Anaerobic energy release in working muscle during 30 s to 3 min of exhausting bicycling.

To examine the anaerobic energy release during intense exercise, 16 healthy young men cycled as long as possible at constant powers chosen to exhaust the subjects in approximately 30 s, 1 min, or 2-3 min. Muscle biopsies were taken before and approximately 10 s after exercise and analyzed for lactate, phosphocreatine (PCr), and other metabolites. O2 uptake was measured for determination of the accumulated O2 deficit (a whole body measure of the anaerobic energy release), and this indirect measure of the anaerobic energy release was compared with a direct value obtained from measured muscle metabolites. Muscle lactate concentration rose by 30.0 +/- 1.2 mmol/kg and muscle PCr concentration fell by 12.4 +/- 0.9 mmol/kg during the 2-3 min of exhausting exercise. The anaerobic ATP production was consequently 58 +/- 2 mmol/kg wet muscle mass, which may be the maximum anaerobic energy release for human muscle during bicycling. Because the anaerobic ATP production was 6 and 32% less for 1 min and 30 s of exercise, respectively, than for 2 min of exercise (P < 0.03), 2 min of exhausting exercise may be required for maximal use of anaerobic sources. Lactate production provided three times more ATP than PCr breakdown for all three exercise durations. There was a close linear relationship between the rates of anaerobic ATP production in muscle and the value estimated for the whole body by the O2 deficit (r = 0.94). This suggests that the accumulated O2 deficit is a valid measure of the anaerobic energy release during bicycling.

Relative importance of aerobic and anaerobic energy release during short-lasting exhausting bicycle exercise.

Anaerobic energy release is of great importance for shortlasting exercise but has been difficult to quantify. In order to determine the amount of anaerobic energy release during shortlasting exercise we let 17 healthy young males exercise on the ergometer bike to exhaustion. The power during exercise was kept constant and selected to cause exhaustion in approximately 30 s, 1 min, or 2-3 min. The O2 uptake was measured continuously during the exercise, and the anaerobic energy release was quantified by the accumulated O2 deficit. The work done as well as the total energy release rose linearly with the exercise duration and was therefore a sum of a component proportional to time plus a constant addition. The accumulated O2 deficit increased from 1.86 +/- 0.07 (SE) mmol/kg for 30 s exercise to 2.25 +/- 0.06 mmol/kg for 1 min exercise and further to 2.42 +/- 0.08 mmol/kg for exercise lasting 2 min or more (P less than 0.01). The accumulated O2 uptake increased linearly with the duration, and as a consequence of this the relative importance of aerobic processes increased from 40% at 30 s duration to 50% at 1 min duration and further to 65% for exercise lasting 2 min. These results show that both aerobic and anaerobic processes contribute significantly during intense exercise lasting from 30 s to 3 min.

Anaerobic capacity determined by maximal accumulated O2 deficit.

We present a method for quantifying the anaerobic capacity based on determination of the maximal accumulated O2 deficit. The accumulated O2 deficit was determined for 11 subjects during 5 exhausting bouts of treadmill running lasting from 15 s to greater than 4 min. The accumulated O2 deficit increased with the duration for exhausting bouts lasting up to 2 min, but a leveling off was found for bouts lasting 2 min or more. Between-subject variation in the maximal accumulated O2 deficit ranged from 52 to 90 ml/kg. During exhausting exercise while subjects inspired air with reduced O2 content (O2 fraction = 13.5%), the maximal O2 uptake was 22% lower, whereas the accumulated O2 deficit remained unchanged. The precision of the method is 3 ml/kg. The method is based on estimation of the O2 demand by extrapolating the linear relationship between treadmill speed and O2 uptake at submaximal intensities. The slopes, which reflect running economy, varied by 16% between subjects, and the relationships had to be determined individually. This can be done either by measuring the O2 uptake at a minimum of 10 different submaximal intensities or by two measurements close to the maximal O2 uptake and by making use of a common Y-intercept of 5 ml.kg-1.min-1. By using these individual relationships the maximal accumulated O2 deficit, which appears to be a direct quantitative expression of the anaerobic capacity, can be calculated after measuring the O2 uptake during one exhausting bout of exercise lasting 2-3 min.

Effect of training on the anaerobic capacity.

Intense exercise of short duration is heavily dependent on energy from anaerobic sources, and subjects successful in anaerobic types of sports may therefore have a larger anaerobic capacity and be able to release energy at a higher rate. Performances in these kinds of sports are improved by training, suggesting that the anaerobic capacity is trainable. The purpose of this investigation was to study the effect of training on anaerobic capacity. We therefore determined the anaerobic capacity, expressed as the maximal accumulated O2 deficit during treadmill running, of untrained, endurance-trained, and sprint-trained young men. In addition, seven women and five men trained for 6 wk, and their anaerobic capacity was compared before and after the training period. There was no difference in anaerobic capacity between the untrained and endurance-trained subjects, whereas the sprinters' anaerobic capacity was 30% larger (P less than 0.001). The women's anaerobic capacity was 17% less than the men's (P = 0.03). Six weeks of training increased the anaerobic capacity by 10%. We conclude that the anaerobic capacity varies significantly between subjects and that it can be improved within 6 wk. Moreover, there was a close relationship between a high anaerobic capacity and a high peak rate of anaerobic energy release.

Lactate release, concentration in blood, and apparent distribution volume after intense bicycling.

To study the release of lactate from muscle and its relationship to the blood lactate concentration during and after intense bicycling, young men cycled at 5.5 W kg(-1) body mass for 2 min to exhaustion or stopped after 1 min (nonexhaustive ride). The leg's release of lactate during and after each ride was taken from the measured blood flow and lactate concentrations in arterial and femoral-venous blood. Muscle biopsies were taken in separate experiments and analyzed for lactate. During the bicycling, 6 to 10% of the lactate produced was released to the blood. During exercise and for the first few minutes after, the rate of lactate release did not differ between 2 min exhaustive and 1 min nonexhaustive bicycling. The integrated release (exercise plus recovery) for the 1 min bicycling was 60 to 80% of the corresponding value of the 2 min exhaustive bicycling. In the late recovery, the blood lactate concentration was 3 to 5 times higher after 2 min exhaustive bicycling than after the 1 min nonexhaustive bicycling. There was thus a mismatch between the amount of lactate released and measured concentration in blood, reflecting a smaller distribution volume after the exhaustive bicycling. The blood lactate concentration may therefore not be a good measure of the lactate production and anaerobic energy release during bicycling.

Lactate elimination and glycogen resynthesis after intense bicycling.

OBJECTIVE: Muscles break down glycogen to lactate during intense exercise, and in the recovery period, glycogen reappears while lactate disappears. The purpose of this study was to examine to what extent lactate is resynthesized to glycogen within the formerly active muscles themselves in man. MATERIAL AND METHODS: Fifteen healthy young men cycled for 2 min to exhaustion. Muscle biopsies were taken from the knee extensor muscle before the exercise, just after the ride, and again after 45 min of recovery. In addition, blood samples were taken from the femoral artery and vein, and the leg blood flow was measured using the ultrasound Doppler technique. The muscle biopsies were analysed for glycogen, lactate and other metabolites, and the blood samples were analysed for lactate and glucose. The exchanges of lactate and glucose of the leg were assessed by multiplying the measured arterio-venous (a-v) differences by the blood flow. RESULTS: During the exercise the muscles broke down 20+/-4 mmol glycogen kg(-1) wet muscle mass and produced 26+/-1 mmol lactate kg(-1). In the recovery period after 24+/-1 mmol lactate kg(-1) had disappeared, of which 48 % was released to the blood, 52 % disappeared within the muscle. An R-value of 0.62 across the leg suggests that none of the lactate was oxidized. Altogether, 10+/-3 mmol glycogen kg(-1) reappeared during recovery. Glucose uptake accounted for 2 mmol kg(-1) and glycolytic intermediates (G-6-P and free glucose) accounted for 4 mmol kg(-1); 4 mmol glycogen kg(-1) (42 %) reappeared from unknown sources. CONCLUSIONS: The present data are compatible with the idea that around half of the lactate produced during intense bicycling is resynthesized to glycogen within the working muscles themselves in the recovery period after the bicycling.

Glycogen breakdown and lactate accumulation during high-intensity cycling.

High-intensity exercise results in a large breakdown of glycogen. The glycogen lost may reappear as hexose phosphates, lactate, or it may be fully oxidized. Part of the lactate produced may be transferred from muscle to blood. There is, however, incomplete information on the relative importance of each endpoint of glycogen breakdown during high intensity exercise. Therefore, 16 healthy men cycled for between 30 s and 3 min until exhaustion. Muscle biopsies were taken from m. vastus lateralis before and immediately after exercise and analysed for glycogen, glucose, glucose-6-phosphate and lactate. In addition the blood lactate concentration was measured at exhaustion, and the O2 uptake was measured throughout the exercise for calculation of glycogen oxidation. The muscle glycogen concentration fell by 17-24 mmol kg-1 wet wt muscle, the muscle glucose and G-6-P concentrations rose by 1 and 4 mmol kg-1 respectively, and the muscle lactate concentration rose by 20-30 mmol kg-1. The blood lactate concentration at exhaustion was 4-9 mmol l-1 above pre-exercise value. Consequently, 60% of the glycogen lost reappeared as lactate within the working muscle, another 20-25% was found as other glycolytic intermediates, 4-13% of the glycogen loss could be accounted for by oxidation. Lactate released to blood could account for approximately 10% of all lactate produced. Therefore, when large muscles are heavily engaged, as during high intensity cycling, most of the glycogen broken down appears as lactate within the working muscle.

[Anaerobic capacity--theoretical basis and methods for practical testing]. / Anaerob kapasitet--teoretisk grunnlag og metoder for praktisk testing.

The ATP turnover rate is raised during highly intensive exercise. Part of the ATP used is regenerated anaerobically independently of oxygen consumption. Lactate production accounts for 75% of the anaerobic ATP production, while breakdown of phosphocreatine accounts for the remaining 25%. Anaerobic processes can provide energy for about one minute's exercise during exhausting exercise lasting several minutes. An athlete may improve his anaerobic capacity by 10% during two months of proper training, and the measured improvement is of significance for athletes. The accumulated oxygen deficit has been introduced to quantify the anaerobic release of energy during exercise. The method is discussed briefly.

Acid-base and electrolyte balance after exhausting exercise in endurance-trained and sprint-trained subjects.

High ability to perform strenuous exercise of short duration is accompanied by a large lactate formation in the exercising muscles, but the disturbances in extracellular acid-base and electrolyte balance might be attenuated compared to subjects with less ability to perform intense exercise. To study this, oxygen deficit, changes in arterial blood acid-base status and plasma electrolytes were studied in six-endurance trained (ET) and six sprint-trained (ST) subjects who exercised on a treadmill at a speed which led to exhaustion within 1 min. During exercise the ET and ST subjects developed an oxygen deficit of 41 and 56 ml oxygen units kg-1 respectively, whereas peak blood lactate concentration post exercise averaged 12.5 and 16.7 mmol l-1. Blood pH followed lactate concentration closely, reaching nadir values of 7.175 and 7.065 for ET and ST subjects respectively. Respiratory compensation and changes in blood bicarbonate and standard base deficit (SBD) concentrations for a given lactate concentration were the same for the two groups, amounting to a change in PCO2 of 0.12 kPa, in bicarbonate concentration of 1.09 mmol l-1 and in SBD of 1.44 mmol l-1 mM-1 change in blood lactate concentration. During exercise the increase in haematocrit, from to 43 to 45% for the ET subjects and from 46 to 50% for the ST subjects, was accompanied by almost parallel relative changes in plasma chloride and sodium concentrations. Whereas haematocrit continued to increase post exercise and followed blood lactate concentration closely, plasma sodium and chloride concentrations decreased to pre-exercise values within 9 min of recovery. The anion gap increased significantly more than blood lactate concentration. Thus, ST subjects were capable of accumulating more lactate in blood compared with ET subjects, but at the expense of a lower pH, since the buffer capacity seemed to be the same for the two groups. The acidosis, which was larger than could be accounted for by lactic acid, was associated with an inexplicably large anion gap.

Plasma potassium changes with high intensity exercise.

1. Exercise seems to change the extracellular potassium concentration far beyond the narrow limits seen in resting subjects. To examine alterations in plasma potassium concentration during exercise, twenty healthy, well-trained men ran on the treadmill at 6 deg inclination with catheters inserted in the femoral vein and artery. 2. During 1 min exhausting exercise plasma potassium concentration rose in parallel in the vein and artery, reaching peak post-exercise values of 8.34 +/- 0.23 mmol l-1 and 8.17 +/- 0.29 mmol l-1. After 3 min recovery the potassium concentration was 0.50 +/- 0.05 mmol l-1 below pre-exercise values. Both the rise of plasma potassium concentration during exercise and the decline during recovery followed exponential time courses with a half-time of 25 s. 3. Exercise at reduced intensity showed that the peak post-exercise potassium concentration was linearly related to the exercise intensity. Individual resting, peak and nadir values were proportionally related. 4. The increased potassium concentration during exercise can be explained in full by the electrical activity in the exercising muscles. Repeated 1 min exhausting exercise bouts revealed no relationship between potassium concentration and plasma pH nor glycogen break-down. 5. All of the observations fit a simple model of potassium efflux from active muscle and elimination from blood with the following characteristics: the efflux increases (decreases) stepwise at the onset (end) of exercise, and the efflux rate during exercise increases with exercise intensity. Potassium is eliminated from blood by a proportional regulator which may be the Na(+)-K+ pump of the exercising muscle. Extracellular potassium is indirectly linked to the pump stimulus, and the rate of reuptake is proportional to the extracellular accumulation. Thus no limited maximal power for potassium uptake was found. The post-exercise undershoot of 0.5 mmol l-1 can be explained by a higher gain of the pump after exercise. 6. The large, rapid changes in the plasma potassium concentration during and after exercise is due to the first order kinetics of the reuptake mechanism rather than to a limited power to take up potassium.

Plasma K+ changes during intense exercise in endurance-trained and sprint-trained subjects.

Active muscle releases K+, and the plasma K+ concentration is consequently raised during exercise. K+ is removed by the Na,K pump, and training may influence the number of pumps. The plasma K+ concentration was therefore studied in five endurance-trained (ET) and six sprint-trained (ST) subjects during and after 1 min of exhausting treadmill running. Non-exhausting bouts of exercise at either lower speed or of shorter duration were also carried out. Blood samples were taken from a catheter in the femoral vein before and at frequent intervals after exercise. The pre-exercise venous plasma [K+] was (mean +/- SEM) 3.68 +/- 0.10 mmol l-1 (ET) and 3.88 +/- 0.06 mmol l-1 (ST). One minute of exhausting exercise was sustained at 5.27 +/- 0.08 m s-1 (ET) and 5.59 +/- 0.06 m s-1 (ST) and caused the plasma K+ concentration to rise by 4.4 +/- 0.3 (ET) and 4.7 +/- 0.3 mmol l-1 (ST; ns) respectively. Three minutes after exercise the K+ concentration was 0.48 +/- 0.08 mmol l-1 (ST) and 0.50 +/- 0.07 mmol l-1 (ST) below the pre-exercise value. During the following 6 min of recovery, the value was unchanged for the ET subjects, while a 0.32 +/- 0.06 mmol l-1 rise was seen for the ST subjects. Exercise at reduced intensity or of reduced duration resulted in smaller changes in the K+ concentration both during exercise and in the post-exercise recovery, and for each subject the lowest post-exercise K+ concentration was therefore inversely related to the peak K+ concentration during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Leg gas exchange, release of glycerol, and uptake of fats after two minutes bicycling to exhaustion.

It is not known to what extent the muscles use fats and carbohydrates as substrate for oxidation after intense, anaerobic types of bicycling. Six healthy young men therefore bicycled at constant power for 2 min to exhaustion. Blood was drawn from indwelling catheters in the femoral artery and vein at intervals during the 1-h postexercise recovery. The blood samples were analysed for concentrations of O2 and CO2, and for free fatty acids (FFA), triacylglycerols (TG), and glycerol in plasma. The blood flow was also measured, and the rate of leg uptake of FFA, TG, and O2 and the release of CO2 and glycerol as well as its gas exchange ratio were calculated and integrated over the recovery period. The leg gas exchange ratio integrated over the exercise plus 1-h recovery period was 0.67 +/- 0.06 (mean +/- SEM ), suggesting pure fat oxidation. There was no statistically significant arterial-femoral-venous difference of FFA across the leg. The concentration of TG in plasma fell by 0.18 +/- 0.09 mmol L(-1) (32%) during the first 10 min of the recovery period, and the leg took up 18 +/- 8 micromol TG kg(-1) body mass (bm) during the whole 1-h recovery period. Free glycerol was released from the leg throughout the recovery period in excess of that released from hydrolysis of TG from plasma, suggesting that 30 +/- 10 micromol TG kg (-1) bm was hydrolysed, probably from intra-muscular stores. If fully oxidized, the triacylglycerols hydrolysed can account for 101% of the measured O2 uptake. Thus, muscle seems to use only triacylglycerols as substrate for its oxidative energy release after intense exercise.

Muscle fluid and electrolyte balance during and following exercise.

During shortlasting exhausting exercise plasma volume is decreased by up to 20%. Water is probably taken up by muscle cells since the concentration of small plasma solutes like Na+ and Cl- increases in parallel with the hemoglobin concentration. During the first 4 min of the recovery phase the extracellular distribution volume for NaCl seems to be restored as evidenced by normalization of the plasma sodium and chloride concentrations. However, the plasma volume is restored at a much slower rate by recapture of isotonic fluid. Interestingly, arterial lactate concentrations are normalized at the same rate. We propose that immediately after end of shortlasting exercise the swollen muscle cells rapidly reduce their volume. Fluid will accumulate in the interstitium since reuptake of fluid into the capillaries is a much slower process.

Glycogen breakdown in different human muscle fibre types during exhaustive exercise of short duration.

The rates of glycogen breakdown during exhaustive intense exercise of three different intensities were determined in type I and subgroups of type II fibres. The exercise intensity corresponded to 122 +/- 2, 150 +/- 7 and 194 +/- 7% of VO2max. Muscle biopsies were taken from both legs before and immediately after exhaustion. Muscle lactate concentration increased by 27 +/- 1, 27 +/- 1 and 20 +/- 2 mmol kg-1 wet wt during the exercise at 122, 150 and 194% VO2max, respectively. The rates of glycogen depletion increased in all fibre types with increasing intensity, and the decline in type I fibres was 30-35% less than in type II fibres at all intensities. No differences were observed between the glycogen depletion rates in subgroups of type II fibres (IIA, IIAB and IIB). During the exercise at 194% VO2max, the rates of glycogen breakdown were 0.35 +/- 0.03 and 0.52 +/- 0.05 mmol s-1 kg-1 wet wt in type I and type II fibres, respectively. For both fibre types, the rates were 32 and 69% lower during the exercise at 150 and 122% VO2max. These data indicate that the glycolytic capacity of type I fibres is 30-35% lower than the capacity of type II fibres, in good agreement with the differences in phosphorylase and phosphofructokinase activities (Essén et al. 1975, Harris et al. 1976). The data also indicate that both fibre types contribute significantly to the anaerobic energy release at powers up till almost 200% VO2max.

Hard training for 5 mo increases Na(+)-K+ pump concentration in skeletal muscle of cross-country skiers.

To study how training affects the Na(+)-K+ pump concentration, 11 male and 9 female elite junior cross-country skiers trained 12-15 h/wk at 60-70% (moderate-intensity group) or 80-90% (high-intensity group) of their maximal O2 uptake for 5 mo. Muscle biopsies taken from the vastus lateralis muscle before and after the training period were analyzed for Na(+)-K+ pump concentration by the [3H]ouabain-binding technique. Before training, the concentration was 343 +/- 11 nmol/kg wet muscle mass (mean +/- SE) for the men and 281 +/- 14 nmol/kg for the women (18% less than for the men, P = 0.003). The Na(+)-K+ pump concentration rose by 49 +/- 11 nmol/kg (16%, P < 0.001) for all subjects pooled during the training period, and there was no difference between the two training groups (P = 0.3) or the sexes (P = 0.5) in this increase. The Na(+)-K+ pump concentration correlated with the maximal O2 uptake (r = 0.6, P = 0.003), with the performance during a 20-min treadmill run (r = 0.6, P = 0.003), and to the rank of the subjects' performance as cross-country skiers (Spearman's rank correlation coefficient = 0.76, P < 0.001). These data could mean that for elite cross-country skiers the performance is related to the Na(+)-K+ pump concentration. However, other studies have shown an equally high pump concentration for far less fit subjects, suggesting that the pump concentration may not be a limiting factor.

Effect of training intensity on muscle lactate transporters and lactate threshold of cross-country skiers.

The training intensity may affect the monocarboxylate transporters MCT1 and MCT4 in skeletal muscle. Therefore, 20 elite cross-country skiers (11 men and nine women) trained hard for 5 months at either moderate (MIG, 60-70% of VO2max) or high intensity (HIG, 80-90%). The lactate threshold, several performance parameters, and the blood lactate concentration (cLa) after exhausting treadmill running were also determined. Muscle biopsies taken from the vastus lateralis muscle before and after the training period were analysed for the two MCTs and for muscle fibre types and six enzymes. The concentration of MCT1 did not change for HIG (P=0.3) but fell for MIG (-12 +/- 3%, P=0.01); the training response differed between the two groups (P=0.05). The concentration of MCT4 did not change during the training period (P > 0.10). The concentration of the two MCTs did not differ between the two sexes (P=0.9). The running speed at the lactate threshold rose for HIG (+3.2 +/- 0.9%, P=0.003), while no change was seen for MIG (P=0.54); the training response differed between the two groups (P=0.04). The cLa after long-lasting exhausting treadmill running correlated with the concentration of MCT1 (rs=0.69, P=0.002), but not with that of MCT4 (rs=0.2, P=0.2). There were no other significant correlations between the concentrations of the two MCTs and the performance parameters, muscle fibre types, or enzymes (r < or = 0.36, P > 0.10). Thus, the training response differed between MIG and HIG both in terms of performance and of the effect on MCT1. Training at high intensity may be more effective for cross-country skiers. Finally, MCT1 may be important for releasing lactate to the blood during long-lasting exercise.

Effect of acupuncture on smoking cessation or reduction: an 8-month and 5-year follow-up study.

BACKGROUND: This study was undertaken to examine whether acupuncture treatment may have a long-term effect on smoking cessation or reduction. METHODS: Altogether 46 healthy men and women who reported smoking 20 +/- 6 cigarettes per day (mean +/- SD) volunteered in the study. They were randomly assigned to a test group (TG) or to a control group (CG) in which presumed anti-smoking acupoints were stimulated (TG) or acupuncture was applied to acupoints considered to have no effect on smoking cessation (CG). Before each treatment, after the last one, and 8 months and 5 years after the last one, each subject answered questionnaires about his or her smoking habits and attitudes. Blood samples for measuring variables related to smoking, i.e., serum cotinine and serum thiocyanate, were taken. RESULTS: During the treatment period the reported cigarette consumption fell on average by 14 (TG) and 7 (CG) cigarettes per day (P < 0.001). For both groups the reported cigarette consumption rose on average by 5-7 cigarettes during the following 8 months, and there was no systematic change thereafter. Consequently, TG showed a maintained reduction in smoking; no lasting effect was seen for CG. The TG reported that cigarettes tasted worse than before the treatments, and also the desire to smoke fell. For TG the serum concentration of cotinine fell, and the values correlated with the reported smoking. CONCLUSIONS: This study confirms that adequate acupuncture treatment may help motivated smokers to reduce their smoking, or even quit smoking completely, and the effect may last for at least 5 years. Acupuncture may affect the subjects' smoking by reducing their taste of tobacco and their desire to smoke. Different acupoints have different effects on smoking cessation.

Arterio-venous differences of blood acid-base status and plasma sodium caused by intense bicycling.

After intense exercise muscle may give off hydrogen ions independently of lactate, perhaps by a mechanism involving sodium ions. To examine this possibility further five healthy young men cycled for 2 min to exhaustion. Blood was drawn from catheters in the femoral artery and vein during exercise and at 1-h intervals after exercise. The blood samples were analysed for pH, blood gases, lactate, haemoglobin, and plasma proteins and electrolytes. Base deficit was calculated directly without using common approximations. The leg blood flow was also measured, thus allowing calculations of the leg's exchange of metabolites. The arterial blood lactate concentration rose to 14.2 +/- 1.0 mmol L-1, the plasma pH fell to 7. 18 +/- 0.02, and the base deficit rose 22% more than the blood lactate concentration did. The femoral-venous minus arterial differences peaked at 1.8 +/- 0.2 mmol L-1 (lactate), -0.24 +/- 0.01 (pH), and 4.5 +/- 0.4 mmol L-1 (base deficit), and -2.5 +/- 0.7 mmol L-1 (plasma sodium concentration corrected for volume changes). Thus, near the end of the exercise and for the first 10 min of the recovery period the leg gave off more hydrogen ions than lactate ions to the blood, and sodium left plasma in proportion to the extra hydrogen ions appearing. The leg's integrated excess release of hydrogen ions of 0.88 +/- 0.45 mmol kg-1 body mass was 67% of the integrated lactate release. Base deficit calculated by the traditional approximate equations underestimated the true value, but the error was less than 10%. We conclude that intense exercise and lactic acidosis may lead to a muscle release of hydrogen ions independent of lactate release, possibly by a Na+,H+ exchange. Hydrogen ions were largely buffered in the red blood cells.

Muscle fibre type and dimension in genetically obese and lean Zucker rats.

Skeletal muscle structure and morphology may be altered in obesity. To study this further, muscles from six genetically obese (fa/fa) and six normal male rats were examined at 15 weeks of age. The gluteus medius, vastus lateralis and rectus abdominis muscles were dissected out and stained for histochemical fibre typing. In addition the fibre cross-sectional area was measured on a graphic tablet. The proportion of fast-twitch fibres was larger in the vastus lateralis and rectus abdominis muscles of the obese rats (P < 0.01); no difference was seen for the gluteus medius muscle. For the normal rats the cross-sectional area of the fast-twitch fibres was 2-3 times larger than the area of slow-twitch fibres in the same muscle. The cross-sectional area of the fast-twitch fibres in the obese rats was 40-47% less than in the control animals (P < 0.003), while no difference between the two groups was found for the slow-twitch fibre area. The data thus suggest that in the genetically obese rats the development of fast-twitch fibres was primarily affected. Moreover, in these animals some muscles may be more affected than others.

Metabolic acidosis and changes in water and electrolyte balance after maximal exercise.

The purpose of this investigation was to study lactate production and the consequent changes in acid-base status, and in water and electrolyte balance, in response to 1 min of maximal exercise in sprint- and endurance-trained subjects. So far, the results from only two subjects (one sprinter and one marathon runner) have been analysed. The rate of lactate production was higher in the sprinter than in the marathon runner, as shown by peak blood lactate concentrations of 20.8 and 13.3 mM for the two subjects, respectively. Arterial blood pH fell from 7.43 to 7.14 in the sprinter and from 7.44 to 7.23 for the marathon runner. The metabolic acidosis was partly compensated for by a lowering of arterial CO2 tension by 0.0775 kPa per 1 mM drop in base excess. In each subject large changes in water and electrolyte balance occurred. Haematocrit increased dramatically in both subjects, and the calculated decrease in plasma volume was 20% for the marathon runner and 30% for the sprinter. In each subject sodium was removed from the circulation in amounts sufficient to keep the plasma sodium concentration constant. Plasma potassium concentration was unrelated to the state of acidosis, being 2.5 mM above the resting concentration immediately after maximal exercise, and dropping by 3 mM in the subsequent 2-3 min of recovery during prevailing acidosis. The degree of lactic acidosis was large in both subjects, although more severe in the sprinter than in the endurance runner. However, buffer capacity and compensatory mechanisms were largely similar in both subjects.