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Biomedical subjects

K Sahlin

Publications and source records attributed to K Sahlin.

At least 19 recordsLinked to original sources
PubMed1995

Effects of prolonged exercise on the contractile properties of human quadriceps muscle.

The contractile properties of the quadriceps muscle were measured in seven healthy male subjects before, during and after prolonged cycling to exhaustion. Special efforts were made to obtain measurements immediately after exercise. The exercise intensity corresponded to about 75% of estimated maximal O2 uptake and time to exhaustion was mean 85 (SEM 9) min. At the end of the cycling heart rate and perceived exertion for the legs were 94% and 97% of maximal values, respectively. Maximal voluntary isometric force (MVC) had decreased after 5 min of exercise to a mean 91 (SEM 4)% of the pre-exercise value (P < 0.05) and decreased further to a mean 82 (SEM 6) and mean 66 (SEM 5)% after 40-min cycling and at exhaustion, respectively. A new finding was that during recovery reversal of MVC occurred in different phases where the half recovery time of the initial rapid phase was about 2 min. The MVC was a mean 80 (SEM 2)% of the pre-exercise value after 30 min and was not affected by superimposed electrical stimulation. Maximal voluntary concentric and eccentric forces decreased to 74% and 80% of initial values at exhaustion (P < 0.05). The kinetics of isometric contraction expressed as the time between 5% and 50% of tension (rise time) and the time between 95% and 50% of tension (relaxation time) were not significantly affected by the prolonged cycling. The electromechanical delay measured as the time between the first electrical stimulus and 5% of tension decreased from a mean 32 (SEM 1) ms at rest to a mean 26.6 (SEM 0.6) ms at fatigue (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Tricarboxylic acid cycle intermediates during incremental exercise in healthy subjects and in patients with McArdle's disease.

1. The importance of the level of tricarboxylic acid cycle intermediates (malate, citrate and fumarate) for energy transduction during exercise has been investigated in six healthy subjects and in two patients with muscle phosphorylase deficiency (McArdle's disease). 2. Healthy subjects cycled for 10 min at low (50 W), moderate [130 +/- 6 W (mean +/- SEM)] and high (226 +/- 12 W) work rates, corresponding to 26, 50 and 80% of their maximal O2 uptake, respectively. Patients with McArdle's disease cycled for 11-13 min at submaximal (40 W) rates, and to fatigue at maximal work rates of 60-90 W. 3. In healthy subjects, phosphocreatine was unchanged during low work rates, but decreased to 79 and 32% of the initial level during moderate and high work rates. In patients with McArdle's disease, phosphocreatine decreased to 82 and 34% of the initial level during submaximal and peak exercise. Muscle lactate increased in healthy subjects during exercise at moderate and high work rates, but remained low in patients with McArdle's disease. 4. In healthy subjects, tricarboxylic acid cycle intermediates were similar at rest and at low work rates (0.48 +/- 0.04 mmol/kg dry weight), but increased to 1.6 +/- 0.2 mmol/kg dry weight and 4.0 +/- 0.3 mmol/kg dry weight at moderate and high work rates. The tricarboxylic acid cycle intermediate level in patients with McArdle's disease was similar to that in healthy subjects at rest, but was markedly reduced during exercise when compared at the same relative intensity. The peak level of tricarboxylic acid cycle intermediates in patients with McArdle's disease was 22% of that in healthy subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effect of hypoxia on muscle oxygenation and metabolism during arm exercise in humans.

The influence of hypoxaemia on anaerobic energy production during arm exercise (AE) has been investigated. Six men were studied during maximal AE and during 10 min of sitting submaximal AE under both normoxic (AEN) and hypoxic (AEH, respiratory hypoxia, 12% O2) conditions. Peak pulmonary oxygen uptake (VO2) during maximal AE in normoxia and hypoxia was 2.25 +/- 0.15 and 2.18 +/- 0.14 l min-1, respectively (P < 0.05). The absolute workload was the same during submaximal AEN and AEH and corresponded to 54% of peak VO2 during normoxic maximal AE. To eliminate the potential influence of differences in catecholamine levels on the metabolic response, the submaximal experiments were performed during beta-adrenoceptor blockade. Oxygen deficit was 1.45 +/- 0.26 and 1.67 +/- 0.191 during AEN and AEH, respectively (n.s.). Oxygen extraction at steady state was lower during AEH than during AEN, and assuming a similar O2 demand this corresponds to a 14% higher muscle blood flow during AEH. At the onset of both AEN and AEH, O2 extraction (a-v O2) across the arm increased transiently above that at steady state, the increase being more pronounced during AEN than during AEH (P < 0.05). Muscle oxygenation, measured by near-infrared spectroscopy, demonstrated an initial decrease which was partially reversed as exercise proceeded. The reversal of muscle O2 desaturation was slower in all subjects during AEH (t1/2 = 2.4 +/- 0.2 min) than during AEN (t1/2 = 1.2 +/- 0.2 min; P < 0.01). After 10 min of exercise, arterial blood lactate was higher (P < 0.05) during AEH (5.5 +/- 0.2 mmol l-1) than during AEN (4.9 +/- 0.6 mmol l-1), whereas arterial plasma ammonia (NH3) was similar. The arteriovenous difference for both lactate and ammonia was similar during AEN and AEH. It is concluded that the high anaerobic energy production at the onset of AE is associated with a transient increase in O2 extraction and a transient decrease in muscle oxygenation. The effects of hypoxaemia on peak VO2, oxygen deficit and blood metabolites are less pronounced than previously described during submaximal leg exercise (LE).

Adult↗
PubMed1994

Effect of muscle mass on lactate formation during exercise in humans.

To elucidate the mechanisms of lactate formation during submaximal exercise, eight men were studied during one- (1-LE) and two-leg (2-LE) exercise (approximately 11-min cycling) using the catheterization technique and muscle biopsies (quadriceps femoris muscle). The absolute exercise intensity and thus the energy demand for the exercising limb was the same [mean 114 (SEM 7) W] during both 1-LE and 2-LE. At the end of exercise partial pressure of O2 and O2 saturation in femoral venous blood were lower and arterial adrenaline and noradrenaline were higher during 2-LE than during 1-LE. Mean arterial blood lactate concentration increased to 10.8 (SEM 0.8) (2-LE) and 5.2 (SEM 0.4) mmol.l-1 (1-LE) after 10 min of exercise. The intramuscular metabolic response to exercise was attenuated during 1-LE [mean, lactate = 49 (SEM 9); glucose 6-P = 3.3 (SEM 0.3); nicotinamide adenine dinucleotide, reduced = 0.17 (SEM 0.02); adenosine 5'-diphosphate 2.7 (SEM 0.1) mmol.kg dry mass-1] compared to 2-LE [76 (SEM 6); 6.1 (SEM 0.7); 0.21 (SEM 0.02); 3.0 (SEM 0.1) mmol.kg dry mass-1, respectively]. To elucidate whether the lower plasma adrenaline concentration could contribute to the attenuated metabolic response, additional experiments were performed on four of the eight subjects with infusion of adrenaline during 1-LE (1-LEE). Average plasma adrenaline concentration was increased during 1-LEE and reached 2-4 times higher levels than during 2-LE. Post-exercise muscle lactate and glucose 6-P contents were higher during 1-LEE than during 1-LE and were similar to those during 2-LE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed1993

Absence of phosphocreatine resynthesis in human calf muscle during ischaemic recovery.

Changes in the metabolites phosphocreatine (PCr), Pi and ATP were quantified by 31P n.m.r. spectroscopy in the human calf muscle during isometric contraction and recovery under ischaemic conditions. Time resolution of the measurements was 10 s. During a 30-60 s ischaemic isometric contraction, PCr decreased linearly at a rate of 1.17%/s (relative to the resting value) at a contraction strength equivalent to 70% of the maximal voluntary contraction (MVC) and at a rate of 2.43%/s at 90% MVC. There was a corresponding increase in Pi but the concentration of ATP did not change. pH decreased linearly during contraction by 4.22 and 8.23 milli-pH units/s at 70 and 90% MVC respectively. During a subsequent 5 min interval of ischaemic recovery, PCr, Pi, ATP, phosphomonoesters and calculated free ADP, free AMP and pH retained the value they had attained by the end of contraction with no significant recovery. Thus it is concluded that anaerobic glycolysis and glycogenolysis is halted momentarily on termination of contraction and that PCr is not resynthesized during ischaemic recovery. This paradoxical arrest of glycolytic flow in spite of the very significantly elevated concentration of potent activators such as Pi and free AMP clearly indicates that parameters other than PCr, ATP, Pi, calculated pH, free ADP and free AMP regulate glycolysis and glycogenolysis of human skeletal muscle very efficiently under ischaemic conditions.

Adenosine Diphosphate↗
PubMed1993

High anaerobic energy release during submaximal arm exercise.

The anaerobic energy release during submaximal arm (AE) and leg exercise (LE) has been estimated from O2 deficit measured at the onset of exercise. Eight male subjects were studied during 8-10 min of arm or leg cycling at the same relative workload (53% of the peak exercise-induced increase in pulmonary oxygen uptake, VO2). The workloads were 78 +/- 4 W during AE and 173 +/- 11 W during LE and VO2 was 1.51 +/- 0.06 1 min-1 for AE and 2.33 +/- 0.15 1 min-1 for LE. The half-time of the VO2 on-response was considerably longer (P < 0.01) during AE (62 +/- 9 s) than during LE (33 +/- 4 s) and the peak blood lactate concentration was higher (P < 0.05) during AE (4.8 +/- 0.5 mmol.l-1) than during LE (3.5 +/- 0.4 mmol.l-1). Oxygen deficit was 1.64 +/- 0.16 and 1.78 +/- 0.16 1 for AE and LE respectively. Oxygen deficit was higher during AE than during LE when related to absolute workload (P < 0.01), or to VO2 at steady state (P < 0.001) or to limb volume (P < 0.001). The proportion of the total energy demand covered by anaerobic energy release at the onset of exercise (0-8 min) was about 54% higher (P < 0.01) during AE than during LE. It is concluded that the energy release to a greater extend is covered by anaerobic processes during AE than during LE.

Adult↗
PubMed1993

High lactate and NH3 release during arm vs. leg exercise is not due to beta-adrenoceptor stimulation.

To investigate the differences in metabolic response between arm exercise (AE) and leg exercise (LE) and to elucidate the underlying mechanisms, seven men were studied during 20 min of AE or LE both with (beta) and without (control, C) nonselective beta-blockade (beta B) (propranolol). The work loads corresponded to 59 and 60% of peak pulmonary O2 uptake (VO2) during LE and AE, respectively. Pulmonary VO2 increased more slowly at the onset of exercise during AEC (half time = 61 +/- 9 s) than during LEC (half time = 35 +/- 3 s) and was not affected by beta B. At the onset of exercise the arteriovenous O2 difference across the exercising limb increased above that of steady state during AEC but not during LEC. This demonstrates that the adjustment of O2 delivery is slower than that of arm VO2 during AE. Despite the smaller exercising muscle mass, the release of lactate and NH3 was about twofold higher during AEC than during LEC. The difference in metabolic response between AE and LE was not altered by beta B. Lactate release was not reduced by beta B but, if anything, tended to increase during both AE and LE (beta vs. C). beta B increased NH3 release during LE (beta vs. C) but not during AE (beta vs. C). We conclude that AE compared with LE at the same relative work load is associated with a greater release of lactate and NH3, indicating a more severe metabolic stress during AE. Furthermore, the present data suggest that the increase in blood lactate at these submaximal exercise intensities is caused by factors other than beta-adrenoceptor stimulation.

Adult↗
PubMed1993

Biochemical indicators of hazardous shoulder-neck loads in light industry.

Prolonged, repetitive handling of light material is known to increase the risk of shoulder-neck disorders. Biological risk indicators related to musculoskeletal exposure, applicable by the general practitioner in the workplace, could provide an instrument for early intervention and rehabilitation. Eight women were studied, all full-time workers performing assembly tasks associated with a high prevalence of shoulder-neck complaints. All subjects were more tender in the shoulder region than young women in low-risk occupations. Heart rate recordings indicated a low general metabolic load during work. Concentrations in antecubital venous blood of several markers for metabolic stress and cellular damage (lactate, ammonia, hypoxanthine, urate, malondialdehyde, potassium, creatine kinase) were normal for all subjects, and showed no increase during 3 consecutive working days. Thus, the blood markers did not reflect hazardous shoulder-neck exposure.

Adult↗
PubMed1992

Repetitive static muscle contractions in humans--a trigger of metabolic and oxidative stress?

Repetitive static exercise (RSE) is a repetitive condition of partial ischaemia/reperfusion and may therefore be connected to the formation of oxygen-derived free radicals and tissue damage. Seven subjects performed two-legged intermittent knee extension exercise repeating at 10 s on and 10 s off at a target force corresponding to about 30% of the maximal voluntary contraction force. The RSE was continued for 80 min (n = 4) or to fatigue (n = 3). Four of the subjects also performed submaximal dynamic exercise (DE) at an intensity of about 60% maximal oxygen uptake (VO2max) for the same period. Whole body oxygen uptake (VO2) increased gradually with time during RSE (P less than 0.05), indicating a decreased mechanical efficiency. This was further supported by a slow increase in leg blood flow (P less than 0.05) and leg oxygen utilization (n.s.) during RSE. In contrast, prolonged RSE had no effect on VO2 during submaximal cycling. Maximal force (measured in six additional subjects) declined gradually during RSE and was not completely restored after 60 min of recovery. After 20 and 80 min (or at fatigue) RSE phosphocreatine (PC) dropped to 74% and 60% of the initial value, respectively. A similar decrease in PC occurred during DE. Muscle and arterial lactate concentrations remained low during both RSE and DE. The three subjects who were unable to continue RSE for 80 min showed no signs of a more severe energy imbalance than the other subjects. A continuous release of K+ occurred during both RSE and DE.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Non-invasive measurements of O2 availability in human skeletal muscle with near-infrared spectroscopy.

The availability of O2 in the human vastus lateralis muscle has been investigated with non-invasive near-infrared spectroscopy (NIRS) using a commercially available unit (RunMan, NIM Inc. Philadelphia). The measuring probe placed above the skin illuminates the underlying tissue and measures the reflected light at two wavelengths (760 and 850 nm). Due to differences in the absorption spectra between HbO2 and Hb the difference in light intensity at these two wavelengths will be a relative index of tissue oxygenation. Prolonged arterial occlusion and static contraction have been studied. Arterial occlusion resulted in a decreased O2 saturation with a half-time of 2.3 +/- 0.2 min (mean +/- SE, n = 4). Restoration of blood flow resulted in a rapid tissue reoxygenation with a half-time of 24 +/- 2 s. Reoxygenation after static contraction occurred with a half time of 19-37 s. The half-time of reoxygenation subsequent to exercise and/or ischemia may be a valuable parameter in sports medicine and in the evaluation of peripheral vascular disease.

Adolescent↗
PubMed1992

Metabolic factors in fatigue.

The supply of energy is of fundamental importance for the ability to sustain exercise. The maximal duration of exercise is negatively related to the relative intensity both during dynamic and static exercise. Since exercise intensity is linearly related to the rate of energy utilisation this suggests that energetic deficiency plays a major role in the aetiology of muscle fatigue. Characteristic metabolic changes in the muscle are generally observed at fatigue--the pattern being different after short term exercise (lactate accumulation and phosphocreatine depletion) from after prolonged exercise at moderate intensity (glycogen depletion). A common metabolic denominator at fatigue during these and many other conditions is a reduced capacity to generate ATP and is expressed by an increased catabolism of the adenine nucleotide pool in the muscle fibre. Transient increases in ADP are suggested to occur during energetic deficiency and may be the cause of fatigue. Experimental evidence from human studies demonstrate that near maximal power output can be attained during acidotic conditions. Decreases in muscle pH is therefore unlikely to affect the contractile machinery by a direct effect. However, acidosis may interfere with the energy supply possibly by reducing the glycolytic rate, and could by this mechanism be related to muscle fatigue.

AMP Deaminase↗
PubMed1991

Changes in plasma hypoxanthine and free radical markers during exercise in man.

Eight men cycled for about 6 minutes at workloads corresponding to 44 and 72% of maximal oxygen uptake and to fatigue at 98% maximal oxygen uptake. Blood samples from a brachial artery and a femoral vein were taken at rest and during exercise. Hypoxanthine, xanthine and urate in plasma were significantly elevated at fatigue and after 10 minutes of recovery. Only hypoxanthine showed a significant arterio-femoral venous difference. The release of hypoxanthine from the legs increased during the recovery period and was three-fold higher 10 minutes post exercise than at the end of exercise. It is concluded that the marked increase in plasma hypoxanthine which occurs during intensive exercise originates from the working muscle whereas the transformation to xanthine and urate may occur in other tissues. Glutathione, methemoglobin and malondialdehyd (MDA) were used as plasma markers of free radicals. Total glutathione (glutathione + glutathionedisulfide) in blood and plasma increased during intensive exercise and may be indicative of free radical formation. However, MDA was not detectable in plasma during any conditions (less than 0.1 mumol x l-1 plasma) and methemoglobin decreased slightly during exercise. Further studies using more specific techniques are required to determine whether the formation of free radicals is increased after brief intensive exercise.

Adult↗
PubMed1991

Regulation of glucose utilization in human skeletal muscle during moderate dynamic exercise.

The effect of bicycle exercise (75% of maximal oxygen uptake) on glucose uptake by the inferior limb (LGU) and glycolysis in human skeletal muscle has been investigated. Biopsies were obtained from the quadriceps femoris muscle before exercise, after 5 and 40 min of exercise, and at fatigue [74.9 +/- 4.7 (SE) min]. LGU was 0.05 +/- 0.02 mmol/min at rest, increased approximately sevenfold after 5 min of exercise, and continued to increase linearly during the first 40 min of exercise. Thereafter LGU stabilized at approximately 1.4 mmol/min until fatigue. Intracellular glucose was low at rest but increased sixfold after 5 min of exercise (P less than 0.01 vs. rest); thereafter, intracellular glucose decreased and was not significantly different from the value at rest after 40 min or at fatigue (P greater than 0.05). D-Glucose 6-phosphate (G-6-P) and alpha-D-glucose 1,6-bisphosphate (G-1,6-P2) (inhibitors of hexokinase) increased significantly after 5 min of exercise (approximately 300% G-6-P; approximately 25% G-1,6-P2) and then decreased continuously. The muscle glycolytic rate (glycogenolysis + glucose uptake) averaged 7.7 mmol.kg dry wt-1.min-1 during the first 40 min of exercise and 3.7 mmol.kg dry wt-1.min-1 during the last 35 min of exercise. The contribution of extracellular glucose to muscle glycolysis was estimated to be only 5 and 19% during the initial and latter phases of exercise, respectively. It is concluded that, during the initial phase of exercise, glucose utilization is limited by phosphorylation, probably due to G-6-P-dependent inhibition of hexokinase.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Deficiency of skeletal muscle succinate dehydrogenase and aconitase. Pathophysiology of exercise in a novel human muscle oxidative defect.

We evaluated a 22-yr-old Swedish man with lifelong exercise intolerance marked by premature exertional muscle fatigue, dyspnea, and cardiac palpitations with superimposed episodes lasting days to weeks of increased muscle fatigability and weakness associated with painful muscle swelling and pigmenturia. Cycle exercise testing revealed low maximal oxygen uptake (12 ml/min per kg; healthy sedentary men = 39 +/- 5) with exaggerated increases in venous lactate and pyruvate in relation to oxygen uptake (VO2) but low lactate/pyruvate ratios in maximal exercise. The severe oxidative limitation was characterized by impaired muscle oxygen extraction indicated by subnormal systemic arteriovenous oxygen difference (a-v O2 diff) in maximal exercise (patient = 4.0 ml/dl, normal men = 16.7 +/- 2.1) despite normal oxygen carrying capacity and Hgb-O2 P50. In contrast maximal oxygen delivery (cardiac output, Q) was high compared to sedentary healthy men (Qmax, patient = 303 ml/min per kg, normal men 238 +/- 36) and the slope of increase in Q relative to VO2 (i.e., delta Q/delta VO2) from rest to exercise was exaggerated (delta Q/delta VO2, patient = 29, normal men = 4.7 +/- 0.6) indicating uncoupling of the normal approximately 1:1 relationship between oxygen delivery and utilization in dynamic exercise. Studies of isolated skeletal muscle mitochondria in our patient revealed markedly impaired succinate oxidation with normal glutamate oxidation implying a metabolic defect at the level of complex II of the mitochondrial respiratory chain. A defect in Complex II in skeletal muscle was confirmed by the finding of deficiency of succinate dehydrogenase as determined histochemically and biochemically. Immunoblot analysis showed low amounts of the 30-kD (iron-sulfur) and 13.5-kD proteins with near normal levels of the 70-kD protein of complex II. Deficiency of succinate dehydrogenase was associated with decreased levels of mitochondrial aconitase assessed enzymatically and immunologically whereas activities of other tricarboxylic acid cycle enzymes were increased compared to normal subjects. The exercise findings are consistent with the hypothesis that this defect impairs muscle oxidative metabolism by limiting the rate of NADH production by the tricarboxylic acid cycle.

Aconitate Hydratase↗
PubMed1990

Adenine nucleotide depletion in human muscle during exercise: causality and significance of AMP deamination.

The predominant route for adenine nucleotide catabolism in skeletal muscle is deamination of AMP to inosine monophosphate (IMP) and ammonia (NH3). Deamination of AMP is enhanced during exercise when the capacity to rephosphorylate ADP is impaired. Thus, in human muscle the formation of IMP (NH3) during exercise is augmented under the following conditions (1) at high intensities, (2) during beta-adrenoceptor blockade, (3) during hypoxia, (4) after detraining, and (5) at low glycogen levels. The formation of IMP is related to the metabolic stress (as indicated by the degree of phosphocreatine breakdown and lactate accumulation), the rate of ATP turnover, and the fiber type composition. During maximal exercise at 100% of VO2max or sustained isometric contractions to fatigue, about 15% of the adenine nucleotide (AN) pool is degraded through deamination of AMP to IMP. It is suggested that the stimulus for increased AMP deamination is increased transient levels of ADP and AMP in the contracting muscle fiber. Deamination of AMP to IMP and NH3 provides a sink for ADP, whereby the ATP/ADP ratio and the phosphorylation potential are kept high, which may be essential for the continuation of the contraction process. This implies that the relative levels of the adenine nucleotides are more important for maintenance of adequate cellular function than the absolute concentration of ATP.

AMP Deaminase↗
PubMed1990

Muscle carnitine metabolism during incremental dynamic exercise in humans.

The changes in muscle content of carnitine and acetylcarnitine have been studied during incremental dynamic exercise. Six subjects exercised for 10 min on an ergometer at 40 and 75% of their maximal oxygen uptake (VO2 max) and to fatigue at 100% of VO2 max (about 4 min). Muscle samples were taken from the quadriceps femoris muscle at rest and after exercise. Muscle content of free carnitine was (means +/- SE) 15.9 +/- 1.7 mmol kg-1 d.wt (dry weight) at rest and remained unchanged after exercise at low intensity but decreased to 5.9 +/- 0.6 and 4.6 +/- 0.5 mmol kg-1 d.wt after exercise at 75 and 100% of VO2 max respectively. Acetylcarnine content at rest was 6.9 +/- 1.9 mmol kg-1 d.wt and increased during exercise in correspondence with the decrease in free carnitine. Muscle content of pyruvate and lactate was unchanged after exercise at 40% of VO2 max but increased at the higher intensities. The parallel increases in acetylcarnitine, pyruvate and lactate indicate that formation of acetylcarnitine is augmented when the availability of glycolytic three-carbon metabolites is high and is consistent with the idea that acetylcarnitine provides a sink for pyruvate and acetyl CoA. This could be of importance for the maintenance of an adequate level of CoA and thus function of the tricarboxylic acid cycle.

Acetyl Coenzyme A↗
PubMed1990

Influence of reduced glycogen level on glycogenolysis during short-term stimulation in man.

The relationship between muscle glycogen concentration and the rate of glycogen breakdown during short, intense contraction has been investigated in man. Prior to the experiment, muscle glycogen content was manipulated by a combination of exercise and diet, and varied from 155 +/- 19 to 350 +/- 25 mmol kg-1 dry muscle (36-81 mmol kg-1 wet wt). The quadriceps femoris muscle was stimulated electrically at a frequency of 20 Hz for 1 min. The blood flow to the leg was occluded during the experiment and muscle biopsies were taken before and after 10, 30 and 60 s stimulation. Force development and glycogenolytic rate were maintained constant during electrical stimulation and similar in all conditions, irrespective of the initial glycogen concentration. The phosphorylase a fraction was increased after 10 s stimulation, but returned to the initial values at the end of the stimulation. Muscle ATP was unaltered during the first 30 s stimulation, but decreased thereafter. The decrease in ATP was accompanied by a stoichiometric increase in inosine monophosphate. Phosphocreatine decreased during stimulation and was almost depleted at the end of stimulation. Muscle lactate and glucose 6-phosphate (Glu 6-P) increased during stimulation. None of these changes was significantly affected by the reduced glycogen contents. It is concluded that the rate of muscle glycogen breakdown is not affected by the initial glycogen level in the range of 155 +/- 19 to 350 +/- 25 mmol kg-1 dry muscle.

Adenosine Triphosphate↗