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.

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.

Examination of the Metamax I and II oxygen analysers during exercise studies in the laboratory.

The performance of the Metamax I and the Metamax II portable analysers for measuring the O2 uptake has been examined during exercise. Healthy subjects ran on the treadmill or bicycled on ergometers while the O2 uptake was measured by the Metamaxes and also by the Douglas bag technique or the Vmax 29 instrument. In the first series of experiments, O2 uptake was measured by each instrument in turn. In later experiments two or more breathing valves were connected in a series, thus enabling measurement of the O2 uptake simultaneously by more than one instrument. The O2 uptake measured by the Metamax analysers rose linearly by the value given by the control methods. However, there were variations of approximately 5% because the relationships differed between subjects. When the data from each subject were examined separately, the error of regression was 0.5-1 micromol s(-1) kg(-1) (2-3%), and the error of regression when relating the O2 uptake to the exercise intensity was similar to that found when using the Douglas bag technique alone. In most cases the lung ventilation reported by the Metamaxes was a few percent less than that given by the control methods, while the fractional extraction of O2 was higher for the Metamaxes. The respiratory exchange ratios (R-value) reported by the Metamaxes were in good agreement with those of the control methods in the range 0.9-1.0 only; for this parameter, the Metamaxes do not seem to be reliable for exercise testing. The O2 uptake and the R-value were also calculated from the raw data reported by the Metamaxes. The calculated values differed somewhat from those reported by the instruments, and the calculated values were more in agreement with those obtained by the Douglas bag technique than those reported by the instrument. This study suggests that the O2 uptake reported by the Metamaxes is precisely measured within subjects but that there are some systematic errors as well as variations between subjects.

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.

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.

Effect of strenuous strength training on the Na-K pump concentration in skeletal muscle of well-trained men.

This study examined how strenuous strength training affected the Na-K pump concentration in the knee extensor muscle of well-trained men and whether leg muscle strength and endurance was related to the pump concentration. First, the pump concentration, taken as 3H-ouabain binding, was measured in top alpine skiers since strength training is important to them. Second, well-trained subjects carried out strenuous eccentric resistance training either 1, 2, or 3 times.week-1 for 3 months. The Na-K pump concentration, the maximal muscle strength in a full squat lift (one repetition maximum, 1 RM), and the muscle endurance, taken as the number of full squat lifts of a mass of 70% of the 1 RM load, were measured before and after the training period. The mean pump concentration of the alpine skiers was 425 (SEM 11) nmol.kg-1 wet muscle mass. The subjects in part two increased their maximal strength in a dose-dependent manner. The muscle endurance increased for all subjects but independently of the training programme. From a mean starting value of 356 (SEM 6) nmol.kg-1 the mean Na-K pump concentration increased by 54 (SEM 15) nmol.kg-1 (+15%, P < 0.001) when the results for all subjects were pooled. The effect was larger for those who had trained twice a week than for those who had trained only once a week (P = 0.025), suggesting that the effect of strength training depended on the amount of training carried out. The muscle strength and endurance were not related to the pump concentration, suggesting that the pumping power of this enzyme did not limit the performance during heavy lifting. However, the individual improvements in the endurance test during the training period correlated with the individual changes in the pump concentration (rSpearman = 0.5; P = 0.01) which could mean that a common factor both increases the pump concentration and makes the muscles more adapted to repeated heavy lifting.

Examination of four different instruments for measuring blood lactate concentration.

Information on the performance of different instruments used to measure blood lactate concentration is incomplete. We therefore examined instruments from Yellow Springs Instruments (YSI 23L and YSI 1500) and three cheaper and simpler instruments: Dr. Lange's LP8+, Lactate Pro from Arkray in the KDK corporation and Accusport from Boehringer Mannheim. First, a number of blood samples were analysed by standard enzymatic photofluorometry (our reference method) and, in addition, by one or more of the instruments mentioned above. Second, measurements using two or more identical instruments were compared. Third, since Lactate Pro and Accusport are small (approximately 100 g, pocket-size), battery-driven, instruments that could be used for outdoor testing, the performance of these instruments was examined at simulated altitudes (O2 pressure of <10 kPa) and at temperatures below -20 degrees C, while screening the instruments as much as possible from the cold. Most of the different instruments showed systematically too high or too low values (10-25% deviation). The observed differences between instruments may affect the "blood lactate threshold" by 2-5%. We found different readings between "equal" YSI 1500 instruments, while we could see no difference when comparing the other instruments of the same type. Lactate Pro gave reliable results at both -21+/-1 degrees C and at simulated altitude. Accusport gave reliable results in the cold, but 1.85+/-0.08 mmol L(-1) (mean+/-SD) too high readings at the simulated altitude. Of the three simpler instruments examined, the Lactate Pro was at least as good as the YSI instruments and superior to the other two.

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.

Effect of training on the activity of five muscle enzymes studied on elite cross-country skiers.

This study examines the effect of training intensity on the activity of enzymes in m. vastus lateralis. Elite junior cross-country skiers of both sexes trained 12-15 h weeks-1 for 5 months at either moderate (60-70% of VO2max, MIG) or high training intensity (80-90% of the VO2max, close to the lactate threshold; HIG). Muscle biopsies for enzyme analyses and fibre typing were taken before and after the training period. Histochemical analyses on single fibres were done for three enzymes (succinate dehydrogenase [SDH], hydroxybutyrate dehydrogenase [HBDH], glycerol-3-phosphate dehydrogenase [GPDH]), while the activity of citrate synthase [CS] and phosphofructokinase [PFK] was measured on whole biopsies. The activity of GPDH was low in ST fibres and high in FT fibres. The activity of SDH and HBDH was high in both ST and FTa fibres but low in the FTb fibres. The HIG increased their performance more than the MIG did during the training period as judged from scores on a 20-min run test. The SDH activity rose by 6% for the HIG (P < 0.02). No effects of training were found in the activities of CS, HBDH or GPDH, neither in the two training groups nor for the two genders (P > or = 0.16). The PFK activity fell by 10% for the HIG (P=0.02), while no change was found for the MIG. For GPDH, CS and SDH the women's activity was approximately 20% less than the value for the men (P < 0.03). For PFK and HBDH there was no sex difference (P > or = 0.27). There were positive correlations between the activity of three of the enzymes (CS, SDH and GPDH) and the performance parameters (VO2max, cross-country skiing and running performance; r > or = 0.6, P < 0.01). No correlations were found between the PFK or HBDH activities and the performance parameters (r < or = 0.16, P > 0.05). This study suggests that intensities near the lactate threshold affect biochemical and physiological parameters examined in this study as well as the performance of elite skiers, and that the rate-limiting enzymes may be more sensitive to training than non-rate-limiting enzymes.

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.

The effect of acute vs chronic treatment with beta-adrenoceptor blockade on exercise performance, haemodynamic and metabolic parameters in healthy men and women.

1. Variable results have been reported on the effect of beta-adrenoceptor blockers on maximal oxygen uptake (VO2 max) and exercise endurance. This may in part be due to different subject populations, but it could also be due to an adaption of metabolic and haemodynamic responses to exercise during chronic treatment with beta-adrenoceptor blockers. The present study was therefore carried out to examine the effect of acute and chronic administration of the non-selective beta-adrenoceptor blocker propranolol on both peak VO2 and exercise performance in the same subjects. Since the effect of beta-adrenoceptor blockade has not been properly investigated in women, eight healthy women were compared with seven men. Progressive bicycle exercise to exhaustion was performed after propranolol 0.15 mg kg-1 i.v. (acute) or 80 mg three times daily for 2 weeks (chronic) or placebo given according to a double-blind crossover design. 2. Mean (s.e. mean) peak VO2, was significantly reduced from 42.3 (1.6) ml min-1 kg-1 during placebo to 40.3 (1.2, P < 0.05) ml min-1 kg-1 after acute and 39.1 (1.2, P < 0.001) ml min-1 kg-1 after chronic propranolol treatment. No significant difference in peak VO2 between the two propranolol treatment regimens was observed (mean difference 1.2, 95% CI -0.1 to 2.4 ml min-1 kg-1). There was no treatment interaction with gender. 3. Cumulative work, 163 (9.3) kJ, was significantly reduced by acute, 148 (7.7, P < 0.001) kJ, and chronic, 147 (7.6, P < 0.001) kJ, administration of propranolol since the time to exhaustion was reduced by 5.3% and 5.3%, respectively. There was no significant difference between the two regimens of propranolol (mean difference 0.2, 95% CI -6.7 to 7.0 kJ) or between the sexes. Maximal knee extensor and handgrip strengths were not affected by propranolol. 4. Whereas sex did not influence ventilatory, haemodynamic or metabolic parameters, some differences were observed between acute and chronic propranolol treatment. During submaximal exercise oxygen uptake was reduced by approximately 2% and RER values increased by 0.04-0.05 after chronic treatment in contrast to no effect of acute propranolol treatment. Heart rate and systolic blood pressure were reduced significantly more after chronic compared with acute propranolol treatment; peak heart rate being 186 (2.2), 147 (2.3) and 134 (2.3) beats min-1, and peak systolic blood pressure being 189 (7), 171 (4) and 161 (4) mmHg after placebo, acute and chronic propranolol administration, respectively. Also the exercise induced rise in potassium and lactate levels were modified differentially; the rise in potassium concentration was less after chronic compared with acute propranolol treatment and lactate levels were reduced only after chronic administration of propranolol. In contrast, ventilation, which was unchanged after propranolol during submaximal exercise, was reduced to similar extent at exhaustion from 108 (6.4) to 97 (7.2) and 96 (5.9) l min-1 after acute and chronic propranolol administration, respectively. Diastolic blood pressure and subjective perception of fatigue were similar across the treatment regimens. 5. The study has demonstrated that acute and chronic administration of propranolol result in different haemodynamic and metabolic response to exercise, although endurance and peak oxygen consumption were reduced to the same extent. The response to propranolol was not significantly different between men and women.

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.

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)

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.

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.

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.