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  • 1.
    Blomstrand, Eva
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Rådegran, Göran
    Saltin, Bengt
    Maximum rate of oxygen uptake by human skeletal muscle in relation to maximal activities of enzymes in the Krebs cycle.1997In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 501 ( Pt 2), p. 455-60Article in journal (Refereed)
    Abstract [en]

    1. Ten subjects performed incremental exercise up to their maximum work rate with the knee extensors of one leg. Measurements of leg blood flow and femoral arteriovenous differences of oxygen were made in order to be able to calculate oxygen uptake of the leg. 2. The volume of the quadriceps muscle was determined from twenty-one to twenty-five computer tomography section images taken from the patella to the anterior inferior iliac spine of each subject. 3. The maximal activities of three enzymes in the Krebs cycle, citrate synthase, oxoglutarate dehydrogenase and succinate dehydrogenase, were measured in biopsy samples taken from the vastus lateralis muscle. 4. The average rate of oxygen uptake over the quadriceps muscle at maximal work, 353 ml min-1 kg-1, corresponded to a Krebs cycle rate of 4.6 mumol min-1 g-1. This was similar to the maximal activity of oxoglutarate dehydrogenase (5.1 mumol min-1 g-1), whereas the activities of succinate dehydrogenase and citrate synthase averaged 7.2 and 48.0 mumol min-1 g-1, respectively. 5. It is suggested that of these enzymes, only the maximum activity of oxoglutarate dehydrogenase can provide a quantitative measure of the capacity of oxidative metabolism, and it appears that the enzyme is fully activated during one-legged knee extension exercise at the maximal work rate.

  • 2.
    Blomstrand, Eva
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Eva Blomstrand's research group.
    Saltin, Bengt
    Effect of muscle glycogen on glucose, lactate and amino acid metabolism during exercise and recovery in human subjects.1999In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 514 ( Pt 1), p. 293-302Article in journal (Refereed)
    Abstract [en]

    1. Eight subjects performed two-legged exercise, one leg with low and the other with normal muscle glycogen content. The purpose was to study the effect of low initial muscle glycogen content on the metabolic response during 1 h of exercise and 2 h of recovery. This model allows direct comparison of net fluxes of substrates and metabolites over the exercising legs receiving the same arterial inflow. 2. Muscle glycogen breakdown during exercise was 60% lower in the leg with a reduced pre-exercise glycogen concentration and the rate of glucose uptake during exercise was 30% higher. 3. The amount of pyruvate that was oxidized during exercise was calculated to be approximately 450 mmol in the low-glycogen leg and 750 mmol in the normal-glycogen leg, which suggests more fat and amino acid oxidation in the low-glycogen leg. 4. During exercise, there was a significant release of amino acids not metabolized in the muscle, e. g. tyrosine and phenylalanine, only from the low-glycogen leg, suggesting an increased rate of net protein degradation in this leg. 5. The release of tyrosine and phenylalanine from the low-glycogen leg during the exercise period and the change in their muscle concentrations yield a net tyrosine and phenylalanine production rate of 1.4 and 1.5 mmol h-1, respectively. The net rate of protein degradation was then calculated to be 7-12 g h-1. 6. The results suggest that the observed differences in metabolism between the low-glycogen and the normal-glycogen leg are induced by the glycogen level per se, since the legs received the same arterial supply of hormones and substrates.

  • 3.
    Calbet, J A L
    et al.
    Department of Physical Education, University of Las Palmas de Gran Canaria, Spain.
    Jensen-Urstad, Mats
    van Hall, Gerrit
    Holmberg, H-C
    Rosdahl, Hans
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Saltin, Bengt
    Maximal muscular vascular conductances during whole body upright exercise in humans.2004In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 558, no Pt 1, p. 319-31Article in journal (Refereed)
    Abstract [en]

    That muscular blood flow may reach 2.5 l kg(-1) min(-1) in the quadriceps muscle has led to the suggestion that muscular vascular conductance must be restrained during whole body exercise to avoid hypotension. The main aim of this study was to determine the maximal arm and leg muscle vascular conductances (VC) during leg and arm exercise, to find out if the maximal muscular vasodilatory response is restrained during maximal combined arm and leg exercise. Six Swedish elite cross-country skiers, age (mean +/-s.e.m.) 24 +/- 2 years, height 180 +/- 2 cm, weight 74 +/- 2 kg, and maximal oxygen uptake (VO2,max) 5.1 +/- 0.1 l min(-1) participated in the study. Femoral and subclavian vein blood flows, intra-arterial blood pressure, cardiac output, as well as blood gases in the femoral and subclavian vein, right atrium and femoral artery were determined during skiing (roller skis) at approximately 76% of VO2max and at VO2max with different techniques: diagonal stride (combined arm and leg exercise), double poling (predominantly arm exercise) and leg skiing (predominantly leg exercise). During submaximal exercise cardiac output (26-27 l min(-1)), mean blood pressure (MAP) (approximately 87 mmHg), systemic VC, systemic oxygen delivery and pulmonary VO2(approximately 4 l min(-1)) attained similar values regardless of exercise mode. The distribution of cardiac output was modified depending on the musculature engaged in the exercise. There was a close relationship between VC and VO2 in arms (r= 0.99, P < 0.001) and legs (r= 0.98, P < 0.05). Peak arm VC (63.7 +/- 5.6 ml min(-1) mmHg(-1)) was attained during double poling, while peak leg VC was reached at maximal exercise with the diagonal technique (109.8 +/- 11.5 ml min(-1) mmHg(-1)) when arm VC was 38.8 +/- 5.7 ml min(-1) mmHg(-1). If during maximal exercise arms and legs had been vasodilated to the observed maximal levels then mean arterial pressure would have dropped at least to 75-77 mmHg in our experimental conditions. It is concluded that skeletal muscle vascular conductance is restrained during whole body exercise in the upright position to avoid hypotension.

  • 4. Calbet, José A L
    et al.
    Losa-Reyna, José
    Peralta, Rafael Torres
    Rasmussen, Peter
    Ponce-González, Jesús Gustavo
    Sheel, A William
    de la Calle-Herrero, Jaime
    Grau, Amelia Guadalupe
    Morales-Alamo, David
    Fuentes, Teresa
    Rodríguez-García, Lorena
    Siebenmann, Christoph
    Boushel, Robert
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Lundby, Carsten
    Limitations to oxygen transport and utilisation during sprint exercise in humans: evidence for a functional reserve in muscle O2 diffusing capacity.2015In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 593, no 20, p. 4649-4664Article in journal (Refereed)
    Abstract [en]

    KEY POINTS SUMMARY: Severe acute hypoxia reduces sprint performance. Muscle VO2 during sprint exercise in normoxia is not limited by O2 delivery, O2 off-loading from haemoglobin or structure-dependent diffusion constraints in the skeletal muscle of young healthy men. A large functional reserve in muscle O2 diffusing capacity exists and remains available at exhaustion during exercise in normoxia, which is recruited during exercise in hypoxia. During whole-body incremental exercise to exhaustion in severe hypoxia leg VO2 is primarily dependent on convective O2 delivery and less limited by diffusion constraints than previously thought. The kinetics of O2 off-loading from haemoglobin does not limit VO2 peak in hypoxia. Our results indicate that the limitation to VO2 during short sprints resides in mechanisms regulating mitochondrial respiration.

    ABSTRACT: To determine the contribution of convective and diffusive limitations to VO2 peak during exercise in humans oxygen transport and haemodynamics were measured in eleven men (22 ± 2 years) during incremental (IE) and 30-s all-out sprints (Wingate test, WgT), in normoxia (Nx, PI O2 :143 mmHg) and hypoxia (Hyp, PI O2 :73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6-7% before both WgTs to left-shift the oxyhaemoglobin dissociation curve. Leg VO2 was measured by the Fick method, and leg blood flow (BF) with thermodilution and muscle O2 diffusing capacity (DMO2 ) was calculated. In the WgT mean power output, leg BF, leg O2 delivery and leg VO2 were 7, 5, 28 and 23% lower in Hyp than Nx (P < 0.05), however, peak WgT DMO2 was higher in hypoxia (51.5 ± 9.7) than Nx (20.5 ± 3.0 ml min(-1) mmHg(-1) , P < 0.05). Despite a similar PaO2 (33.3 ± 2.4 and 34.1 ± 3.3 mmHg), mean capillary PO2 (16.7 ± 1.2 and 17.1 ± 1.6 mmHg), and peak perfusion during IE and WgT in Hyp, DMO2 and leg VO2 were 12 and 14% higher during WgT than IE in Hyp (both, P < 0.05). DMO2 was apparently insensitive to COHb (COHb: 0.7 vs 7%, in IE Hyp and WgT Hyp). At exhaustion, the Y equilibration index was well above 1.0 in both conditions, reflecting greater convective than diffusive limitation to the O2 transfer both in Nx and Hyp. In conclusion, muscle VO2 during sprint exercise is not limited by O2 delivery, the O2 off-loading from haemoglobin or structure-dependent diffusion constraints in the skeletal muscle. These findings reveal a remarkable functional reserve in muscle O2 diffusing capacity. This article is protected by copyright. All rights reserved.

  • 5.
    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.

  • 6.
    Krustrup, Peter
    et al.
    Inst of exercise and sport sciences dept of human physiology, August Krogh inst, University of Copenhagen .
    Secher, Niels H
    Relu, Mihai U
    Hellsten, Ylva
    Söderlund, Karin
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Bangsbo, Jens
    Neuromuscular blockade of slow twitch muscle fibres elevates muscle oxygen uptake and energy turnover during submaximal exercise in humans.2008In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 586, no Pt 24, p. 6037-48Article in journal (Refereed)
    Abstract [en]

    We tested the hypothesis that a greater activation of fast-twitch (FT) fibres during dynamic exercise leads to a higher muscle oxygen uptake (VO2 ) and energy turnover as well as a slower muscle on-kinetics. Subjects performed one-legged knee-extensor exercise for 10 min at an intensity of 30 W without (CON) and with (CUR) arterial injections of the non-depolarizing neuromuscular blocking agent cisatracurium. In CUR, creatine phosphate (CP) was unaltered in slow twitch (ST) fibres and decreased (P < 0.05) by 28% in FT fibres, whereas in CON, CP decreased (P < 0.05) by 33% and 23% in ST and FT fibres, respectively. From 127 s of exercise, muscle VO2 was higher (P < 0.05) in CUR compared to CON (425 +/- 25 (+/- S.E.M.) versus 332 +/- 30 ml min(-1)) and remained higher (P < 0.05) throughout exercise. Using monoexponential fitting, the time constant of the exercise-induced muscle VO2 response was slower (P < 0.05) in CUR than in CON (55 +/- 6 versus 33 +/- 5 s). During CUR and CON, muscle homogenate CP was lowered (P < 0.05) by 32 and 35%, respectively, and also muscle lactate production was similar in CUR and CON (37.8 +/- 4.1 versus 35.2 +/- 6.2 mmol). Estimated total muscle ATP turnover was 19% higher (P < 0.05) in CUR than in CON (1196 +/- 90 versus 1011 +/- 59 mmol) and true mechanical efficiency was lower (P < 0.05) in CUR than in CON (26.2 +/- 2.0 versus 30.9 +/- 1.5%). In conclusion, the present findings provide evidence that FT fibres are less efficient than ST fibres in vivo at a contraction frequency of 1 Hz, and that the muscle VO2 kinetics is slowed by FT fibre activation.

  • 7. Löscher, W N
    et al.
    Cresswell, Andrew G
    Thorstensson, Alf
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Excitatory drive to the alpha-motoneuron pool during a fatiguing submaximal contraction in man.1996In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 491 ( Pt 1), p. 271-80Article in journal (Refereed)
    Abstract [en]

    1. This study was undertaken to examine changes of excitatory drive to the triceps surae alpha-motoneuron pool during fatiguing submaximal isometric contractions in man. Eight healthy subjects maintained isometric plantar flexions at 30 percent of maximum voluntary contraction (MVC) until the limit of endurance (range, 6-9 min). 2. Excitability of the alpha-motoneuron pool to Ia afferent stimulation (H reflex), electromyograms (EMG) and maximum compound motor unit action potentials (Mmax) from the lateral (LG) and medial heads (MG) of the gastrocnemius as well as from the soleus muscle (Sol) were recorded throughout the contraction. Superimposed maximum twitch torques (twitch occlusion) and isometric torque fluctuations (tremor) were also recorded as indirect measures of excitatory drive. 3. H reflexes were studied at different levels of underlying voluntary contraction to assess the relationship between H reflex amplitude and excitatory drive. With increasing levels of underlying contraction up to MVC, superimposed H reflex amplitude increased for LG in six subjects, for MG in all eight and for Sol in five. In the remaining cases, H reflex amplitude first increased and then plateaued between 30-50% of MVC. 4. H/Mmax ratios increased during fatigue in those muscles that showed an H reflex amplitude increase with high levels of underlying contraction. In these cases, LG and MG H/Mmax increased significantly after about 50 and 20% of endurance time onward, respectively, whereas Sol H/Mmax demonstrated a significant increase up to 40% of endurance time. 5. EMG root mean square (r.m.s.) increased linearly throughout the contraction for all three muscles, while tremor r.m.s. increased in a non-linear way, with a steeper increase from 60% of endurance time onward. Superimposed twitch amplitude decreased significantly from 25% of endurance time onward. 6. It is concluded that during fatiguing isometric contractions at 30% of MVC, the excitatory drive to the triceps surae alpha-motoneuron pool increases. This is thought to be a compensatory mechanism to facilitate recruitment of new, unfatigued motor units (MUs), and/or to increase MU firing rates. The facts that the twitch is not abolished at endurance limit and that the EMG does not attain its unfatigued MVC level are strong indications that central fatigue occurred during the sustained submaximal contraction.

  • 8. Malm, Christer
    et al.
    Sjödin, The Late Bertil
    Sjöberg, Berit
    Lenkei, Rodica
    Renström, Per
    Lundberg, Ingrid E
    Ekblom, Björn
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Björn Ekblom's research group.
    Leukocytes, cytokines, growth factors and hormones in human skeletal muscle and blood after uphill or downhill running.2004In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 556, no Pt 3, p. 983-1000Article in journal (Refereed)
    Abstract [en]

    Muscular adaptation to physical exercise has previously been described as a repair process following tissue damage. Recently, evidence has been published to question this hypothesis. The purpose of this study was to investigate inflammatory processes in human skeletal muscle and epimysium after acute physical exercise with large eccentric components. Three groups of subjects (n= 19) performed 45 min treadmill running at either 4 deg (n= 5) or 8 deg (n= 9) downhill or 4 deg uphill (n= 5) and one group served as control (n= 9). One biopsy was taken from each subject 48 h post exercise. Blood samples were taken up to 7 days post exercise. Compared to the control group, none of the markers of inflammation in muscle and epimysium samples was different in any exercised group. Only subjects in the Downhill groups experienced delayed onset of muscle soreness (DOMS) and increased serum creatine kinase activity (CK). The detected levels of immunohistochemical markers for T cells (CD3), granulocytes (CD11b), leukaemia inhibitory factor (LIF) and hypoxia-inducible factor 1beta (HIF-1beta) were greater in epimysium from exercised subjects with DOMS ratings >3 (0-10 scale) compared to exercised subjects without DOMS but not higher than controls. Eccentric physical exercise (downhill running) did not result in skeletal muscle inflammation 48 h post exercise, despite DOMS and increased CK. It is suggested that exercise can induce DOMS by activating inflammatory factors present in the epimysium before exercise. Repeated physical training may alter the content of inflammatory factors in the epimysium and thus reduce DOMS.

  • 9. Mogensen, Martin
    et al.
    Bagger, Malene
    Pedersen, Preben
    Fernstrom, Maria
    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.
    Cycling efficiency in humans is related to low UCP3 content and to type I fibres but not to mitochondrial efficiency2006In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 571, no 3, p. 669-681Article in journal (Refereed)
    Abstract [en]

    The purpose of this study was to investigate the hypothesis that cycling efficiency in vivo is related to mitochondrial efficiency measured in vitro and to investigate the effect of training status on these parameters. Nine endurance trained and nine untrained male subjects ( , respectively) completed an incremental submaximal efficiency test for determination of cycling efficiency (gross efficiency, work efficiency (WE) and delta efficiency). Muscle biopsies were taken from m. vastus lateralis and analysed for mitochondrial respiration, mitochondrial efficiency (MEff; i.e. P/O ratio), UCP3 protein content and fibre type composition (% MHC I). MEff was determined in isolated mitochondria during maximal (state 3) and submaximal (constant rate of ADP infusion) rates of respiration with pyruvate. The rates of mitochondrial respiration and oxidative phosphorylation per muscle mass were about 40% higher in trained subjects but were not different when expressed per unit citrate synthase (CS) activity (a marker of mitochondrial density). Training status had no influence on WE (trained 28.0 +/- 0.5, untrained 27.7 +/- 0.8%, N.S.). Muscle UCP3 was 52% higher in untrained subjects, when expressed per muscle mass (P < 0.05 versus trained). WE was inversely correlated to UCP3 (r=-0.57, P < 0.05) and positively correlated to percentage MHC I (r= 0.58, P < 0.05). MEff was lower (P < 0.05) at submaximal respiration rates (2.39 +/- 0.01 at 50% ) than at state 3 (2.48 +/- 0.01) but was neither influenced by training status nor correlated to cycling efficiency. In conclusion cycling efficiency was not influenced by training status and not correlated to MEff, but was related to type I fibres and inversely related to UCP3. The inverse correlation between WE and UCP3 indicates that extrinsic factors may influence UCP3 activity and thus MEff in vivo.

  • 10. Pinniger, G J
    et al.
    Nordlund Ekblom, Maria
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Steele, J R
    Cresswell, Andrew G
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    H-reflex modulation during passive lengthening and shortening of the human triceps surae.2001In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 534, no Pt 3, p. 913-23Article in journal (Refereed)
    Abstract [en]

    1. The present study investigated the effects of lengthening and shortening actions on H-reflex amplitude. H-reflexes were evoked in the soleus (SOL) and medial gastrocnemius (MG) of human subjects during passive isometric, lengthening and shortening actions performed at angular velocities of 0, +/-2, +/-5 and +/-15 deg s(-1). 2. H-reflex amplitudes in both SOL and MG were significantly depressed during passive lengthening actions and facilitated during passive shortening actions, when compared with the isometric H-reflex amplitude. 3. Four experiments were performed in which the latencies from the onset of movement to delivery of the stimulus were altered. Passive H-reflex modulation during lengthening actions was found to begin at latencies of less than 60 ms suggesting that this inhibition was due to peripheral and/or spinal mechanisms. 4. It is postulated that the H-reflex modulation seen in the present study is related to the tonic discharge of muscle spindle afferents and the consequent effects of transmission within the Ia pathway. Inhibition of the H-reflex at less than 60 ms after the onset of muscle lengthening may be attributed to several mechanisms, which cannot be distinguished using the current protocol. These may include the inability to evoke volleys in Ia fibres that are refractory following muscle spindle discharge during rapid muscle lengthening, a reduced probability of transmitter release from the presynaptic terminal (homosynaptic post-activation depression) and presynaptic inhibition of Ia afferents from plantar flexor agonists. Short latency facilitation of the H-reflex may be attributed to temporal summation of excitatory postsynaptic potentials arising from muscle spindle afferents during rapid muscle lengthening. At longer latencies, presynaptic inhibition of Ia afferents cannot be excluded as a potential inhibitory mechanism.

  • 11.
    Rosdahl, Hans
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Ungerstedt, Urban
    Jorfeldt, Lennart
    Henriksson, Jan
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Interstitial glucose and lactate balance in human skeletal muscle and adipose tissue studied by microdialysis.1993In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 471, p. 637-57Article in journal (Refereed)
    Abstract [en]

    1. Microdialysis was used to gain insight into the substrate exchanges in the interstitial space of skeletal muscle and adipose tissue. Probes were inserted in the quadriceps femoris muscle and para-umbilical subcutaneous adipose tissue of thirteen subjects and microdialysis was performed at different flow rates (1-4 microliters min-1) and during changes in tissue blood flow. 2. When ethanol (5 mM) is included in the perfusion solution, the ethanol clearance from the probe is a measure of tissue blood flow. Blood flow changes induced by adenosine or vasopressin perfusion, by exercise or by circulatory occlusion resulted in ethanol clearance values of 69-139% of the basal level. The ethanol clearance was higher in skeletal muscle than in adipose tissue (32-62%, P < 0.001), a difference compatible with a higher blood flow in muscle tissue. 3. The fraction of the interstitial glucose concentration that was recovered with the microdialysis was similar in skeletal muscle (the absolute values being 1.70 +/- 0.14 mM at 1 microliter min-1 and 0.59 +/- 0.05 mM at 4 microliters min-1) and adipose tissue (1.89 +/- 0.20 mM at 1 microliter min-1; 0.54 +/- 0.05 mM at 4 microliters min-1) and correlated inversely with the tissue ethanol clearance, both in the basal state and during changes in tissue blood flow (muscle: r = -0.56 to -0.67; adipose tissue r = -0.72 to -0.95). Coefficients of variation were 6-8% (glucose) and 11-16% (lactate) and were similar during isometric exercise. The reproducibility of the technique (comparison of two contralateral probes; perfusion flow rate 4 microliters min-1) was 5.3-8.3% (ethanol) and 23.9-20.8% (glucose) in muscle (n = 6) and adipose tissue (n = 4) respectively. 4. The skeletal muscle dialysate lactate concentration (1 microliter min-1: 1.16 +/- 0.2 mM) was higher than in adipose tissue (0.76 +/- 0.08 mM, P < 0.05), where the absolute amount of lactate that could be removed from the tissue (at 4 microliters min-1) was only half of that in skeletal muscle (0.8 +/- 0.11 vs. 1.76 +/- 0.23 nmol min-1, P < 0.05). The dialysate lactate level was not affected in either tissue by large changes in the interstitial glucose concentration indicating that in neither tissue is blood glucose a significant source of lactate formation. 5. The blood flow effects on the dialysate glucose concentration are the likely consequence of probe glucose drainage artificially shifting the balance between the supply and consumption of interstitial glucose.(ABSTRACT TRUNCATED AT 400 WORDS)

  • 12.
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    Boosting fat burning with carnitine: an old friend comes out from the shadow.2011In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 589, no Pt 7, p. 1509-10Article in journal (Refereed)
  • 13.
    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. Karolinska institutet.
    Fernström, Maria
    Karolinska institutet.
    Svensson, Michael
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences. Karolinska institutet.
    Tonkonogi, Michail
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences. Karolinska institutet.
    No evidence of an intracellular lactate shuttle in rat skeletal muscle.2002In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 541, no Pt 2, p. 569-74Article in journal (Refereed)
    Abstract [en]

    The concerted view is that cytosolic pyruvate is transferred into mitochondria and after oxidative decarboxylation further metabolized in the tricarboxylic acid cycle. Recently this view has been challenged. Based on experimental evidence from rat skeletal muscle it has been concluded that mitochondria predominantly oxidize lactate in vivo and that this constitutes part of an 'intracellular lactate shuttle'. This view appears to be gaining acceptance in the scientific community and due to its conceptual importance, confirmation by independent experiments is required. We have repeated the experiments in mitochondria isolated from rat soleus muscle. Contrary to the previously published findings we cannot find any mitochondrial respiration with lactate. Analysis of lactate dehydrogenase (LDH) by spectrophotometry demonstrated that the activity in the mitochondrial fraction was only 0.7 % of total activity. However, even when external LDH was added to mitochondria, there were no signs of respiration with lactate. In the presence of conditions where lactate is converted to pyruvate (external additions of both LDH and NAD(+)), mitochondrial oxygen consumption increased. Furthermore, we provide theoretical evidence that direct mitochondrial lactate oxidation is energetically unlikely. Based on the present data we conclude that direct mitochondrial lactate oxidation does not occur in skeletal muscle. The presence of an 'intracellular lactate shuttle' can therefore be questioned.

  • 14.
    Tokuno, Craig
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Laboratory for Biomechanics and Motor Control.
    Taube, W
    Cresswell, Andrew G
    Changes in cortical and corticospinal excitability during standing2007In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793Article in journal (Refereed)
  • 15.
    Tonkonogi, Michail
    et al.
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Harris, B
    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 oxidative function in human saponin-skinned muscle fibres: effects of prolonged exercise.1998In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 510 ( Pt 1), p. 279-86Article in journal (Refereed)
    Abstract [en]

    1. The influence of prolonged exhaustive exercise on mitochondrial oxidative function was investigated in ten men. 2. Muscle biopsies were taken before and after exercise and mitochondrial respiration investigated in fibre bundles made permeable by pretreatment with saponin. 3. After exercise, respiration in the absence of ADP increased by 18 % (P < 0.01), but respiration at suboptimal ADP concentration (0.1 mM) and maximal ADP-stimulated respiration (1 mM ADP) remained unchanged. 4. In the presence of creatine (20 mM), mitochondrial affinity for ADP increased markedly and respiration at suboptimal ADP concentration (0.1 mM) was similar (pre-exercise) or higher (post-exercise; P < 0.05) than with 1 mM ADP alone. The increase in respiratory rate with creatine was correlated to the relative type I fibre area (r = 0.84). Creatine-stimulated respiration increased after prolonged exercise (P < 0.01). 5. The respiratory control index (6.8 +/- 0.4, mean +/- s.e.m.) and the ratio between respiration at 0.1 and 1 mM ADP (ADP sensitivity index, 0.63 +/- 0.03) were not changed after exercise. The sensitivity index was negatively correlated to the relative type I fibre area (r = -0.86). 6. The influence of exercise on muscle oxidative function has for the first time been investigated with the skinned-fibre technique. It is concluded that maximal mitochondrial oxidative power is intact or improved after prolonged exercise, while uncoupled respiration is increased. The latter finding may contribute to the elevated post-exercise oxygen consumption. The finding that the sensitivity of mitochondrial respiration for ADP and creatine are related to fibre-type composition indicates intrinsic differences in the control of mitochondrial respiration between fibres.

  • 16. Walsh, B
    et al.
    Tonkonogi, Michail
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Söderlund, Karin
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences.
    Hultman, E
    Saks, V
    Sahlin, Kent
    Swedish School of Sport and Health Sciences, GIH, Department of Sport and Health Sciences, Research group for Mitokondriell funktion och metabolisk kontroll.
    The role of phosphorylcreatine and creatine in the regulation of mitochondrial respiration in human skeletal muscle.2001In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 537, no Pt 3, p. 971-8Article in journal (Refereed)
    Abstract [en]

    1. The role of phosphorylcreatine (PCr) and creatine (Cr) in the regulation of mitochondrial respiration was investigated in permeabilised fibre bundles prepared from human vastus lateralis muscle. 2. Fibre respiration was measured in the absence of ADP (V(0)) and after sequential additions of submaximal ADP (0.1 mM ADP, V(submax)), PCr (or Cr) and saturating [ADP] (V(max)). 3. V(submax) increased by 55 % after addition of saturating creatine (P < 0.01; n = 8) and half the maximal effect was obtained at 5 mM [Cr]. In contrast, V(submax) decreased by 54 % after addition of saturating phosphorylcreatine (P < 0.01; n = 8) and half the maximal effect was obtained at 1 mM [PCr]. V(max) was not affected by Cr or PCr. 4. V(submax) was similar when PCr and Cr were added simultaneously at concentrations similar to those in muscle at rest (PCr/Cr = 2) and at low-intensity exercise (PCr/Cr = 0.5). At conditions mimicking high-intensity exercise (PCr/Cr = 0.1), V(submax) increased to 60 % of V(max) (P < 0.01 vs. rest and low-intensity exercise). 5. Eight of the subjects participated in a 16 day Cr supplementation programme. Following Cr supplementation, V(0) decreased by 17 % (P < 0.01 vs. prior to Cr supplementation), whereas ADP-stimulated respiration (with and without Cr or PCr) was unchanged. 6. For the first time evidence is given that PCr is an important regulator of mitochondrial ADP-stimulated respiration. Phosphorylcreatine decreases the sensitivity of mitochondrial respiration to ADP whereas Cr has the opposite effect. During transition from rest to high-intensity exercise, decreases in the PCr/Cr ratio will effectively increase the sensitivity of mitochondrial respiration to ADP. The decrease in V(0) after Cr supplementation indicates that intrinsic changes in membrane proton conductance occur.

  • 17. 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
    Krook, A
    Zierath, J R
    Marathon running increases ERK1/2 and p38 MAP kinase signalling to downstream targets in human skeletal muscle.2001In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 536, no Pt 1, p. 273-82Article in journal (Refereed)
    Abstract [en]

    1. We tested the hypothesis that long-distance running activates parallel mitogen-activated protein kinase (MAPK) cascades that involve extracellular signal regulated kinase 1 and 2 (ERK1/2) and p38 MAPK and their downstream substrates. 2. Eleven men completed a 42.2 km marathon (mean race time 4 h 1 min; range 2 h 56 min to 4 h 33 min). Vastus lateralis muscle biopsies were obtained before and after the race. Glycogen content was measured spectrophotometrically. ERK1/2 and p38 MAPK phosphorylation was determined by immunoblot analysis using phosphospecific antibodies. Activation of the downstream targets of ERK1/2 and p38 MAPK, MAPK-activated protein kinase-1 (MAPKAP-K1; also called p90 ribosomal S6 kinase, p90rsk), MAPK-activated protein kinase-2 (MAPKAP-K2), mitogen- and stress-activated kinase 1 (MSK1) and mitogen- and stress-activated kinase 2 (MSK2) was determined using immune complex assays. 3. Muscle glycogen content was reduced by 40 +/- 6 % after the marathon. ERK1/2 phosphorylation increased 7.8-fold and p38 MAPK phosphorylation increased 4.4-fold post-exercise. Prolonged running did not alter ERK1/2 and p38 MAPK protein expression. The activity of p90rsk, a downstream target of ERK1/2, increased 2.8-fold after the marathon. The activity of MAPKAPK-K2, a downstream target of p38 MAPK, increased 3.1-fold post-exercise. MSK1 and MSK2 are downstream of both ERK1/2 and p38 MAPK. MSK1 activity increased 2.4-fold post-exercise. MSK2 activity was low, relative to MSK1, with little activation post-exercise. 4. In conclusion, prolonged distance running activates MAPK signalling cascades in skeletal muscle, including increased activity of downstream targets: p90rsk, MAPKAP-K2 and MSK. Activation of these downstream targets provides a potential mechanism by which exercise induces gene transcription in skeletal muscle.

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