Effect of lowered muscle temperature on the physiological response to exercise in men

The effect of low muscle temperature on the response to dynamic exercise was studied in six healthy men who performed 42 min of exercise on a cycle ergometer at an intensity of 70% of their maximal O2 uptake. Experiments were performed under control conditions, i.e. from rest at room temperature, and following 45 min standing with legs immersed in a water bath at 12 degrees C. The water bath reduced quadriceps muscle temperature (at 3 cm depth) from 36.4 (SD 0.5) degrees C to 30.5 (SD 1.7) degrees C. Following cooling, exercise heart rate was initially lower, the mean difference ranged from 13 (SD 4) beats.min-1 after 6 min of exercise, to 4 (SD 2) beats.min-1 after 24 min of exercise. Steady-state oxygen uptake was consistently higher (0.2 l.min-1). However, no difference could be discerned in the kinetics of oxygen uptake at the onset of exercise. During exercise after cooling a significantly higher peak value was found for the blood lactate concentration compared to that under control conditions. The peak values were both reached after approximately 9 min of exercise. After 42 min of exercise the blood lactate concentrations did not differ significantly, indicating a faster rate of removal during exercise after cooling. We interpreted these observations as reflecting a relatively higher level of muscle hypoxia at the onset of exercise as a consequence of a cold-induced vasoconstriction. The elevated steady-state oxygen uptake may in part have been accounted for by the energetic costs of removal of the extra lactate released into the blood consequent upon initial tissue hypoxia.     

Leg and arm lactate and substrate kinetics during exercise

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72-76% maximal O(2) uptake. A high lactate appearance rate (R(a), 184 +/- 17 micromol x kg(-1) x min(-1)) but a low arterial lactate concentration ( approximately 2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of approximately 2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was approximately 45% at rest and approximately 95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate R(a) during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged.     

Disposal of lactate during and after strenuous exercise in humans

Heavy dynamic exercise using both arm and leg muscles was performed to exhaustion by seven well-trained subjects. The aerobic and anaerobic energy utilization was determined and/or calculated. O2 uptake during exercise and during 1 h of recovery was measured as well as splanchnic and muscle metabolite exchange. Glycogen and lactate content in the quadriceps femoris was determined before exercise, immediately after exercise, and after a recovery period. In four male subjects the estimated mean lactate production during exercise was 830 mmol. The splanchnic uptake of lactate during recovery was 80 mmol, and the calculated maximum amount oxidized during the recovery period was 330 mmol. About 60 mmol were accounted for in the body water at the end of the rest period. The remaining 360 mmol of lactate were apparently resynthesized into glycogen in muscle via gluconeogenesis. It is concluded that approximately 50% of the lactate formed during heavy exercise is transformed to glycogen via glyconeogenesis in muscle during recovery and that lactate uptake by the liver is only 10%.     

Epinephrine-induced changes in muscle carbohydrate metabolism during exercise in male subjects

Epinephrine increases glycogenolysis in resting skeletal muscle, but less is known about the effects of epinephrine on exercising muscle. To study this, epinephrine was given intraarterially to one leg during two-legged cycle exercise in nine healthy males. The epinephrine-stimulated (EPI) and non-stimulated (C) legs were compared with regard to glycogen, glucose, glucose 6-phosphate (G6P), alpha-glycerophosphate (alpha-GP), and lactate contents in muscle biopsies taken before and after the 45-min submaximal exercise, as well as brachial arterial-femoral venous (a-fv) differences for epinephrine, norepinephrine, lactate, glucose, and O2 during exercise. During exercise the arterial plasma epinephrine concentration was 4.8 +/- 0.8 nmol/l and the femoral venous epinephrine concentrations were 10.3 +/- 2.1 and 3.9 +/- 0.6 nmol/l, respectively, in the EPI and C leg. During exercise the a-fv difference for lactate was greater (-0.41 +/- 0.14 vs. -0.21 +/- 0.14 mmol/l; P less than 0.001), and the a-fv difference for glucose was smaller (0.07 +/- 0.12 vs. 0.24 +/- 0.12 mmol/l; P less than 0.01) in the EPI than in the C leg, but the a-fv differences for O2 were similar. Muscle glycogen depletion (137 +/- 63 vs. 99 +/- 43 mmol/kg dry muscle; P less than 0.1) and the muscle concentrations of glucose (P less than 0.05), alpha-GP (P less than 0.1), G6P (P greater than 0.1), and lactate (P greater than 0.1) tended to be higher in the EPI than the C leg after exercise. These findings suggest that physiological concentrations of epinephrine may enhance muscle glycogenolysis during submaximal exercise in male subjects.     

Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise

Nine bodybuilders performed heavy-resistance exercise activating the quadriceps femoris muscle. Intermittent 30-s exhaustive exercise bouts comprising 6-12 repetitions were interspersed with 60-s periods for 30 min. Venous blood samples were taken repeatedly during and after exercise for analyses of plasma free fatty acid (FFA) and glycerol concentration. Muscle biopsies were obtained from the vastus lateralis muscle before and after exercise and assayed for glycogen, glycerol-3-phosphate, lactate and triglyceride (TG) content. The activities of citrate synthase (CS), lactate dehydrogenase, hexokinase (HK), myokinase, creatine kinase and 3-hydroxyacyl-CoA dehydrogenase (HAD), were analysed. Histochemical staining procedures were used to assess fibre type composition, fibre area and capillary density. TG content before and after exercise averaged (SD) 23.9 (13.3) and 16.7 (6.4) mmol kg-1 dry wt. The basal triglyceride content varied sixfold among individuals and the higher the levels the greater was the change during exercise. The glycogen content decreased (P less than 0.001) from 690 (82) to 495 (95) mmol kg-1 dry wt. and lactate and glycerol-3-phosphate increased (P less than 0.001) to 79.5 (5.5) and 14.5 (7.3) mmol kg-1 dry wt., respectively, after exercise. The HK and HAD/CS content respectively correlated with glycogen or TG content at rest and with changes in these metabolites during exercise. FFA and glycerol concentrations increased slightly (P less than 0.001) during exercise. Lipolysis may, therefore, provide energy during heavy-resistance exercise of relatively short duration. Also, storage and utilization of intramuscular substrates appear to be influenced by the metabolic profile of muscle.     

Effect of ambient temperature on human skeletal muscle metabolism during fatiguing submaximal exercise.

To examine the effect of ambient temperature on metabolism during fatiguing submaximal exercise, eight men cycled to exhaustion at a workload requiring 70% peak pulmonary oxygen uptake on three separate occasions, at least 1 wk apart. These trials were conducted in ambient temperatures of 3 degrees C (CT), 20 degrees C (NT), and 40 degrees C (HT). Although no differences in muscle or rectal temperature were observed before exercise, both muscle and rectal temperature were higher (P < 0.05) at fatigue in HT compared with CT and NT. Exercise time was longer in CT compared with NT, which, in turn, was longer compared with HT (85 +/- 8 vs. 60 +/- 11 vs. 30 +/- 3 min, respectively; P < 0.05). Plasma epinephrine concentration was not different at rest or at the point of fatigue when the three trials were compared, but concentrations of this hormone were higher (P < 0.05) when HT was compared with NT, which in turn was higher (P < 0.05) compared with CT after 20 min of exercise. Muscle glycogen concentration was not different at rest when the three trials were compared but was higher at fatigue in HT compared with NT and CT, which were not different (299 +/- 33 vs. 153 +/- 27 and 116 +/- 28 mmol/kg dry wt, respectively; P < 0.01). Intramuscular lactate concentration was not different at rest when the three trials were compared but was higher (P < 0.05) at fatigue in HT compared with CT. No differences in the concentration of the total intramuscular adenine nucleotide pool (ATP + ADP + AMP), phosphocreatine, or creatine were observed before or after exercise when the trials were compared. Although intramuscular IMP concentrations were not statistically different before or after exercise when the three trials were compared, there was an exercise-induced increase (P < 0.01) in IMP. These results demonstrate that fatigue during prolonged exercise in hot conditions is not related to carbohydrate availability. Furthermore, the increased endurance in CT compared with NT is probably due to a reduced glycogenolytic rate.     

Muscle metabolism during intense, heavy-resistance exercise

The objective of this study was to examine the muscle metabolic changes occurring during intense and prolonged, heavy-resistance exercise. Muscle biopsies were obtained from the vastus lateralis of 9 strength trained athletes before and 30 s after an exercise regimen comprising 5 sets each of front squats, back squats, leg presses and knee extensions using barbell or variable resistance machines. Each set was executed until muscle failure, which occurred within 6-12 muscle contractions. The exercise: rest ratio was approximately 1:2 and the total performance time was 30 min. Concentrations of adenosine triphosphate (ATP), creatine phosphate (CP), creatine, glycogen, glucose, glucose-6-phosphate (G-6-P), alpha-glycerophosphate (alpha-G-P) and lactate were determined on freeze-dried tissue samples using fluorometric assays. Blood samples were analyzed for lactate and glucose. The exercise produced significant reductions in ATP (p less than 0.01) and CP (p less than 0.001), while alpha-G-P more than doubled (p less than 0.05), glucose increased tenfold (p less than 0.001) and G-6-P fourfold (p less than 0.001). Muscle lactate concentration at cessation of exercise averaged 17.3 mmol X kg-1 w. w. Glycogen concentration decreased (p less than 0.001) from 160 to 118 mmol X kg-1 w. w. It is concluded that high intensity, heavy resistance exercise is associated with a high rate of energy utilization through phosphagen breakdown and activation of glycogenolysis.     

Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (VO2) during exercise and their relationship to performance, 20 healthy, active subjects underwent 30 min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1 (SD 4.0) min (P < 0.001) and cycling endurance time was prolonged from 20.9 (SD 5.5) to 26.6 (SD 11.8) min (P < 0.01) after respiratory training. The VO2 did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8 (SD 1.9) mmol x l(-1), P < 0.001] as well as at the end of the endurance exercise [10.4 (SD 3.6) vs 9.6 (SD 2.7) mmol x l(-1), P < 0.01] test after respiratory training. We speculate that the reduction in blood lactate concentration was most likely caused by an improved lactate uptake by the trained respiratory muscles. However, reduced exercise blood lactate concentrations per se are unlikely to explain the improved cycling performance after respiratory endurance training.     

Metabolic response to maximal exercise of 800 and 2,000 m in the thoroughbred horse

To define the metabolic response to maximal exercise in the thoroughbred horse under field conditions, muscle biopsies and venous blood samples were taken from five horses after a single 800-m gallop and from four horses after a single 2,000-m gallop. Muscle and blood samples were also collected during 60 min of recovery. After exercise muscle ATP contents were decreased by 30 +/- 7 (SD) and 47 +/- 3% after the 800- and 2,000-m gallops, respectively. As indicators of purine catabolism, ammonia and uric acid increased in plasma, the accumulation being greater after the 2,000-m gallop. Blood ammonia peaked immediately after exercise and uric acid after 40-60 min of recovery. Muscle glycogen utilization over the 800- and 2,000-m gallops averaged 2.68 +/- 0.90 and 1.06 +/- 0.12 mmol glucosyl units.kg dry muscle-1.s-1, respectively, and the total used amounted to 27.3 +/- 6.6 and 32.5 +/- 8.8% of the initial store. Muscle lactate accumulation averaged 123.5 +/- 49.7 and 167.3 +/- 20.7 mmol/kg dry muscle, respectively, and declined during recovery with half times of 22.9 +/- 4.2 and 18.9 +/- 6.6 min. Blood lactate peaked 5-10 min after exercise. Exercise resulted in only a small increase in muscle glycerol content, but this continued to rise during recovery reaching 9-12 mmol/kg dry muscle after 20 min. During this time the increase in muscle glycerol content exactly matched the decline in glycerol 3-phosphate.     

Hyperoxia decreases muscle glycogenolysis, lactate production, and lactate efflux during steady-state exercise

The aim of this study was to determine whether the decreased muscle and blood lactate during exercise with hyperoxia (60% inspired O2) vs. room air is due to decreased muscle glycogenolysis, leading to decreased pyruvate and lactate production and efflux. We measured pyruvate oxidation via PDH, muscle pyruvate and lactate accumulation, and lactate and pyruvate efflux to estimate total pyruvate and lactate production during exercise. We hypothesized that 60% O2 would decrease muscle glycogenolysis, resulting in decreased pyruvate and lactate contents, leading to decreased muscle pyruvate and lactate release with no change in PDH activity. Seven active male subjects cycled for 40 min at 70% VO2 peak on two occasions when breathing 21 or 60% O2. Arterial and femoral venous blood samples and blood flow measurements were obtained throughout exercise, and muscle biopsies were taken at rest and after 10, 20, and 40 min of exercise. Hyperoxia had no effect on leg O2 delivery, O2 uptake, or RQ during exercise. Muscle glycogenolysis was reduced by 16% with hyperoxia (267 +/- 19 vs. 317 +/- 21 mmol/kg dry wt), translating into a significant, 15% reduction in total pyruvate production over the 40-min exercise period. Decreased pyruvate production during hyperoxia had no effect on PDH activity (pyruvate oxidation) but significantly decreased lactate accumulation (60%: 22.6 +/- 6.4 vs. 21%: 31.3 +/- 8.7 mmol/kg dry wt), lactate efflux, and total lactate production over 40 min of cycling. Decreased glycogenolysis in hyperoxia was related to an approximately 44% lower epinephrine concentration and an attenuated accumulation of potent phosphorylase activators ADPf and AMPf during exercise. Greater phosphorylation potential during hyperoxia was related to a significantly diminished rate of PCr utilization. The tighter metabolic match between pyruvate production and oxidation resulted in a decrease in total lactate production and efflux over 40 min of exercise during hyperoxia.     

Variations in heart rate at blood lactate threshold due to exercise mode in elite cross-country skiers

This study attempted to quantify the difference in heart rate and exercise stage at which blood lactate threshold (T(bla)) occurs using 3 different modes of exercise: running, double poling (DP) on roller skis, and skating (SK) on roller skis. Nine elite collegiate cross-country ski racers (4 men, 5 women) served as test subjects. Testing was conducted on a motorized FitNex treadmill, specially designed for roller skiing. Heart rate was monitored via telemetry with values averaged over the last 30 seconds of each stage. A 40-micro l blood sample was obtained at the fingertip at the end of each 4-minute stage, and 25 micro l was analyzed for whole blood lactate concentration. The T(bla) was determined by the first exercise stage that elicited a concentration over 4.0 mmol.L(-1). The same test protocol was used for all 3 exercise modes. Mean heart rate, in beats per minute (b.min(-1)), at T(bla) was not significantly different (P < or = 0.05) for SK (mean 187 +/- 14 b.min(-1) SD) vs. running (mean 187 +/- 12 b.min(-1) SD); however, heart rate was significantly lower at T(bla) for DP (mean 161 +/- 17 b.min(-1) SD) vs. running and DP vs. SK. The mean exercise protocol stage that induced a blood lactate value which exceeded T(bla) was significantly different (P < or = 0.05) for running (5.22 +/- 1.20 mmol.L(-1) SD) vs. DP (1.89 +/- 0.78 mmol.L(-1) SD), running vs. SK (3.67 +/- 0.71 mmol.L(-1) SD), and SK vs. DP. It was concluded that T(bla) occurs at a lower heart rate and exercise stage during DP as compared with SK or running. Therefore, it stands to reason that the heart rate at T(bla) may vary based on mode of exercise, and when using heart rate to estimate blood lactate concentration, coaches and athletes should be aware that different modes of exercise elicit a different blood lactate concentration at a given heart rate depending on exercise mode used.     

Metabolic adaptations to training precede changes in muscle mitochondrial capacity.

To determine whether increases in muscle mitochondrial capacity are necessary for the characteristic lower exercise glycogen loss and lactate concentration observed during exercise in the trained state, we have employed a short-term training model involving 2 h of cycling per day at 67% maximal O2 uptake (VO2max) for 5-7 consecutive days. Before and after training, biopsies were extracted from the vastus lateralis of nine male subjects during a continuous exercise challenge consisting of 30 min of work at 67% VO2max followed by 30 min at 76% VO2max. Analysis of samples at 0, 15, 20, and 60 min indicated a pronounced reduction (P less than 0.05) in glycogen utilization after training. Reductions in glycogen utilization were accompanied by reductions (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 15 min [37.4 +/- 9.3 (SE) vs. 20.2 +/- 5.3], 30 min (30.5 +/- 6.9 vs. 17.6 +/- 3.8), and 60 min (26.5 +/- 5.8 vs. 17.8 +/- 3.5) of exercise. Maximal aerobic power, VO2max (l/min) was unaffected by the training (3.99 +/- 0.21 vs. 4.05 +/- 0.26). Measurements of maximal activities of enzymes representative of the citric acid cycle (succinic dehydrogenase and citrate synthase) were similar before and after the training. It is concluded that, in the voluntary exercising human, altered metabolic events are an early adaptive response to training and need not be accompanied by changes in muscle mitochondrial capacity.     

Muscle ATP turnover rate during isometric contraction in humans

ATP turnover and glycolytic rates during isometric contraction in humans have been investigated. Subjects contracted the knee extensor muscles at two-thirds maximal voluntary force to fatigue (mean +/- SE, 53 +/- 4 s). Biopsies were obtained before and after exercise and analyzed for high-energy phosphates and glycogenolytic-glycolytic intermediates. Total ATP turnover was 190 +/- 7 mmol/kg dry muscle, whereas the average turnover rate was 3.7 +/- 0.2 mmol . kg dry muscle-1 . S-1. The average ATP turnover rate was positively correlated with the percentage of fast-twitch fibers in the postexercise biopsy (r = 0.71; P less than 0.05) and negatively correlated with contraction duration to fatigue (r = -0.88; P less than 0.05). At fatigue, phosphocreatine ranged from 1 to 11 mmol/kg dry muscle (86-99% depletion of value at rest), whereas lactate ranged from 59 to 101. The mean glycolytic rate was 0.83 +/- 0.05 mmol . kg dry muscle-1 . S-1 and was positively correlated with the rate of glucose 6-phosphate accumulation (r = 0.83; P less than 0.05). It is concluded that a major determinant of the ATP turnover rate is the muscle fiber composition, which is probably explained by a higher turnover rate in fast-twitch fibers; fatigue is more closely related to a low phosphocreatine content than to a high lactate content; and the increase in prephosphofructokinase intermediates is important for stimulating glycolysis during contraction.     

Lactate as substrate for glycogen resynthesis after exercise

Muscle glycogen levels in the perfused rat hemicorpus preparation were reduced two-thirds by electrical stimulation plus exposure to epinephrine (10(-7) M) for 30 min. During the contraction period muscle lactate concentrations increased from a control level of 3.6 +/- 0.6 to a final value of 24.1 +/- 1.6 mumol/g muscle. To determine whether the lactate that had accumulated in muscle during contraction could be used to resynthesize glycogen, glycogen levels were determined after 1-3 h of recovery from the contraction period during which time the perfusion medium (flow-through system) contained low (1.3 mmol/l) or high (10.5 or 18 mmol/l) lactate concentrations but no glucose. With the low perfusate lactate concentration, muscle lactate levels declined to 7.2 +/- 0.8 mumol/g muscle by 3 h after the contraction period and muscle glycogen levels did not increase (1.28 +/- 0.07 at 3 h vs. 1.35 +/- 0.09 mg glucosyl U/g at end of exercise). Lactate disappearance from muscle was accounted for entirely by output into the venous effluent. With the high perfusate lactate concentrations, muscle lactate levels remained high (13.7 +/- 1.7 and 19.3 +/- 2.0 mumol/g) and glycogen levels increased by 1.11 and 0.86 mg glucosyl U/g, respectively, after 1 h of recovery from exercise. No more glycogen was synthesized when the recovery period was extended. Therefore, it appears that limited resynthesis of glycogen from lactate can occur after the contraction period but only when arterial lactate concentrations are high; otherwise the lactate that builds up in muscle during contraction will diffuse into the bloodstream.     

Continuous intramuscular pH measurement during the recovery from brief, maximal exercise in man

Muscle pH and temperature were measured before, and continuously for 30 min after, a 30-s maximal sprint exercise in ten subjects. These measurements were made with a needle-tipped pH electrode and a thermocouple placed in vastus lateralis. Venous blood samples were collected for pH, lactate and catecholamine estimations and measurements were also made of the arterial blood pressure and heart rate. The muscle and venous pH decreased from 7.17 +/- 0.01 (mean +/- SEM) and 7.39 +/- 0.01 to 6.57 +/- 0.04 and 7.04 +/- 0.03, respectively, in response to the exercise. No significant recovery occurred in either pH measurement for 10 min, after which muscle pH increased to 7.03 +/- 0.03 and venous pH to 7.29 +/- 0.01 by 30 min. Muscle temperature increased by 2.1 degrees C with exercise and also failed to return to pre-exercise values by 30 min. Blood lactate concentration increased from 0.75 +/- 0.04 mmol l-1 before exercise to a peak value of 15.76 +/- 0.35 mmol l-1 5 min after completion of the exercise, and then declined slowly to 10.30 +/- 0.61 mmol l-1 by 30 min. Arterial blood pressure increased transiently with exercise but recovered rapidly, whereas the exercise-induced tachycardia was sustained throughout the recovery period. The recovery from the metabolic and cardiovascular responses to maximal sprint exercise in man is incomplete 30 min after cessation of the exercise.     

Effects of hyperoxia on skeletal muscle carbohydrate metabolism during transient and steady-state exercise.

This study compared the effects of inspiring either a hyperoxic (60% O(2)) or normoxic gas (21% O(2)) while cycling at 70% peak O(2) uptake on 1) the ATP derived from substrate phosphorylation during the initial minute of exercise, as estimated from phosphocreatine degradation and lactate accumulation, and 2) the reliance on carbohydrate utilization and oxidation during steady-state cycling, as estimated from net muscle glycogen use and the activity of pyruvate dehydrogenase (PDH) in the active form (PDH(a)), respectively. We hypothesized that 60% O(2) would decrease substrate phosphorylation at the onset of exercise and that it would not affect steady-state exercise PDH activity, and therefore muscle carbohydrate oxidation would be unaltered. Ten active male subjects cycled for 15 min on two occasions while inspiring 21% or 60% O(2), balance N(2). Blood was obtained throughout and skeletal muscle biopsies were sampled at rest and 1 and 15 min of exercise in each trial. The ATP derived from substrate-level phosphorylation during the initial minute of exercise was unaffected by hyperoxia (21%: 52.2 +/- 11.1; 60%: 54.0 +/- 9.5 mmol ATP/kg dry wt). Net glycogen breakdown during 15 min of cycling was reduced during the 60% O(2) trial vs. 21% O(2) (192.7 +/- 25.3 vs. 138.6 +/- 16.8 mmol glycosyl units/kg dry wt). Hyperoxia had no effect on PDH(a), because it was similar to the 21% O(2) trial at rest and during exercise (21%: 2.20 +/- 0.26; 60%: 2.25 +/- 0.30 mmol.kg wet wt(-1).min(-1)). Blood lactate was lower (6.4 +/- 1.0 vs. 8.9 +/- 1.0 mM) at 15 min of exercise and net muscle lactate accumulation was reduced from 1 to 15 min of exercise in the 60% O(2) trial compared with 21% (8.6 +/- 5.1 vs. 27.3 +/- 5.8 mmol/kg dry wt). We concluded that O(2) availability did not limit oxidative phosphorylation in the initial minute of the normoxic trial, because substrate phosphorylation was unaffected by hyperoxia. Muscle glycogenolysis was reduced by hyperoxia during steady-state exercise, but carbohydrate oxidation (PDH(a)) was unaffected. This closer match between pyruvate production and oxidation during hyperoxia resulted in decreased muscle and blood lactate accumulation. The mechanism responsible for the decreased muscle glycogenolysis during hyperoxia in the present study is not clear.     

Effect of beta-adrenergic blockade on lactate turnover in exercising dogs

Dogs with indwelling catheters in the jugular vein and in the carotid artery ran on the treadmill (slope: 15%, speed: 133 m/min). Lactate turnover and glucose turnover were measured using [U-14C]lactate and [3-3H]glucose as tracers, according to the primed constant-rate infusion method. In addition, the participation of plasma glucose in lactate production (Ra-L) was measured with [U-14C]glucose. Propranolol was given either (A) before exercise (250 micrograms/kg, iv) or (B) in form of a primed infusion administered to the dog running at a steady rate. Measurements of plasma propranolol concentration showed that in type A experiments plasma propranolol fell in 45 min below the lower limit of the complete beta-blockade. In the first 15 min of work Ra-L rose rapidly; then it fell below that of the control (exercise) values. During steady exercise, the elevated Ra-L was decreased by propranolol infusion close to resting values. beta-Blockade doubled the response of glucose production, utilization, and metabolic clearance rate to exercise. In exercising dogs approximately 40-50% of Ra-L arises from plasma glucose. This value was increased by the blockade to 85-90%. It is concluded that glycogenolysis in the working muscle has a dual control: 1) an intracellular control operating at the beginning of exercise, and 2) a hormonal control involving epinephrine and the beta-adrenergic receptors.     

Skeletal muscle metabolism during exercise is influenced by heat acclimation

The influence of heat acclimation on skeletal muscle metabolism during submaximal exercise was studied in 13 healthy men. The subjects performed 30 min of cycle exercise (70% of individual maximal O2 uptake) in a cool [21 degrees C, 30% relative humidity (rh)] and a hot (49 degrees C, 20% rh) environment before and again after they were heat acclimated. Aerobic metabolic rate was lower (0.1 l X min-1; P less than 0.01) during exercise in the heat compared with the cool both before and after heat acclimation. Muscle and plasma lactate accumulation with exercise was greater (P less than 0.01) in the hot relative to the cool environment both before and after acclimation. Acclimation lowered (P less than 0.01) aerobic metabolic rate as well as muscle and plasma lactate accumulation in both environments. The amount of muscle glycogen utilized during exercise in the hot environment did not differ from that in the cool either before or after acclimation. These findings indicate that accumulation of muscle lactate is increased and aerobic metabolic rate is decreased during exercise in the heat before and after heat acclimation; increased muscle glycogen utilization does not account for the increased muscle lactate accumulation during exercise under extreme heat stress; and heat acclimation lowers the aerobic metabolic rate and muscle and blood lactate accumulation during exercise in a cool as well as a hot environment.     

The significance of the aerobic-anaerobic transition for the determination of work load intensities during endurance training.

Anaerobic and aerobic-anaerobic threshold (4 mmol/l lactate), as well as maximal capacity, were determined in seven cross country skiers of national level. All of them ran in a treadmill exercise for at least 30 min at constant heart rates as well as at constant running speed, both as previously determined for the aerobic-anaerobic threshold. During the exercise performed with a constant speed, lactate concentration initially rose to values of nearly 4 mmol/l and then remained essentially constant during the rest of the exercise. Heart rate displayed a slight but permanent increase and was on the average above 170 beats/min. A new arrangement of concepts for the anaerobic and aerobic-anaerobic threshold (as derived from energy metabolism) is suggested, that will make possible the determination of optimal work load intensities during endurance training by regulating heart rate.     

Oxidative metabolism and anaerobic glycolysis during repeated exercise

The purpose of the present study was to examine aerobic and muscle anaerobic energy production during supramaximal repeated exercise. Eight subjects performed three 2-min bouts of cycling (EX1-EX3) at an intensity corresponding to about 125 % of VO2 max separated by 15 min of rest. Ventilatory variables were measured breath by breath during the exercise and a muscle biopsy was taken before and after each exercise bout. Blood samples were collected before and after each cycling period and during the recovery periods. Total work in the first 2 min bout of cycling, EX1, [46.3 +/- 2.1 KJ] was greater than in the second, EX2, (p < 0.01) and in the third, EX3, (p < 0.05). The ATP utilization [4.0 +/- 1.4 mmol x (kg dry weight)(-1), EX1] during the three exercise bouts was the same. The decrement in muscle phosphocreatine (PCr) [46.8 +/- 8.5 mmol x (kg dry weight)(-1), EX1] was also similar for the three exercise bouts. Muscle lactate accumulation was greater (p < 0.05) during EX1 compared to EX2 and EX3. The total oxygen consumption was the same for the three exercise bouts, but when it is corrected for the total work performed, oxygen uptake during EX2 (153 +/- 9 ml x KJ(-1)) and EX3 (150 +/- 9 ml x KJ(-1)) was higher (p < 0.01 and p < 0.05, respectively) than during EX1 (139 +/- 8 ml x KJ(-1)). The present data suggest that oxidative metabolism does not compensate for the reduction of anaerobic glycolysis during repeated fatiguing exercise.