1. The activity of pyruvate dehydrogenase (PDH) was measured in samples of triceps muscle obtained in 15 males, before and after immobilization for 5 weeks and 5 months of strength training carried out in random order with cross-over of treatment. 2. Although the total PDH activity was unchanged at 300 nmol min −1 g −1 , the proportion in the active form increased after strength training (62 ± 10.1%) and decreased after immobilization (12 ± 2.3%) compared with control (36 ± 3.4%). 3. In six subjects measurements were repeated after 10 min maximal exercise (arm ergometer). The proportion of PDH in the active form increased least after immobilization (to 52 ± 13.6%), compared with control (95 ± 11.7%) and post-training (98 ± 6.6%). 4. After exercise muscle glycogen fell to the greatest extent and lactate rose the least in the post-training state, with opposite findings post-immobilization, suggesting that PDH activation contributes to the control of lactate formation in muscle during heavy exercise, and that the effects of training and immobilization are mediated at least in part through changes in the activation of this regulatory enzyme.
1. The activity of pyruvate dehydrogenase in its active and inactive forms was measured in biopsy samples obtained from the vastus lateralis muscle of healthy subjects before and after exercise. 2. At rest, 40 ± 4% (mean ± sem ) of the enzyme was in the active form. 3. After progressive aerobic exercise to exhaustion ( n = 5), 88 ± 2·3% was in the active form. 4. After intermittent supramaximal short-term exercise (1 min exercise, 3 min rest) to exhaustion ( n = 6), 60 ± 2·2% was in the active form. 5. After isometric maximal exercise of 65 ± 3·6 s duration ( n = 3), only 39 ± 1% of the enzyme was in the active form. 6. Muscle glycogen depletion was greatest with intermittent exercise and least with isometric maximal exercise; in contrast, the increase in muscle lactate was least with progressive exercise (1·3 to 9·4 μmol/g), intermediate in intermittent maximal exercise (1·2 to 13·1 μmol/g) and greatest after isometric exercise (1·8 to 17·6 μmol/g). There were no significant differences between the three studies in the changes in lactate/pyruvate ratios. 7. In three subjects who exercised with one leg, activation of the enzyme was twice as great in the exercised as in the inactive leg. 8. The ratio of active to total enzyme in biopsies of resting muscle was greater in four well-trained athletes than in four untrained control subjects (70% compared with 41% respectively). 9. The activation of pyruvate dehydrogenase appears to play an important part in regulating the use of glycogen and glucose during exercise in man.
1. Five males were studied on three occasions, after oral administration of CaCO 3 (control), NH 4 Cl (acidosis) and NaHCO 3 (alkalosis), in a dose of 0.3 g/kg, taken over a 3 h period at rest. The subjects then exercised on a cycle ergometer for 20 min at 33% maximal oxygen uptake ( V o 2 max.), followed by 20 min at 66% and at 95% V o 2 max. until exhaustion. 2. Endurance at 95% V o 2 max. was longest with alkalosis (5.44 ± 1.05 min), shortest with acidosis (3.13 ± 0.97 min) and intermediate in the control study (4.56 ± 1.31 min); venous blood pH at exhaustion was 7.33 ± 0.02 (mean ±1 sem ), 7.13 ± 0.02 and 7.26 ± 0.02 respectively. 3. Concentrations of plasma lactate at exhaustion were 7.10 ± 0.8 mmol/l 4.0 ± 0.5 and 7.9 ± 0.9 mmol/l in the control, acidosis and alkalosis studies respectively. 4. Muscle lactate increased most from rest to exhaustion with alkalosis to 17.1 ± 2.5 μmol/g and least with acidosis to 12.2 ± 1.4 μmol/g. Muscle glycogen depletion was comparable in control and alkalosis studies. 5. The lower plasma lactate concentration during exercise in acidosis compared with control and alkalosis appears to be due to an inhibition of muscle glycolysis combined with a reduction in lactate efflux from muscle.
1. To investigate differences between the metabolic effects of light and heavy exercise, five healthy males (mean maximal oxygen intake 3.92 litres/min) exercised for 40 min at 36% maximum power (light work) and 70% maximum power (heavy work) on separate days, after an overnight fast. 2. A steady state was achieved in both studies between 20 and 40 min in: oxygen intake (1.42 and 2.64 litres/min respectively); respiratory exchange ratio (0.89 and 1.01); plasma lactate concentration (1.78 and 9.94 mmol/l). 3. Plasma palmitate turnover rate ( 14 C) was unchanged from resting values in light work but was decreased by 40% (from 104 ± 16 to 63 ± 8 μmol/min) in heavy work. Heavy work was associated with falls in the plasma concentrations of all free fatty acids measured: palmitic acid (C 16:0 ), oleic acid (C 18:1 ), stearic acid (C 18:0 ), linoleic acid (C 18:2 ) and palmitoleic acid (C 16:1 ). 4. In contrast to the fall in palmitate turnover the increase in plasma glycerol was greater in heavy exercise (0.054–0.229 mmol/l) than in light exercise (0.053–0.094 mmol/l), suggesting that lipolysis was occurring which did not lead to influx of free fatty acids into plasma. 5. In light exercise fat metabolism may be controlled to favour adipose tissue lipolysis and extraction of free fatty acids by muscle from the circulation, whereas in heavy exercise adipose tissue lipolysis is inhibited and hydrolysis of muscle triglycerides may play a more important part. 6. The finding of a high respiratory exchange ratio may not exclude the use of fat as a major fuel source in exercise associated with lactate production.
1. The ability to metabolize lactate at rest and during exercise was studied in six male subjects by using a constant infusion of sodium l(+)-lactate at a rate of 0·05 mmol min −1 kg −1 . Twenty minute periods of rest and exercise at two work rates were used, amounting to 25% and 50% of maximal O 2 uptake (V̇o 2 max.) in four subjects and 50% and 66% of V̇o 2 max. in two subjects. Control measurements were made with saline infusion. In all studies a steady state in blood lactate was achieved. 2. At rest lactate infusion was associated with an increase of 3·51 mmol/l (± sd 0·70) in plasma lactate. The increase was smaller in exercise and in a given subject was the same at both work rates; plasma lactate was on average 1·21 mmol/l (±sd 1·11) higher during lactate infusion than the control measurement at the same power output. In one subject lactate values in exercise were unchanged by lactate infusion. 3. At rest lactate infusion was associated with an increase in O 2 intake and CO 2 output, the respiratory exchange ratio was unchanged, and plasma HCO − 3 rose by 1·85 mmol/l. 4. During exercise lactate infusion was associated with a smaller and variable increase in O 2 intake. CO 2 output was less, the respiratory exchange ratio fell, and plasma HCO − 3 rose by 6·1 mmol/l. 5. Exercise is accompanied by an increased capacity to metabolize lactate aerobically. Decreasing lactate metabolism appears to play no part in the increase in plasma lactate concentration with increasing exercise, at least to 66% of the maximal O 2 intake.
1. Seven healthy males were studied during cycle ergometer exercise at 33%, 66% and 90% of V̇o 2 max. on three occasions when NH 4 Cl, NaHCO 3 or CaCO 3 (as a control substance) were administered in gelatin capsules double blind and in randomized order. Plasma growth hormone (HGH), lactic acid and hydrogen ion concentration ([H + ])weremeasured at frequent intervals. 2. Ammonium chloride produced highest blood [H + ] and NaHCO 3 the lowest. These differences were maintained during exercise and in recovery. Plasma lactic acid concentrations were similar at rest. At 66%, 90% V̇o 2 max. and recovery lactic acid was highest with NaHCO 3 and lowest with NH 4 Cl. 3. Exercise stimulated HGH secretion in all studies and the elevation was proportional to the intensity of the exercise. NH 4 Cl caused a variable elevation of HGH at rest and 33% V̇o 2 max. At 66% V̇o 2 max., plasma HGH was significantly elevated to similar concentrations in all studies and, at 90% V̇o 2 max., HGH was highest with NaHCO 3 . 4. An infusion of sodium l(+)-lactate producing plasma lactate concentrations of 3–5 mmol/l did not influence HGH secretion. 5. Exercise is a physiological stimulus to HGH secretion and the mechanism is independent of blood [H + ] and lactate concentrations.