblom, Maria M
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Thorstensson, Alf
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Cresswell, Andrew G
    Central and peripheral contributions to fatigue in relation to level of activation during repeated maximal voluntary isometric plantar flexions.2004In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 96, no 1, p. 218-25Article in journal (Refereed)
    Abstract [en]

    This study aimed to investigate central and peripheral contributions to fatigue during repeated maximal voluntary isometric plantar flexions (MVCs). Changes in joint torque, level of activation (LOA), resting twitch amplitude (RT), electromyographic signals (EMG), and presynaptic inhibition of Ia afferents were investigated during 9 bouts of 10 MVCs. MVCs lasted for 2 s and were separated by 1 s. The interval between bouts was 10 s. Electrical stimulation was applied to the tibial nerve; at rest to evoke RTs, M waves, and two (1.5-s interval) H reflexes; with the soleus EMG at 30% of that during MVC to evoke M waves and two H reflexes; and during MVCs to measure LOA. Over the nine bouts, LOA decreased by 12.6% and RT by 16.2%. EMG root mean square during MVCs remained unchanged for the soleus and tibialis anterior muscles, but it decreased for medial gastrocnemius. Peripheral fatigue (decrease in RT) was positively correlated to LOA, whereas central fatigue (decrease in LOA) was not. Depression of both H reflexes suggests that presynaptic inhibition after the first bout was partly induced by homosynaptic postactivation depression of the Ia terminal. The H-reflex-to-M-wave ratio increased with fatigue in both passive and active states, with no change in the ratio of the second H reflex to the first, thereby indicating a decrease of presynaptic inhibition during fatigue. The results indicate that both central and peripheral mechanisms contributed to the fatigue observed during repeated MVCs and that the development of peripheral fatigue was influenced by the level of voluntary activation and initial plantar flexor torque.

  • 13. Nybo, Lars
    et al.
    Nielsen, Bodil
    Blomstrand, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Moller, Kirsten
    Secher, Niels
    Neurohumoral responses during prolonged exercise in humans.2003In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 95, no 3, p. 1125-31Article in journal (Refereed)
    Abstract [en]

    This study examined neurohumoral alterations during prolonged exercise with and without hyperthermia. The cerebral oxygen-to-carbohydrate uptake ratio (O2/CHO = arteriovenous oxygen difference divided by arteriovenous glucose difference plus one-half lactate), the cerebral balances of dopamine, and the metabolic precursor of serotonin, tryptophan, were evaluated in eight endurance-trained subjects during exercise randomized to be with or without hyperthermia. The core temperature stabilized at 37.9 +/- 0.1 degrees C (mean +/- SE) in the control trial, whereas it increased to 39.7 +/- 0.2 degrees C in the hyperthermic trial, with a concomitant increase in perceived exertion (P < 0.05). At rest, the brain had a small release of tryptophan (arteriovenous difference of -1.2 +/- 0.3 micromol/l), whereas a net balance was obtained during the two exercise trials. Both the arterial and jugular venous dopamine levels became elevated during the hyperthermic trial, but the net release from the brain was unchanged. During exercise, the O2/CHO was similar across trials, but, during recovery from the hyperthermic trial, the ratio decreased to 3.8 +/- 0.3 (P < 0.05), whereas it returned to the baseline level of approximately 6 within 5 min after the control trial. The lowering of O2/CHO was established by an increased arteriovenous glucose difference (1.1 +/- 0.1 mmol/l during recovery from hyperthermia vs. 0.7 +/- 0.1 mmol/l in control; P < 0.05). The present findings indicate that the brain has an increased need for carbohydrates during recovery from strenuous exercise, whereas enhanced perception of effort as observed during exercise with hyperthermia was not related to alterations in the cerebral balances of dopamine or tryptophan.

  • 14.
    Psilander, Niklas
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    Eftestøl, Einar
    University of Oslo, Norway.
    Cumming, Kristoffer Toldnes
    Norwegian School of Sport Sciences, Norway.
    Juvkam, Inga
    University of Oslo, Norway.
    Ekblom, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Sunding, Kerstin
    Karolinska Institutet.
    Wernbom, Mathias
    Göteborg University.
    Holmberg, Hans-Christer
    Mid Sweden University.
    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.
    Bruusgaard, Jo C
    University of Oslo, Norway..
    Raastad, Truls
    Norwegian School of Sport Sciences, Norway.
    Gundersen, Kristian
    University of Oslo, Norway..
    Effects of training, detraining, and retraining on strength, hypertrophy, and myonuclear number in human skeletal muscle2019In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 126, no 6, p. 1636-1645Article in journal (Refereed)
    Abstract [en]

    Previously trained mouse muscles acquire strength and volume faster than naïve muscles; it has been suggested that this is related to increased myonuclear density. The present study aimed to determine whether a previously strength-trained leg (mem-leg) would respond better to a period of strength training than a previously untrained leg (con-leg). Nine men and 10 women performed unilateral strength training (T1) for 10 weeks, followed by 20 weeks of detraining (DT) and a 5-week bilateral retraining period (T2). Muscle biopsies were taken before and after each training period and analyzed for myonuclear number, fiber volume, and cross-sectional area (CSA). Ultrasound and one repetition of maximum leg extension were performed to determine muscle thickness (MT) and strength. CSA (~17%), MT (~10%), and strength (~20%) increased during T1 in the mem-leg. However, the myonuclear number and fiber volume did not change. MT and CSA returned to baseline values during DT, but strength remained elevated (~60%), supporting previous findings of a long-lasting motor learning effect. MT and strength increased similarly in the mem-leg and con-leg during T2, whereas CSA, fiber volume, and myonuclear number remained unaffected. In conclusion, training response during T2 did not differ between the mem-leg and con-leg. However, this does not discount the existence of human muscle memory since no increase in the number of myonuclei was detected during T1 and no clear detraining effect was observed for cell size during DT; thus, the present data did not allow for a rigorous test of the muscle memory hypothesis.

  • 15.
    Rundqvist, Håkan Claes
    et al.
    Karolinska Institutet .
    Esbjörnsson, Mona
    Karolinska Institutet .
    Rooyackers, Olav
    Huddinge University Hospital .
    Osterlund, Ted
    Karolinska Institutet.
    Moberg, Marcus
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Eva Blomstrand's research group.
    Apró, William
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Eva Blomstrand'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.
    Jansson, Eva
    Karolinska Institutet .
    Influence of nutrient ingestion on amino acid transporters and protein synthesis in human skeletal muscle after sprint exercise2017In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 123, no 6, p. 1501-1515Article in journal (Refereed)
    Abstract [en]

    Nutrient ingestion is known to increase the exercise-induced stimulation of muscle protein synthesis following resistance exercise. Less is known about the effect of nutrients on muscle protein synthesis following sprint exercise. At two occasions separated by one month, twelve healthy subjects performed three 30-s sprints with 20-min rest between bouts. In randomized order, they consumed a drink with essential amino acids and maltodextrin (nutrient) or flavored water (placebo). Muscle biopsies were obtained 80 and 200 min after the last sprint and blood samples were taken repeatedly during the experiment. Fractional synthetic rate (FSR) was measured by continuous infusion of L-[(2)H5]-phenylalanine up to 200 min postexercise. The mRNA and protein expression of SNAT2 were both 1.4-fold higher (P < 0.05) after nutrient intake compared to placebo at 200 min postexercise. Phosphorylated Akt, mTOR and p70S6k was 1.7- to 3.6-fold higher (P<0.01) 80 min after the last sprint with nutrient ingestion as compared to placebo. In addition, FSR was higher (P<0.05) with nutrients when plasma phenylalanine (FSRplasma) was used as a precursor, but not when intracellular phenylalanine (FSRmuscle) was used. Significant correlations were also found between FSRplasma on the one hand and plasma leucine and serum insulin on the other hand in the nutrient condition. The results show that nutrient ingestion induces the expression of the amino acid transporter SNAT2, stimulates Akt/mTOR signaling and most likely the rate of muscle protein synthesis following sprint exercise.

  • 16. Râdegran, Göran
    et al.
    Blomstrand, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Saltin, Bengt
    Peak muscle perfusion and oxygen uptake in humans: importance of precise estimates of muscle mass.1999In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 87, no 6, p. 2375-80Article in journal (Refereed)
    Abstract [en]

    The knee extensor exercise model was specifically developed to enable in vivo estimates of peak muscle blood flow and O(2) uptake in humans. The original finding, using thermodilution measurements to measure blood flow in relation to muscle mass [P. Andersen and B. Saltin. J. Physiol. (Lond.) 366: 233-249, 1985], was questioned, however, as the measurements were two- to threefold higher than those previously obtained with the (133)Xe clearance and the plethysmography technique. As thermodilution measurements have now been confirmed by other methods and independent research groups, we aimed to address the impact of muscle mass estimates on the peak values of muscle perfusion and O(2) uptake. In the present study, knee extensor volume was determined from multiple measurements with computer tomography along the full length of the muscle. In nine healthy humans, quadriceps muscle volume was 2.36 +/- 0.17 (range 1. 31-3.27) liters, corresponding to 2.48 +/- 0.18 (range 1.37-3.43) kg. Anthropometry overestimated the muscle volume by approximately 21-46%, depending on whether quadriceps muscle length was estimated from the patella to either the pubic bone, inguinal ligament, or spina iliaca anterior superior. One-legged, dynamic knee extensor exercise up to peak effort of 67 +/- 7 (range 55-100) W rendered peak values for leg blood flow (thermodilution) of 5.99 +/- 0.66 (range 4.15-9.52) l/min and leg O(2) uptake of 856 +/- 109 (range 590-1,521) ml/min. Muscle perfusion and O(2) uptake reached peak values of 246 +/- 24 (range 149-373) and 35.2 +/- 3.7 (range 22.6-59. 6) ml. min(-1). 100 g muscle(-1), respectively. These peak values are approximately 19-33% larger than those attained by applying anthropometric muscle mass estimates. In conclusion, the present findings emphasize that peak perfusion and O(2) uptake in human skeletal muscle may be up to approximately 30% higher than previous anthropometric-based estimates that use equivalent techniques for blood flow measurements.

  • 17.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Comments on Point: Counterpoint: Muscle lactate and H⁺ production do/do not have a 1:1 association in skeletal muscle. Why add complexity/confusion to a simple issue?2011In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 110, no 5, p. 1494-Article in journal (Refereed)
  • 18.
    Sahlin, Kent
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Nielsen, Jens Steen
    Mogensen, Martin
    Tonkonogi, Michail
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Repeated static contractions increase mitochondrial vulnerability towards oxidative stress in human skeletal muscle2007In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 101, p. 833-839Article in journal (Refereed)
    Abstract [en]

    Repeated static contractions (RSC) induce large fluctuations in tissue oxygen tension and increase the generation of reactive oxygen species (ROS). This study investigated the effect of RSC on muscle contractility, mitochondrial respiratory function, and in vitro sarcoplasmatic reticulum (SR) Ca2+-kinetics in human muscle. Ten male subjects performed 5 bouts of static knee extension with 10 min rest in between. Each bout of RSC (target torque 66% of maximal voluntary contraction torque, MVC) was maintained to fatigue. Muscle biopsies were taken pre-exercise and 0.3 and 24 h post-exercise from vastus lateralis. Mitochondria were isolated and respiratory function measured after incubation with H2O2 (HPX) or control medium (CON). Mitochondrial function was not affected by RSC during CON. However, RSC exacerbated mitochondrial dysfunction during HPX resulting in decreased respiratory control index, decreased mitochondrial efficiency (P/O ratio) and increased non-coupled respiration (HPX/CON post vs. pre-exercise). SR Ca2+ uptake rate was lower 0.3 h vs. 24 h post-exercise, whereas SR Ca2+ release rate was unchanged. RSC resulted in long-lasting changes in muscle contractility including reduced maximal torque, low frequency fatigue (LFF) and faster torque relaxation. It is concluded that RSC increases mitochondrial vulnerability towards ROS, reduces SR Ca2+ uptake rate and causes LFF. Although conclusive evidence is lacking we suggest that these changes are related to increased formation of ROS during RSC.

  • 19.
    Sahlin, Kent
    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 G
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology. Stockholm University.
    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.
    Bakkman, Linda
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology. Karolinska Institutet.
    Fernström, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology. Karolinska Institutet.
    Rozhdestvenskaya, Zinaida
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology.
    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.
    Nedergaard, Jan
    Stockholm University.
    Ekblom, Björn T
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology, Björn Ekblom's research group.
    Tonkonogi, Michail
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Åstrand Laboratory of Work Physiology. University of Dalarna.
    Ultra-endurance exercise increases the production of reactive oxygen species in isolated mitochondria from human skeletal muscle.2010In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 108, no 4, p. 780-787Article in journal (Refereed)
    Abstract [en]

    Exercise-induced oxidative stress is important for the muscular adaptation to training but may also cause muscle damage. We hypothesized that prolonged exercise would increase mitochondrial production of reactive oxygen species (ROS) measured in vitro and that this correlates with oxidative damage. Eight male athletes (24-32 years) performed ultra-endurance exercise (kayaking/running/cycling) with an average work intensity of 55% VO2peak for 24 h. Muscle biopsies were taken from vastus lateralis before exercise, immediately after exercise and after 28 h of recovery. The production of H2O2 was measured fluorometrically in isolated mitochondria with the Amplex red and peroxidase system. Succinate-supported mitochondrial H2O2 production was significantly increased after exercise (73% higher, P=0.025) but restored to the initial level at recovery. Plasma level of free fatty acids (FFA) increased 4-fold and exceeded 1.2 mmol l(-1) during the last 6 h of exercise. Plasma FFA at the end of exercise was significantly correlated to mitochondrial ROS production (r=0.74, P<0.05). Mitochondrial content of 4-hydroxy-nonenal-adducts (a marker of oxidative damage) was increased only after recovery and was not correlated with mitochondrial ROS production. Total thiol-group level and glutathione peroxidase activity were elevated after recovery. In conclusion: ultra-endurance exercise increases ROS production in isolated mitochondria but this is reversed after 28 h recovery. Mitochondrial ROS production was not correlated with oxidative damage of mitochondrial proteins, which was increased at recovery but not immediately after exercise. Key words: antioxidative defence, fatty acids, oxidative stress.

  • 20.
    Schantz, Peter
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Källman, Mi
    Levels of the NADH shuttle enzymes and cytochrome b5 reductase in human skeletal muscle: effect of strength training1989In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 67, no 1, p. 123-127Article in journal (Refereed)
  • 21. Seynnes, Olivier R
    et al.
    Bojsen-Møller, Jens
    Albracht, Kirsten
    Arndt, Anton
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Cronin, Neil J
    Finni, Taija
    Magnusson, S Peter
    Ultrasound-Based Testing Of Tendon Mechanical Properties: A Critical Evaluation.2015In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 118, no 2, p. 133-141Article in journal (Refereed)
    Abstract [en]

    In the past twenty years, the use of ultrasound-based methods has become a standard approach to measure tendon mechanical properties in vivo. Yet, the multitude of methodological approaches adopted by various research groups probably contributes to the large variability of reported values. The technique of obtaining and relating tendon deformation to tensile force in vivo has been applied differently, depending on practical constraints or scientific points of view. Divergence can be seen in i) methodological considerations such as the choice of anatomical features to scan and to track, force measurements or signal synchronisation and ii), in physiological considerations related to the viscoelastic behaviour or length measurements of tendons. Hence, the purpose of the present review is to assess and discuss the physiological and technical aspects connected to in vivo testing of tendon mechanical properties. In doing so, our aim is to provide the reader with a systematic, qualitative analysis of ultrasound-based techniques. Finally, a list of recommendations is proposed for a number of selected issues.

  • 22.
    Tannerstedt, Jörgen
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Apró, William
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Blomstrand, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Maximal lengthening contractions induce different signaling responses in the type I and type II fibers of human skeletal muscle.2009In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 106, no 4, p. 1412-8Article in journal (Refereed)
    Abstract [en]

    The molecular mechanisms by which resistance exercise enlarges muscle mass, particularly the mass of fast-twitch type II fibers, are likely to involve enhanced phosphorylation/activation of key enzymes regulating protein synthesis. The hypothesis is that resistance exercise influences the phosphorylation of such key signaling proteins to a greater extent in type II than in type I fibers. Six recreationally active male subjects performed four sets of six maximal lengthening contractions with one leg. Muscle biopsies were taken from the vastus lateralis before and immediately after exercise and following 1 and 2 h of recovery. Samples were freeze-dried, and individual muscle fibers were dissected out and identified as type I or type II after staining for myosin ATPase. Phosphorylation of p70(S6k) on Thr(389) and S6 in type II fibers was increased three-to fourfold and six- to ninefold (P < 0.05), respectively, 1 and 2 h after exercise, whereas phosphorylation in type I fibers remained unchanged. Phosphorylation of Akt, mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK) was unaltered in both fiber types, whereas that of eukaryotic elongation factor 2 (eEF2) was attenuated 20-45% (P < 0.05) in type II fibers during recovery. Phosphorylation of ERK1/2 was elevated six- to sevenfold (P < 0.05) immediately after exercise, and p38 MAPK phosphorylation was increased three- to fourfold (P < 0.05) for as long as 1 h after exercise in both types of fibers, although the level was markedly higher in type II fibers (P < 0.05). In conclusion, the elevation of p70(S6k) and the reduction of eEF2 phosphorylation in the type II fibers following resistance exercise suggest stimulation of protein synthesis, which may contribute to a more pronounced enlargement of these fibers. Our findings also suggest that p70(S6k) is activated, at least in part, via pathways not involving Akt-mTOR and MAPK.

  • 23.
    Tokuno, Craig D
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Garland, S Jayne
    Carpenter, Mark G
    Thorstensson, Alf
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Cresswell, Andrew G
    Sway-dependent modulation of the triceps surae H-reflex during standing.2008In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 104, no 5, p. 1359-65Article in journal (Refereed)
    Abstract [en]

    Previous research has shown that changes in spinal excitability occur during the postural sway of quiet standing. In the present study, it was of interest to examine the independent effects of sway position and sway direction on the efficacy of the triceps surae Ia pathway, as reflected by the Hoffman (H)-reflex amplitude, during standing. Eighteen participants, tested under two different experimental protocols, stood quietly on a force platform. Percutaneous electrical stimulation was applied to the posterior tibial nerve when the position and direction of anteroposterior (A-P) center of pressure (COP) signal satisfied the criteria for the various experimental conditions. It was found that, regardless of sway position, a larger amplitude of the triceps surae H-reflex (difference of 9-14%; P = 0.005) occurred when subjects were swaying in the forward compared with the backward direction. The effects of sway position, independent of the sway direction, on spinal excitability exhibited a trend (P = 0.075), with an 8.9 +/- 3.7% increase in the H-reflex amplitude occurring when subjects were in a more forward position. The observed changes to the efficacy of the Ia pathway cannot be attributed to changes in stimulus intensity, as indicated by a constant M-wave amplitude, or to the small changes in the level of background electromyographic activity. One explanation for the changes in reflex excitability with respect to the postural sway of standing is that the neural modulation may be related to the small lengthening and shortening contractions occurring in the muscles of the triceps surae.

  • 24. Wang, Li
    et al.
    Psilander, Niklas
    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.
    Mascher, Henrik
    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.
    Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle.2011In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 111, no 5, p. 1335-1344Article in journal (Refereed)
    Abstract [en]

    Combining endurance and strength training (concurrent training) may change the adaptation compared with single mode training. However, the site of interaction and the mechanisms are unclear. We have investigated the hypothesis that molecular signaling of mitochondrial biogenesis after endurance exercise is impaired by resistance exercise. Ten healthy subjects performed either only endurance exercise (E: 1h cycling at ~65% of VO(2max)) or endurance exercise followed by resistance exercise (ER: 1h cycling + 6 sets of leg press at 70-80% of 1 repetition maximum) in a randomized cross-over design. Muscle biopsies were obtained before and after exercise (1 and 3h Post cycling). The mRNA of genes related to mitochondrial biogenesis (PGC-1α, PRC) and substrate regulation (PDK4) increased after both E and ER, but the mRNA levels were about 2-fold higher after ER (P<0.01). Phosphorylation of proteins involved in the signaling cascade of protein synthesis (mTOR, S6K1 and eEF2) was altered after ER but not after E. Moreover, ER induced a larger increase in mRNA of genes associated with positive mTOR signaling (cMyc and Rheb). Phosphorylation of AMPK, ACC and Akt increased similarly at 1h Post (P<0.01) after both types of exercise. Contrary to our hypothesis, the results demonstrate that resistance exercise, performed after endurance exercise, amplifies the adaptive signaling response of mitochondrial biogenesis compared with single-mode endurance exercise. The mechanism may relate to a crosstalk between signaling pathways mediated by mTOR. The results suggest that concurrent training may be beneficial for the adaptation of muscle oxidative capacity.

  • 25. Wibom, Rolf
    et al.
    Hultman, Erik
    Johansson, Mats
    Matherei, Kaj
    Constantin-Teodosiu, Dimitri
    Schantz, Peter
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Adaptation of mitochondrial ATP-production in human skeletal muscle to endurance training and detraining1992In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, no 73, p. 2004-2010Article in journal (Refereed)
  • 26. Yu, M
    et al.
    Blomstrand, Eva
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Chibalin, A V
    Wallberg-Henriksson, H
    Zierath, J R
    Krook, A
    Exercise-associated differences in an array of proteins involved in signal transduction and glucose transport.2001In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 90, no 1, p. 29-34Article in journal (Refereed)
    Abstract [en]

    Vastus lateralis muscle biopsies were obtained from endurance-trained (running approximately 50 km/wk) and untrained (no regular physical exercise) men, and the expression of an array of insulin-signaling intermediates was determined. Expression of insulin receptor and insulin receptor substrate-1 and -2 was decreased 44% (P < 0.05), 57% (P < 0.001), and 77% (P < 0.001), respectively, in trained vs. untrained muscle. The downstream signaling target, Akt kinase, was not altered in trained subjects. Components of the mitogenic signaling cascade were also assessed. Extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase expression was 190% greater (P < 0.05), whereas p38 mitogen-activated protein kinase expression was 32% lower (P < 0.05), in trained vs. untrained muscle. GLUT-4 protein expression was twofold higher (P < 0.05), and the GLUT-4 vesicle-associated protein, the insulin-regulated aminopeptidase, was increased 4.7-fold (P < 0. 05) in trained muscle. In conclusion, the expression of proteins involved in signal transduction is altered in skeletal muscle from well-trained athletes. Downregulation of early components of the insulin-signaling cascade may occur in response to increased insulin sensitivity associated with endurance training.

  • 27.
    Åstrand, PO
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Bergh, U
    Kilbom, A
    A 33-yr follow-up of peak oxygen uptake and related variables of former physical education students.1997In: Journal of applied physiology, ISSN 8750-7587, E-ISSN 1522-1601, Vol. 82, no 6, p. 1844-52Article in journal (Refereed)
    Abstract [en]

    In 1949, 27 female and 26 male physical education students were studied at a mean age of 22 and 25 yr, respectively. They were restudied in 1970 and 1982. Measurements included oxygen uptake, heart rate, and pulmonary ventilation during submaximal and maximal exercise on a cycle ergometer and treadmill. After 21 yr, peak aerobic power was significantly reduced, from 2.90 to 2.18 l/min and from 4.09 to 3.28 l/min for women and men, respectively. After another 12 yr, the 1970 maxima were not reduced further. From 1949 to 1982 there was a decrease in peak heart rate from 196 to 177 beats/min in women and from 190 to 175 beats/min in men (P < 0.05). Highest pulmonary ventilation did not change significantly. At an oxygen uptake of 1.5 l/min, the heart rate was the same in 1949 as in 1982. In conclusion, the physical fitness level of the subjects was well above average for these ages. From 1970 to 1982 there was no decline in the average peak aerobic power, a finding possibly related to increased habitual physical activity.

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