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Biomedical subjects

E Hultman

Publications and source records attributed to E Hultman.

At least 19 recordsLinked to original sources
PubMed1995

Glycogen resynthesis in human muscle fibre types following exercise-induced glycogen depletion.

1. Studies investigating muscle glycogen resynthesis in man have usually examined mixed-fibred biopsies or have used histochemical methods to estimate single fibre resynthesis. Since the accuracy of the latter is open to debate, this study investigated glycogen resynthesis in type I and II fibres using biochemical methods of analysis. 2. Seven subjects performed one-legged cycling exercise to exhaustion. During the initial 2 h of recovery, subjects consumed 3 g of glucose (kg body mass (BM))-1, and a high carbohydrate diet thereafter. Muscle biopsy samples were obtained from both legs at exhaustion, and from the exercised leg after 3, 10 and 24 h of recovery. 3. In the initial 3 h of recovery, there was a 25 +/- 8% higher rate of resynthesis in type I compared with type II fibres (41 +/- 3 and 31 +/- 4 mmol glucosyl units (kg dry mass (DM))-1 h-1, respectively; P < 0.05). Between 3 and 10 h of recovery, resynthesis in type I fibres declined by 60 +/- 13% to 15 +/- 4 mmol glucosyl units (kg DM)-1 h-1 (P < 0.01), whilst the rate in type II fibres was maintained. Good agreement was found when relating the mixed-fibred muscle glycogen concentration to the mean concentration found in type I and type II fibres (r = 0.96). 4. A discrepancy was found to exist with histochemically derived data reported in the literature. The higher initial glycogen resynthesis rate in type I fibres may be attributable to fibre-type differences in glucose uptake and disposal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Human skeletal muscle protein: effect of malnutrition, elective surgery and total parenteral nutrition.

1. The concentration of alkali-soluble protein, DNA and RNA in percutaneous muscle biopsy specimens was analysed. Tissue alkali-soluble protein/DNA ratio is a measure of muscle protein concentration, while tissue RNA/DNA ratio may reflect the capacity for protein synthesis. 2. Patients with weight loss due to cancer (n = 6) were compared with metabolically healthy patients before elective surgery (n = 7). Alkali-soluble protein/DNA and RNA/DNA ratios in the weight loss group were 248 (14) g/g and 1.3 (0.1) g/g respectively as compared with 404 (13) g/g and 2.1 (0.1) g/g in otherwise healthy patients. All of the alkali-soluble protein/DNA ratios and 5/6 of the RNA/DNA ratios in the weight loss group were below the 95% confidence interval for the healthy control subjects. 3. Patients undergoing elective open cholecystectomy (n = 7) were studied preoperatively and on days 3, 10, 20 and 30 post-operatively. The alkali-soluble protein/DNA ratio remained unchanged on post-operative day 3 but decreased by 8.7% (P < 0.01), 9.6% (P < 0.05) and 20.4% (P < 0.01) on days 10, 20 and 30 respectively in patients eating at will after the operation. No significant post-operative changes in alkali-soluble protein/DNA ratio were seen in patients given post-operative total parenteral nutrition with (n = 9) or without (n = 7) glycyl-glutamine supplementation for 3 days after surgery. 4. In conclusion, patients with weight loss due to malignant disease have a low muscle protein concentration. Elective surgery of medium magnitude results in a decrease in muscle protein lasting for more than 30 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Fuel selection, muscle fibre.

The fuel selection of muscle fibres at rest is dependent on substrate availability. Increased lipid availability results in an increase citrate concentration with inhibition of glycolysis. Fat utilization also increases the concentration ratio acetyl-CoA:CoASH, with inhibition of PDH transformation to the active form. The result is an inhibition of carbohydrate utilization in conformity with the classical glucose-fatty acid style. During exercise fuel selection is dependent on the intensity of exercise, the recruitment pattern of fibre type and the availability of fuels. During exercise at maximum intensity the main fuels are PCr and muscle glycogen, the highest energy release occurring with type II fibres. At exercise intensities between 70 and 100% VO2max carbohydrate is the main fuel after the intake of normal mixed or carbohydrate-rich diets. No inhibition of PDHa formation was observed by increased concentration ratio acetyl-CoA:CoASH during the exercise, but the activation and transport of fatty-acyl groups from NEFA may be inhibited by a decrease in the concentration of CoASH. This mechanism may limit the contribution of fat to metabolism during exercise at intensities above 60% VO2max, after an intake of carbohydrate-rich diets. After carbohydrate starvation or an infusion of a fat emulsion, there was a substantial increase in the utilization of fat which, after the infusion, was concomitant with a high PDHa and a high lactate production. This is thought to be due to a decrease in glycolysis and in the catalytic activity of PDHa, especially in type I fibres, while lactate production continues in type II fibres. When exercise intensities fall below 60% VO2max, fat becomes the dominant fuel during prolonged exercise. At the same time the recruitment pattern is shifted toward type I fibres which have the lowest activation threshold and the highest oxidative capacity.

Acetyl Coenzyme A↗
PubMed1995

Effects of epinephrine infusion on muscle glycogenolysis during intense aerobic exercise.

The purpose of this study was to determine whether an epinephrine (Epi) infusion would enhance muscle glycogenolysis during intense aerobic exercise. Epi was infused at rates that produced the same plasma Epi concentrations observed after caffeine (Caf) ingestion. Seven male subjects cycled for 15 min at 80% maximal O2 uptake during four different trials. Trial 1 was preceded by a 9 mg/kg oral dose of Caf to determine resting and exercise plasma Epi concentrations. Trial 2 was used to determine the Epi infusion rates needed to mimic the plasma Epi levels found with Caf. Trials 3 and 4 were randomized and consisted of either an Epi infusion or a saline infusion (control, Con). During Epi and Con trials muscle samples were obtained from the vastus lateralis at 0, 3, and 15 min of exercise. Plasma Epi levels were similar between Caf and Epi and were elevated twofold compared with Con. At 5 min of exercise the plasma Epi concentrations were 1.51 +/- 0.26, 2.61 +/- 0.34, and 2.97 +/- 0.45 nM for the Con, Caf, and Epi trials, respectively. Plasma Epi increased to 3.08 +/- 0.56, 5.45 +/- 1.11, and 5.86 +/- 1.03 nM at 14 min of exercise in the Con, Caf, and Epi trials, respectively. Muscle glycogenolysis was not different between trials (Con 220.5 +/- 25.3 vs. Epi 240.6 +/- 12.1 mmol/kg dry muscle). In addition, the degradation of muscle ATP and phosphocreatine and the accumulation of muscle lactate, ADP, and AMP were similar between trials.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Skeletal muscle pyruvate dehydrogenase activity during acetate infusion in humans.

Pyruvate dehydrogenase activity (PDHa), acetyl group, and citrate accumulation were examined in human skeletal muscle at rest and during cycling exercise while acetate was infused. Eight subjects received 400 mmol of sodium acetate (Ace) at a constant rate during 20 min of rest, 5 min of cycling at 40% maximal O2 uptake (VO2max) and 15 min of cycling at 80% VO2max. Two weeks later experiments were repeated while 400 mmol of sodium bicarbonate was infused in the control condition (CON). Ace infusion increased muscle acetyl-coenzyme A (acetyl-CoA), citrate, and acetylcarnitine. A decline in resting PDHa during 20 min of Ace infusion (0.37 +/- 0.08 vs. 0.16 +/- 0.03 mmol.min-1.kg wet wt-1) coincided with an elevation in the acetyl-CoA-to-free CoA ratio (acetyl-CoA/CoASH; 0.28 +/- 0.04 to 0.73 +/- 0.14). After 20 min of CON infusion, resting PDHa (0.32 +/- 0.06 mmol.min-1.kg wet wt-1) was similar to PDHa before Ace infusion. During exercise, acetyl-CoA, citrate, and acetyl-CoA/CoASH were further elevated, and the differences that existed at rest were resolved. PDHa increased to the same extent in Ace and CON, in which it was 44-47% transformed after 5 min at 40% VO2max and completely transformed after 15 min at 80% VO2max. At rest PDHa was regulated by variations in acetyl-CoA/CoASH secondary to enhanced acetate metabolism. Conversely, during exercise PDHa regulation appeared independent of variations in acetyl-CoA/CoASH. The resting data are consistent with a central role for PDHa and citrate in the regulation of the glucose-fatty acid cycle in skeletal muscle, as classically proposed. However, in the present study Ace infusion was not effective in perturbing the glucose-fatty acid cycle during exercise.

Acetates↗
PubMed1995

Exercise causes branched-chain oxoacid dehydrogenase dephosphorylation but not AMP deaminase binding.

The responses of AMP deaminase (AMPD) and branched-chain oxoacid dehydrogenase (BCOAD) to moderate (70% maximal O2 consumption for 90 min) followed by intense (90% maximal O2 consumption to exhaustion) cycling exercise were evaluated in the active skeletal muscle of human subjects (n = 8). The exercise conditions invoke different energy demands and ammonia production rates. Active muscle and plasma ammonia concentrations continuously increased throughout moderate exercise in the absence of significant inosine 5-monophosphate accumulation. The free activity of AMPD decreased during moderate exercise (by approximately 25-35%), whereas myosin-bound activity did not change. BCOAD was significantly dephosphorylated (activated) at 5 min and was continuously dephosphorylated during moderate exercise (to a maximum of approximately 21%). Ammonia accumulation rate increased dramatically during the higher intensity exercise accompanied by inosine monophosphate accumulation of approximately 2 mmol/kg dry muscle. The higher intensity exercise caused no further changes in AMPD activity distribution or BCOAD dephosphorylation. Resting muscle percent bound AMPD was notably higher than values previously reported for rat muscle. Increases in percent bound AMPD during exercise were the result of decreases in the sum of free and bound activities and not increases in bound activity. The results of this study do not support a role for myosin binding in the activation of AMPD in human skeletal muscle.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗
PubMed1995

Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance.

BACKGROUND: Cardiac creatine levels are depressed in chronic heart failure. Oral supplementation of creatine to healthy volunteers has been shown to increase physical performance. AIM: To evaluate the effects of creatine supplementation on ejection fraction, symptom-limited physical endurance and skeletal muscle strength in patients with chronic heart failure. METHODS: With a double-blind, placebo-controlled design 17 patients (age 43-70 years, ejection fraction < 40) were supplemented with creatine 20 g daily for 10 days. Before and on the last day of supplementation ejection fraction was determined by radionuclide angiography as was symptom-limited 1-legged knee extensor and 2-legged exercise performance on the cycle ergometer. Muscle strength as unilateral concentric knee extensor performance (peak torque, Nm at 180 degrees/s) was also evaluated. Skeletal muscle biopsies were taken for the determination of energy-rich phosphagens. RESULTS: Ejection fraction at rest and at work did not change. Performance before creatine supplementation did not differ between placebo and creatine groups. While no change was seen in the placebo group compared to baseline, creatine supplementation increased skeletal muscle total creatine and creatine phosphate by 17 +/- 4% (P < 0.05) and 12 +/- 4% (P < 0.05), respectively. Increments were seen only in patients with < 140 mmol total creatine/kg d.w. (P < 0.05). One-legged performance (21%, P < 0.05), 2-legged performance (10%, P < 0.05), and peak torque, Nm (5%, P < 0.05) increased. Both peak torque and 1-legged performance increased linearly with increased skeletal muscle phosphocreatine (P < 0.05). The increments in 1-legged, 2-legged and peak torque were significant compared to the placebo group, (P < 0.05). CONCLUSIONS: One week of creatine supplementation to patients with chronic heart failure did not increase ejection fraction but increased skeletal muscle energy-rich phosphagens and performance as regards both strength and endurance. This new therapeutic approach merits further attention.

Administration, Oral↗
PubMed1994

The metabolic responses of human type I and II muscle fibres during maximal treadmill sprinting.

1. Muscle biopsy samples were obtained from the vastus lateralis of six healthy volunteers before and after 30 s of treadmill sprinting. A portion of each biopsy sample was used for mixed-fibre metabolite analysis. Single fibres were dissected from the remaining portion of each biopsy and were used for ATP, phosphocreatine (PCr) and glycogen determination. 2. Before exercise, PCr and glycogen contents were higher in type II fibres (79.3 +/- 2.7 and 472 +/- 35 mmol (kg dry matter (DM)-1, respectively) compared with type I fibres (71.3 +/- 3.0 mmol (kg DM)-1, P < 0.01 and 375 +/- 25 mmol (kg DM)-1, P < 0.001, respectively). 3. Peak power output was 885 +/- 66 W and declined by 65 +/- 3% during exercise. Phosphocreatine and glycogen degradation in type II fibres during exercise (74.3 +/- 2.5 and 126.3 +/- 15.8 mmol (kg DM)-1, respectively) was greater than the corresponding degradation in type I fibres (59.1 +/- 2.9 mmol (kg DM)-1, P < 0.001 and 77.0 +/- 14.3 mmol (kg DM)-1, P < 0.01, respectively). The decline in ATP during exercise was similar when comparing fibre types (P > 0.05). 4. Compared with previous studies involving similar durations of maximal cycling exercise, isokinetic knee extension and intermittent isometric contraction, the rates of substrate utilization recorded in type I fibres were extremely high, being close to the rapid rates observed in this fibre type during intense contraction with limb blood flow occluded.

Adenosine Triphosphate↗
PubMed1994

Effect of oral creatine supplementation on skeletal muscle phosphocreatine resynthesis.

Biopsy samples were obtained from the vastus lateralis muscle of eight subjects after 0, 20, 60, and 120 s of recovery from intense electrically evoked isometric contraction. Later (10 days), the same procedures were performed using the other leg, but subjects ingested 20 g creatine (Cr)/day for the preceding 5 days. Muscle ATP, phosphocreatine (PCr), free Cr, and lactate concentrations were measured, and total Cr was calculated as the sum of PCr and free Cr concentrations. In five of the eight subjects, Cr ingestion substantially increased muscle total Cr concentration (mean 29 +/- 3 mmol/kg dry matter, 25 +/- 3%; range 19-35 mmol/kg dry matter, 15-32%) and PCr resynthesis during recovery (mean 19 +/- 4 mmol/kg dry matter, 35 +/- 6%; range 11-28 mmol/kg dry matter, 23-53%). In the remaining three subjects, Cr ingestion had little effect on muscle total Cr concentration, producing increases of 8-9 mmol/kg dry matter (5-7%), and did not increase PCr resynthesis. The data suggest that a dietary-induced increase in muscle total Cr concentration can increase PCr resynthesis during the 2nd min of recovery from intense contraction.

Administration, Oral↗
PubMed1994

Plasma volume and ion regulation during exercise after low- and high-carbohydrate diets.

This study compared plasma volume (PV) and ion regulation during prolonged exercise in control vs. glycogen-depleted (GD) conditions, with emphasis on the initial minutes of exercise. In two trials separated by 1-2 wk, four adult males cycled at 75% of peak oxygen consumption (VO2) until exhaustion (50 +/- 7 min for GD) or until the GD exhaustion time in the control trial. Blood was sampled from catheters placed in the brachial artery and retrograde in the femoral vein (fv). Arterial PV decreased rapidly and by 15 min PV was 83% (control) and 88% (GD) of initial. The decrease in PV was accompanied by a net osmotic flux of water from plasma and inactive tissues to contracting muscles. The significantly greater decrease in PV in control compared with GD was associated with a higher muscle lactate content (Lac-; 36 vs. 17 mumol/g dry wt, respectively). Increases in plasma [Cl-] and [Na+] were less than predicted from decreased PV, indicating net loss of these ions from the plasma compartment. Increases in arterial and fv [K+] were 50% greater than could be accounted for by decreased PV, corresponding with increased arterial and fv plasma K+ contents. The rapid net release of K+ and Lac- from contracting muscle during the first few minutes of exercise in both trials was abolished (control) or reversed (GD) within 15 min of beginning exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Nutritional status, muscle composition and plasma and muscle free amino acids in renal transplant patients.

To investigate the effects of renal transplantation (Rtx) on the nutritional status, muscle composition and the plasma and muscle free amino acid (AA) pattern, three groups of altogether 30 renal transplant patients (group I n = 10; 46 +/- 14 [SD] days after Trx), (group II n = 10; 13 +/- 2 months after Rtx) and (group III n = 10; 9 +/- 2 years after Rtx) underwent anthropometric measurements, blood sampling and percutaneous muscle biopsy. The immunosuppressive therapy consisted of prednisolone, azathioprine and cyclosporine-A. The results were compared with data from age-matched healthy subjects. Renal function was impaired in groups I, II and III. Serum albumin was decreased in groups I and II. The patients of group II had an increased percentage of body fat, triceps and subscapular skin folds and total sum of skinfolds. In group I the ratio alkaline-soluble protein (ASP) to DNA, which is a sensitive index of protein depletion on the cellular level, was decreased. Muscle magnesium content was decreased whereas the muscle DNA, sodium and chloride contents were increased. The mean plasma concentration of most essential AA (EAA) was essentially normal except phenylalanine which was increased in groups I and II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Influence of oral creatine supplementation of muscle torque during repeated bouts of maximal voluntary exercise in man.

1. The present experiment was undertaken to investigate the influence of oral creatine supplementation, shown previously to increase the total creatine content of human skeletal muscle (Harris RC, Soderlund K, Hultman E. Clin Sci 1992; 83: 367-74), on skeletal muscle isokinetic torque and the accumulation of plasma ammonia and blood lactate during five bouts of maximal exercise. 2. Twelve subjects undertook five bouts of 30 maximal voluntary isokinetic contractions, interspersed with 1 min recovery periods, before and after 5 days of placebo (4 x 6 g of glucose/day, n = 6) or creatine (4 x 5 g of creatine plus 1 g of glucose/day, n = 6) oral supplementation. Muscle torque production and plasma ammonia and blood lactate accumulation were measured during and after exercise on each treatment. 3. No difference was seen when comparing muscle peak torque production during exercise before and after placebo ingestion. After creatine ingestion, muscle peak torque production was greater in all subjects during the final 10 contractions of exercise bout 1 (P < 0.05), throughout the whole of exercise bouts 2 (P < 0.01), 3 (P < 0.05) and 4 (P = 0.057) and during contractions 11-20 of the final exercise bout (P < 0.05), when compared with the corresponding measurements made before creatine ingestion. Plasma ammonia accumulation was lower during and after exercise after creatine ingestion. No differences were found when comparing blood lactate levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Energy metabolism in single human muscle fibres during intermittent contraction with occluded circulation.

1. Glycogenolysis in type I and II muscle fibres was investigated in five healthy volunteers during electrical stimulation of the quadriceps muscle group with blood flow occluded. 2. The quadriceps femoris muscles were stimulated intermittently (1.6 s stimulation, 1.6 s rest) at a frequency of 50 Hz for 64 s and isometric contraction force was recorded. Muscle biopsies were obtained at rest prior to and immediately after stimulation. Single muscle fibres were dissected free and were identified as type I and II fibres. ATP, phosphocreatine (PCr) and glycogen contents were measured luminometrically and enzymatically in single fibres and mixed fibre muscle. 3. Electrical stimulation resulted in a marked decline in contraction force and near total depletion of PCr in both fibre types. The ATP turnover rate (P < 0.05) and the magnitude of the decline in ATP (P < 0.05) were greater in type II fibres. Prior to stimulation the muscle glycogen content was 32% higher in type II fibres compared with type I fibres (P < 0.01). During stimulation the rate of glycogenolysis in type II fibres (4.32 +/- 0.54 mmol (kg dry matter (DM)-1 s-1 was twofold greater than the rate in type I fibres (2.05 +/- 0.70 mmol (kg DM)-1 s-1, P < 0.05). 4. The data suggest that the relatively higher rate of glycogenolysis observed in type I fibres during intermittent electrical stimulation with occluded circulation (2.05 +/- 0.70 mmol (kg DM)-1 s-1), when compared with the corresponding rate recorded during intense contraction with circulation intact (0.18 +/- 0.14 mmol (kg DM)-1 s-1, P < 0.05), may result from an accelerated ATP turnover rate in this fibre type increasing the cellular concentrations of free AMP and inosine 5'-monophosphate (IMP), which are known activators of glycogen phosphorylase. 5. The similarity in the rate of type II fibre glycogenolysis during contraction with circulatory occlusion (4.32 +/- 0.54 mmol (kg DM)-1 s-1), when compared with the corresponding rate recorded during non-occluded circulation (3.54 +/- 0.53 mmol (kg DM)-1 s-1, P > 0.05), is in agreement with the suggestion that glycogenolysis in this fibre type is already occurring at a near-maximal rate with circulation intact.

Adult↗
PubMed1993

Pyruvate dehydrogenase activity and acetyl group accumulation during exercise after different diets.

Pyruvate dehydrogenase activity (PDHa) and acetyl group accumulation were examined in human skeletal muscle at rest and during exercise after different diets. Five males cycled at 75% of maximal O2 uptake (VO2 max) to exhaustion after consuming a low-carbohydrate diet (LCD) for 3 days and again 1-2 wk later for the same duration after consuming a high-carbohydrate diet (HCD) for 3 days. Resting PDHa was lower after a LCD (0.20 +/- 0.04 vs. 0.69 +/- 0.05 mmol.min-1.kg wet wt-1; P < 0.05) and coincided with a greater intramuscular acetyl-CoA-to-CoASH ratio, acetyl-CoA content, and acetylcarnitine content. PDHa increased during exercise in both conditions but at a lower rate in the LCD condition compared with the HCD condition (1.46 +/- 0.25 vs. 2.65 +/- 0.23 mmol.min-1.kg wet wt-1 at 16 min and 1.88 +/- 0.20 vs. 3.11 +/- 0.14 at the end of exercise; P < 0.05). During exercise muscle acetyl-CoA and acetylcarnitine content and the acetyl-CoA-to-CoASH ratio decreased in the LCD condition but increased in the HCD condition. Under resting conditions PDHa was influenced by the availability of fat or carbohydrate fuels acting through changes in the acetyl-CoA-to-CoASH ratio. However, during exercise the activation of PDHa occurred independent of changes in the acetyl-CoA-to-CoASH ratio, suggesting that other factors are more important.

Acetyl Coenzyme A↗
PubMed1993

Regulation of fat-carbohydrate interaction in skeletal muscle during intense aerobic cycling.

Six male subjects received either a saline (control) or Intralipid infusion during 30 min rest and 15 min cycling at 85% maximal O2 uptake (VO2max) to examine the regulation of fat-carbohydrate interaction (glucose-fatty acid cycle) in skeletal muscle. Muscle biopsies were sampled immediately before and at 3 and 15 min of exercise in both trials. A muscle biopsy was also taken at -30 min rest in the Intralipid trial. Intralipid infusion significantly elevated plasma free fatty acids above control during rest (0.21 +/- 0.04 to 0.94 +/- 0.09 mM) and exercise (5 min: 1.27 +/- 0.15 mM; 15 min: 1.42 +/- 0.13 mM). Muscle glycogen degradation was significantly lower in the Intralipid trial (109.7 +/- 29.3 vs. 194.7 +/- 32.1 mmol/kg dry muscle). Muscle lactate accumulation after 15 min was similar in both trials (control, 60.7 +/- 12.2 and Intralipid, 60.9 +/- 12.4 mmol/kg dry muscle). Muscle citrate increased at rest during Intralipid (0.32 +/- 0.06 to 0.58 +/- 0.06 mmol/kg dry muscle) but was not different between trials at 3 min (control, 0.73 +/- 0.07 and Intralipid, 0.68 +/- 0.06 mmol/kg dry muscle) and 15 min of cycling. Resting acetyl-CoA was unaffected by Intralipid and increased similarly in both trials at 3 min of cycling (control, 59.0 +/- 10.3 and Intralipid, 50.7 +/- 13.6 mumol/kg dry muscle) and remained unchanged at 15 min. Pyruvate dehydrogenase activity increased five- to sevenfold during exercise and was similar in both trials (15 min: control, 2.42 +/- 0.30 and Intralipid, 2.79 +/- 0.41 mmol.min-1 x kg wet wt-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetyl Coenzyme A↗
PubMed1993

PDC activity and acetyl group accumulation in skeletal muscle during isometric contraction.

The activity of pyruvate dehydrogenase complex (PDC) was studied in the human quadriceps femoris muscle during isometric contraction induced by intermittent electrical stimulation at 20 Hz. Muscle biopsy samples were obtained at rest and after 10, 20, and 46 contractions. The active form of PDC (PDCa) increased from a mean value of 26% of the total PDC at rest to mean values of 46, 78, and 80%, respectively. Muscle biopsy samples were also obtained at rest, after 46 contractions with limb blood flow intact or occluded, and after 2 min of oxidative recovery. In another experiment, muscle biopsy samples were obtained at rest, after 10 min of resting ischemia, and after 46 contractions with limb blood flow occluded. The transformation of PDC to PDCa was nearly complete, regardless of whether the blood flow was intact or occluded. However, the accumulation of acetyl groups observed during stimulation with intact blood flow was abolished when the blood flow was occluded. The absence of NADH oxidation during anoxia had no effect on the contraction-induced transformation of PDC to PDCa, but it inhibited the flux through the enzyme reaction.

Acetyl Coenzyme A↗