Effect of pedaling rates and myosin heavy chain composition in the vastus lateralis muscle on the power generating capability during incremental cycling in humans

In this study, we have determined power output reached at maximal oxygen uptake during incremental cycling exercise (P(I, max)) performed at low and at high pedaling rates in nineteen untrained men with various myosin heavy chain composition (MyHC) in the vastus lateralis muscle. On separate days, subjects performed two incremental exercise tests until exhaustion at 60 rev min(-1) and at 120 rev min(-1). In the studied group of subjects P(I, max) reached during cycling at 60 rev min(-1) was significantly higher (p=0.0001) than that at 120 rev min(-1) (287+/-29 vs. 215+/-42 W, respectively for 60 and 120 rev min(-1)). For further comparisons, two groups of subjects (n=6, each) were selected according to MyHC composition in the vastus lateralis muscle: group H with higher MyHC II content (56.8+/-2.79 %) and group L with lower MyHC II content in this muscle (28.6+/-5.8 %). P(I, max) reached during cycling performed at 60 rev min(-1) in group H was significantly lower than in group L (p=0.03). However, during cycling at 120 rev min(-1), there was no significant difference in P(I, max) reached by both groups of subjects (p=0.38). Moreover, oxygen uptake (VO(2)), blood hydrogen ion [H(+)], plasma lactate [La(-)] and ammonia [NH(3)] concentrations determined at the four highest power outputs completed during the incremental cycling performed at 60 as well as 120 rev min(-1), in the group H were significantly higher than in group L. We have concluded that during an incremental exercise performed at low pedaling rates the subjects with lower content of MyHC II in the vastus lateralis muscle possess greater power generating capabilities than the subjects with higher content of MyHC II. Surprisingly, at high pedaling rate, power generating capabilities in the subjects with higher MyHC II content in the vastus lateralis muscle did not differ from those found in the subjects with lower content of MyHC II in this muscle, despite higher blood [H(+)], [La(-)] and [NH(3)] concentrations. This indicates that at high pedaling rates the subjects with higher percentage of MyHC II in the vastus lateralis muscle perform relatively better than the subjects with lower percentage of MyHC II in this muscle.     

VO2/power output relationship and the slow component of oxygen uptake kinetics during cycling at different pedaling rates: relationship to venous lactate accumulation and blood acid-base balance.

In this experiment we studied the effect of different pedalling rates during cycling at a constant power output (PO) 132+/-31 W (mean+/-S.D.), corresponding to 50% VO2 max, on the oxygen uptake and the magnitude of the slow component of VO2 kinetics in humans. The PO corresponded to 50% of VO2 max, established during incremental cycling at a pedalling rate of 70 rev.min(-1). Six healthy men aged 22.2+/-2.0 years with VO2 max 3.89+/-0.92 l.min(-1), performed on separate days constant PO cycling exercise lasting 6 min at pedalling rates 40, 60, 80, 100 and 120 rev.min(-1), in random order. Antecubital blood samples for plasma lactate [La]pl and blood acid-base balance variables were taken at 1 min intervals. Oxygen uptake was determined breath-by-breath. The total net oxygen consumed throughout the 6 min cycling period at pedalling rates of 40, 60, 80, 100 and 120 rev.min(-1) amounted to 7.727+/-1.197, 7.705+/-1.548, 8.679+/-1.262, 9.945+/-1.435 and 13.720+/-1.862 l, respectively for each pedalling rate. The VO2 during the 6 min of cycling only rose slowly by increasing the pedalling rate in the range of 40-100 rev.min(-1). This increase, was 0.142 l per 20 rev.min(-1) on the average. Plasma lactate concentration during the sixth minute of cycling changed little within this range of pedalling rates: the values were 1.83+/-0.70, 1.80+/-0.48, 2.33+/-0.88 and 2.52+/-0.33 mmol.l(-1). The values of [La]pl reached in the 6th minute of cycling were not significantly different from the pre-exercise levels. Blood pH was also not affected by the increase of pedalling rate in the range of 40-100 rev.min(-1). However, an increase of pedalling rate from 100 to 120 rev.min(-1) caused a sudden increase in the VO2 amounting to 0.747 l per 20 rev.min(-1), accompanied by a significant increase in [La]pl from 1.21+/-0.26 mmol.l(-1) in pre-exercise conditions to 5.92+/-2.46 mmol.l(-1) reached in the 6th minute of cycling (P<0.01). This was also accompanied by a significant drop of blood pH, from 7.355+/-0.039 in the pre-exercise period to 7.296+/-0.060 in the 6th minute of cycling (P < 0.01). The mechanical efficiency calculated on the basis of the net VO2 reached between the 4th and the 6th minute of cycling amounted to 26.6+/-2.7, 26.4+/-2.0, 23.4+/-3.4, 20.3+/-2.6 and 14.7+/-2.2%, respectively for pedalling rates of 40, 60, 80, 100 and 120 rev.min(-1). No significant increase in the VO2 from the 3rd to the 6th min (representing the magnitude of the slow component of VO2 kinetics) was observed at any of the pedalling rates (-0.022+/-0.056, -0.009+/-0.029, 0.012+/-0.073, 0.030+/-0.081 and 0.122+/-0.176 l.min(-1) for pedalling rates of 40, 60, 80, 100 and 120 rev.min(-1), respectively). Thus a significant increase in [La]pl and a decrease in blood pH do not play a major role in the mechanism(s) responsible for the slow component of VO2 kinetics in humans.     

Effect of different cycling frequencies during incremental exercise on the venous plasma potassium concentration in humans

The effect of different muscle shortening velocity was studied during cycling at a pedalling rate of 60 and 120 rev.min(-1) on the [K+]v in humans. Twenty-one healthy young men aged 22.5+/-2.2 years, body mass 72.7+/-6.4 kg, VO2 max 3.720+/-0.426 l. min(-1), performed an incremental exercise test until exhaustion. The power output increased by 30 W every 3 min, using an electrically controlled ergometer Ergoline 800 S (see Zoladz et al. J. Physiol. 488: 211-217, 1995). The test was performed twice: once at a cycling frequency of 60 rev.min(-1) (test A) and a few days later at a frequency of 120 rev. min(-1) (test B). At rest and at the end of each step (i.e. the last 15 s) antecubital venous blood samples for [K+]p were taken. Gas exchange variables were measured continuously (breath-by-breath) using Oxycon Champion Jaeger. The pre-exercise [K+]v in both tests was not significantly different amounting to 4.24+/-0.36 mmol.l(-1) in test A, and 4.37+/-0.45 mmol.l(-1) in test B. However, the [K+]p during cycling at 120 rev. min(-1) was significantly higher (p<0.001, ANOVA for repeated measurements) at each power output when compared to cycling at 60 rev.min(-1). The maximal power output reached 293+/-31 W in test A which was significantly higher (p<0.001) than in test B, which amounted to 223+/-40 W. The VO2max values in both tests reached 3.720+/-0.426 l. min(-1) vs 3.777+/-0.514 l. min(-1). These values were not significantly different. When the [K+]v was measured during incremental cycling exercise, a linear increase in [K+]v was observed in both tests. However, a significant (p<0.05) upward shift in the [K+]v and a % VO2max relationship was detected during cycling at 120 rev.min(-1). The [K+]v measured at the VO2max level in tests A and B amounted to 6.00+/-0.47 mmol.l-1 vs 6.04+/-0.41 mmol.l-1, respectively. This difference was not significant. It may thus be concluded that: a) generation of the same external mechanical power output during cycling at a pedalling rate of 120 rev.min(-1) causes significantly higher [K+]v changes than when cycling at 60 rev.min(-1), b) the increase of venous plasma potassium concentration during dynamic incremental exercise is linearly related to the metabolic cost of work expressed by the percentage of VO2max (increase as reported previously by Vollestad et al. J. Physiol. 475: 359-368, 1994), c) there is a tendency towards upward up shift in the [K+]v and % VO2max relation during cycling at 120 rev.min(-1) when compared to cycling at 60 rev.min(-1).     

Effect of different muscle shortening velocities during prolonged incremental cycling exercise on the plasma growth hormone, insulin, glucose, glucagon, cortisol, leptin and lactate concentrations.

BACKGROUND: Strenuous exercise was reported to involve the alteration in the release of some "stress" hormones such as growth hormone (GH), cortisol, catecholamines and appropriate adjustment of energy metabolism but the relative contribution of these hormones to metabolic response, to cycling exercise performed at different muscle shortening velocities, has not been clarified. AIMS: The purpose of this experiment was to assess the effect of applying different pedalling rates during a prolonged incremental cycling exercise test on the changes in the plasma levels of growth hormone, cortisol, insulin, glucagon and leptin in humans. Material and METHODS: Fifteen healthy non-smoking men (means +/- SD: age 22.9 +/- 2.4 years; body mass 71.9 +/- 8.2 kg; height 178 +/- 6 cm; with VO2max of 3.896 +/- 0.544 1 x min(-1), assessed in laboratory tests, were subjects in this study. The subjects performed in two different days a prolonged incremental exercise tests at two different pedalling rates, one of them at 60 and another at 120 rev x min(-1). During this tests the power output has increased by 30 W every 6 minutes. The tests were stopped when the subject reached about 70 % of the VO2max. RESULTS AND CONCLUSIONS: We have found that choosing slow or fast pedalling rates (60 or 120 rev min(-1)), while generating the same external mechanical power output, had no effect on the pattern of changes in plasma cortisol, insulin, glucagon, glucose and leptin concentrations. But, generation of the same external mechanical power output at 120 rev min(-1) causes more stepper increase (p < 0.01) in the plasma growth hormone concentration [GH]pl and plasma lactate concentrations [La]pl when compared to that observed during cycling at 60 rev x min(-1). We have also found that the onset of a significant increase in [GH]pl during cycling at 60 rev x min(-1) was not accompanied by significant increase in [La]pl. While during cycling at 120 rev x min(-1) the onset of a significant increase in [La]pl occurred without increase in [GH]pl, but with continuation of exercise when plasma [La]pl increased, there was also a parallel rise in plasma [GH]pl, as reported before. This results indicates that the increase in [GH]pl during exercise is not closely related to the increase in [La]pl.     

Cycling efficiency and pedalling frequency in road cyclists

The purpose of this study was to determine the influence of pedalling rate on cycling efficiency in road cyclists. Seven competitive road cyclists participated in the study. Four separate experimental sessions were used to determine oxygen uptake (VO(2)) and carbon dioxide output (VCO(2)) at six exercise intensities that elicited a VO(2) equivalent to 54, 63, 73, 80, 87 and 93% of maximum VO(2) (VO(2max)). Exercise intensities were administered in random order, separated by rest periods of 3-5 min; four pedalling frequencies (60, 80, 100 and 120 rpm) were randomly tested per intensity. The oxygen cost of cycling was always lower when the exercise was performed at 60 rpm. At each exercise intensity, VO(2) showed a parabolic dependence on pedalling rate (r = 0.99-1, all P < 0.01) with a curvature that flattened as intensity increased. Likewise, the relationship between power output and gross efficiency (GE) was also best fitted to a parabola (r = 0.94-1, all P < 0.05). Regardless of pedalling rate, GE improved with increasing exercise intensity (P < 0.001). Conversely, GE worsened with pedalling rate (P < 0.001). Interestingly, the effect of pedalling cadence on GE decreased as a linear function of power output (r = 0.98, n = 6, P < 0.001). Similar delta efficiency (DE) values were obtained regardless of pedalling rate [21.5 (0.8), 22.3 (1.2), 22.6 (0.6) and 23.9 (1.0)%, for the 60, 80, 100 and 120 rpm, mean (SEM) respectively]. However, in contrast to GE, DE increased as a linear function of pedalling rate (r = 0.98, P < 0.05). The rate at which pulmonary ventilation increased was accentuated for the highest pedalling rate (P < 0.05), even after accounting for differences in exercise intensity and VO(2) (P < 0.05). Pedalling rate per se did not have any influence on heart rate which, in turn, increased linearly with VO(2). These results may help us to understand why competitive cyclists often pedal at cadences of 90-105 rpm to sustain a high power output during prolonged exercise.     

Electromyographic data do not support a progressive recruitment of muscle fibers during exercise exhibiting a VO2 slow component

The origin of the slow component (SC) of oxygen uptake kinetics, presenting during exercise above the ventilatory threshold (VT), remains unclear. Possible physiologic mechanisms include a progressive recruitment of type II muscle fibers. The purpose of this study was to examine alterations in muscle activity through electromyography (EMG) and mean power frequency (MPF) analysis during heavy cycling exercise. Eight trained cyclists (mean +/- S.E.; age = 30 +/- 3 years, height = 1771 +/- 4 cm, weight = 73.8 +/- 6.5 kg, VO2max = 4.33 +/- 0.28 l min(-1)) completed transitions from 20W to a workload equaling 50% of the difference between V(T) and VO2max. VO2 was monitored using a breath-by-breath measurement system, and EMG data were gathered from surface electrodes placed on the gastrocnemius lateralis and vastus lateralis oblique. Breath-by-breath data were time aligned, averaged, interpolated to 1-s intervals, and modeled with non-linear regression. Mean power frequency (MPF) and RMS EMG values were calculated for each minute during the exercise bout. Additionally, MPF was determined using both isolated EMG bursts and complete pedal revolutions. All subjects exhibited a VO2 SC (mean amplitude = 0.98 +/- 0.16 l min(-1)), yet no significant differences were observed during the exercise bout in MPF or RMS EMG data (p > 0.05) using either analysis technique. While it is possible that the sensitivity of EMG may be insufficient to identify changes in muscle activity theorized to affect the VO2 SC, the data indicated no relationship between MPF/EMG and the SC during heavy cycling.     

The effects of high intensity training upon respiratory gas exchanges during fixed term maximal incremental exercise in man

The response of respiratory gas exchanges to a 6 week high intensity training program was examined in 5 healthy males during fixed term maximal incremental treadmill exercise. Training was performed 3 d.wk-1 and consisted of a progressive series of repeated 15 sec and 30 sec maximal runs, and weight training exercises for the leg extensor muscles. Respiratory gases during the tests were continuously monitored using an on-line system. Muscle biopsy samples were obtained from the m. vastus lateralis before and after training for histochemical determination of fibre distribution based on myosin ATP-ase activity, and fibre cross-sectional area based on NADH-Tetrazolium Reductase activity. Training significantly increased the proportion of type IIa fibres (+5.9 +/- 2.0%, p less than 0.001) and decreased type I fibres (-6.3 +/- 2.0%, p less than 0.001), the distribution of type IIb fibres remained unchanged (+0.4 +/- 0.9%). Muscle cross-sectional area also showed a significant increase after training in type I (+318 +/- 215 microns 2, p less than 0.05), IIa (+652 +/- 207 microns 2, p less than 0.001) and IIb (+773 +/- 196 microns 2, p less than 0.001) fibres. During fixed term maximal incremental exercise the mean carbon dioxide output (VCO2) and mean respiratory exchange ratio (R = VCO2/VO2) were significantly increased (p less than 0.01) after training. The R-time relationship was at all times shifted to the left after training, being significantly (p less than 0.01) so over the final five min of exercise. No changes in mean exercise oxygen uptake (VO2), maximum oxygen uptake (VO2max) and maximum heart rate (FHRmax) were observed between tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determinants of endurance in well-trained cyclists

Fourteen competitive cyclists who possessed a similar maximum O2 consumption (VO2 max; range, 4.6-5.0 l/min) were compared regarding blood lactate responses, glycogen usage, and endurance during submaximal exercise. Seven subjects reached their blood lactate threshold (LT) during exercise of a relatively low intensity (group L) (i.e., 65.8 +/- 1.7% VO2 max), whereas exercise of a relatively high intensity was required to elicit LT in the other seven men (group H) (i.e., 81.5 +/- 1.8% VO2 max; P less than 0.001). Time to fatigue during exercise at 88% of VO2 max was more than twofold longer in group H compared with group L (60.8 +/- 3.1 vs. 29.1 +/- 5.0 min; P less than 0.001). Over 92% of the variance in performance was related to the % VO2 max at LT and muscle capillary density. The vastus lateralis muscle of group L was stressed more than that of group H during submaximal cycling (i.e., 79% VO2 max), as reflected by more than a twofold greater (P less than 0.001) rate of glycogen utilization and blood lactate concentration. The quality of the vastus lateralis in groups H and L was similar regarding mitochondrial enzyme activity, whereas group H possessed a greater percentage of type I muscle fibers (66.7 +/- 5.2 vs. 46.9 +/- 3.8; P less than 0.01). The differing metabolic responses to submaximal exercise observed between the two groups appeared to be specific to the leg extension phase of cycling, since the blood lactate responses of the two groups were comparable during uphill running. These data indicate that endurance can vary greatly among individuals with an equal VO2 max.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of depletion exercise and light training on muscle glycogen supercompensation in men

Supercompensated muscle glycogen can be achieved by using several carbohydrate (CHO)-loading protocols. This study compared the effectiveness of two "modified" CHO-loading protocols. Additionally, we determined the effect of light cycle training on muscle glycogen. Subjects completed a depletion (D, n = 15) or nondepletion (ND, n = 10) CHO-loading protocol. After a 2-day adaptation period in a metabolic ward, the D group performed a 120-min cycle exercise at 65% peak oxygen uptake (VO2 peak) followed by 1-min sprints at 120% VO2 peak to exhaustion. The ND group performed only 20-min cycle exercise at 65% VO2 peak. For the next 6 days, both groups ate the same high-CHO diets and performed 20-min daily cycle exercise at 65% VO2 peak followed by a CHO beverage (105 g of CHO). Muscle glycogen concentrations of the vastus lateralis were measured daily with 13C magnetic resonance spectroscopy. On the morning of day 5, muscle glycogen concentrations had increased 1.45 (D) and 1.24 (ND) times baseline (P < 0.001) but did not differ significantly between groups. However, on day 7, muscle glycogen of the D group was significantly greater (p < 0.01) than that of the ND group (130 +/- 7 vs. 104 +/- 5 mmol/l). Daily cycle exercise decreased muscle glycogen by 10 +/- 2 (D) and 14 +/- 5 mmol/l (ND), but muscle glycogen was equal to or greater than preexercise values 24 h later. In conclusion, a CHO-loading protocol that begins with a glycogen-depleting exercise results in significantly greater muscle glycogen that persists longer than a CHO-loading protocol using only an exercise taper. Daily exercise at 65% VO2 peak for 20 min can be performed throughout the CHO-loading protocol without negatively affecting muscle glycogen supercompensation.     

Effects of prior heavy exercise on VO(2) kinetics during heavy exercise are related to changes in muscle activity.

We hypothesized that the elevated primary O(2) uptake (VO(2)) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peak VO(2)) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary VO(2) response was increased after prior heavy leg exercise (from mean +/- SE 2.11 +/- 0.12 to 2.44 +/- 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 +/- 2.3 to 25.2 +/- 3.3 s), and the amplitude of the VO(2) slow component was reduced (from 0.79 +/- 0.08 to 0.40 +/- 0.08 l/min, P < 0.05). The elevated primary VO(2) amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 +/- 108 vs. 604 +/- 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 +/- 0.9 vs. 80.6 +/- 1.0 Hz). The results of the present study indicate that the increased primary VO(2) amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.     

EMG versus oxygen uptake during cycling exercise in trained and untrained subjects.

The aim of this study was to test the hypothesis that bicycle training may improve the relationship between the global SEMG energy and VO2. We already showed close adjustment of the root mean square (RMS) of the surface electromyogram (SEMG) to the oxygen uptake (VO2) during cycling exercise in untrained subjects. Because in these circumstances an altered neuromuscular transmission which could affect SEMG measurement occurred in untrained individuals only, we searched for differences in the SEMG vs. VO2 relationship between untrained subjects and well-trained cyclists. Each subject first performed an incremental exercise to determine VO2max and the ventilatory threshold, and second a constant-load threshold cycling exercise, continued until exhaustion. SEMG from both vastus lateralis muscles was continuously recorded. RMS was computed. M-Wave was periodically recorded. During incremental exercise: (1) a significant non-linear positive correlation was found between RMS increase and VO2 increase in untrained subjects, whereas the relationship was best fitted by a straight line in trained cyclists; (2) the RMS/VO2 ratio decreased progressively throughout the incremental exercise, its decline being significantly and markedly accentuated in trained cyclists; (3) in untrained subjects, significant M-wave alterations occurred at the end of the trial. These M-wave alterations could explain the non-linear RMS increase in these individuals. During constant-load exercise: (1) after an initial increase, the VO2 ratio decreased progressively to reach a plateau after 2 min of exercise, but no significant inter-group differences were noted; (2) no M-wave changes were measured in the two groups. We concluded that the global SEMG energy recorded from the vastus lateralis muscle is a good estimate of metabolic energy expenditure during incremental cycling exercise only in well-trained cyclists.     

Effect of pH on metabolic and cardiorespiratory responses during progressive exercise

Six healthy male subjects performed three exercise tests in which the power output was increased by 100 kpm/min each minute until exhaustion. The studies were carried out after oral administration of CaCO3 (control), NH4Cl (metabolic acidosis), and NaHCO3 (metabolic alkalosis). Ventilation (VE), O2 intake (VO2), and CO2 output (VCO2) were monitored continuously. Arterialized-venous blood samples were drawn at specific times and analyzed for pH, PCO2, and lactate concentration. Resting pH (mean +/- SE) was lowest in acidosis (7.29 +/- 0.01) and highest in alkalosis (7.46 +/- 0.02). A lower peak power output (kpm/min) was achieved in acidosis (1,717 +/- 95) compared with control (1,867 +/- 120) alkalosis (1,867 +/- 125). Submaximal VO2 and VCO2 were similar, but peak VO2 and VCO2 were lower in acidosis. Plasma lactate concentration was lower at rest and during exercise in acidosis. Although lactate accumulation was reduced in acidosis, increases in hydrogen ion concentration were similar in the three conditions. We conclude that acid-base changes influence the maximum power output that may be sustained in incremental dynamic exercise and modify plasma lactate appearance, but have little effect on hydrogen ion appearance in plasma.     

Effect of fatigue on maximal power output at different contraction velocities in humans.

The effect of fatigue as a result of a standard submaximal dynamic exercise on maximal short-term power output generated at different contraction velocities was studied in humans. Six subjects performed 25-s maximal efforts on an isokinetic cycle ergometer at five different pedaling rates (60, 75, 90, 105, and 120 rpm). Measurements of maximal power output were made under control conditions [after 6 min of cycling at 30% maximal O2 uptake (VO2max)] and after fatiguing exercise that consisted of 6 min of cycling at 90% VO2max with a pedaling rate of 90 rpm. Compared with control values, maximal peak power measured after fatiguing exercise was significantly reduced by 23 +/- 19, 28 +/- 11, and 25 +/- 11% at pedaling rates of 90, 105, and 120 rpm, respectively. Reductions in maximum peak power of 11 +/- 8 and 14 +/- 8% at 60 and 75 rpm, respectively, were not significant. The rate of decline in peak power during the 25-s control measurement was least at 60 rpm (5.1 +/- 2.3 W/s) and greatest at 120 rpm (26.3 +/- 13.9 W/s). After fatiguing exercise, the rate of decline in peak power at pedaling rates of 105 and 120 rpm decreased significantly from 21.5 +/- 9.0 and 26.3 +/- 13.9 W/s to 10.0 +/- 7.3 and 13.3 +/- 6.9 W/s, respectively. These experiments indicate that fatigue induced by submaximal dynamic exercise results in a velocity-dependent effect on muscle power. It is suggested that the reduced maximal power at the higher velocities was due to a selective effect of fatigue on the faster fatigue-sensitive fibers of the active muscle mass.     

Comparison of incremental and steady state tests of endurance training

To compare the results obtained by incremental or constant work load exercises in the evaluation of endurance conditioning, a 20-week training programme was performed by 9 healthy human subjects on the bicycle ergometer for 1 h a day, 4 days a week, at 70-80% VO2max. Before and at the end of the training programme, (1) the blood lactate response to a progressive incremental exercise (18 W increments every 2nd min until exhaustion) was used to determine the aerobic and anaerobic thresholds (AeT and AnT respectively). On a different day, (2) blood lactate concentrations were measured during two sessions of constant work load exercises of 20 min duration corresponding to the relative intensities of AeT (1st session) and AnT (2nd session) levels obtained before training. A muscle biopsy was obtained from vastus lateralis at the end of these sessions to determine muscle lactate. AeT and AnT, when expressed as % VO2max, increased with training by 17% (p less than 0.01) and 9% (p less than 0.05) respectively. Constant workload exercise performed at AeT intensity was linked before training (60% VO2max) to a blood lactate steady state (4.8 +/- 1.4 mmol.l-1) whereas, after training, AeT intensity (73% VO2max) led to a blood lactate accumulation of up to 6.6 +/- 1.7 mmol.l-1 without significant modification of muscle lactate (7.6 +/- 3.1 and 8.2 +/- 2.8 mmol.kg-1 wet weight respectively). It is concluded that increase in AeT with training may reflect transient changes linked to lower early blood lactate accumulation during incremental exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of exercise on the fiber composition of skeletal muscle

Biopsy samples from the vastus lateralis muscle (VLM) of man were examined for fiber composition at rest and at selected intervals during prolonged exercise ranging in intensity from 40% to 75% of the total body maximal oxygen uptake (VO2max) and one-min bouts of exercise at 150% VO2max. Because of the heterogeneity of fibers in human VLM, studies were also completed where the effect of exercise on the fiber composition of the rat soleus muscle (SM) was examined. In some animals the SM from one hindlimb was removed 9 days prior to their being exercised after which the remaining SM was removed. Exercise reduced muscle glycogen in all experiments. In the studies with man, blood lactate exceeded 17 mmoles/l after the heavy exercise but was largely unchanged by endurance exercise. Colonic temperature of the exercised rats exceeded 40 degrees C. In studies where fibers were identified only as type I and type II, type II fibers in the VLM of all samples (16) taken at rest averaged 61.2 +/- 12.5% as compared to 59.0 +/- 12.0% after exercise (54 biopsy samples). In a second series of studies with man where the subtypes of type II fibers were identified, there were also no differences in fiber composition of the VLM after varying periods of exercise. Glycogen content and percent fiber composition were the same in right and left SM obtained from rested rats. Exercise (30 to 40 min) did not alter the fiber composition of the rat SM. These data demonstrate that the histochemically demonstratable myofibrillar actomyosin ATPase of skeletal muscle is not altered by a single exercise bout.     

Skeletal muscle oxygenation during incremental exercise

The purpose of this study was to investigate the relationship between muscle oxygenation level at exhaustion and maximal oxygen uptake (VO2max) in an incremental cycling exercise. Nine male subjects took part in an incremental exhaustive cycling exercise, and then cuff occlusion was performed. Changes in oxy-(deltaHbO2) and deoxy-(deltaHb) hemoglobin concentrations in the vastus lateralis muscle were measured with a near infrared spectroscopy (NIRS). Muscle oxygenation during incremental exercise was expressed as a percentage (%Moxy) of the maximal range observed during an arterial occlusion as the lower reference point. A systematic decrease was observed in %Moxy with increasing intensity. A significant relationship was observed between %Moxy at exhaustion and VO2max (p < 0.01). We concluded that the one of the limiting factor of VO2max is the muscle oxygen diffusion capacity, and %Moxy during exercise could be one of the indexes of muscle oxygen diffusion capacity.     

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.     

Adaptations in skeletal muscle exercise metabolism to a sustained session of heavy intermittent exercise

The purpose of this study was to investigate the hypothesis that a single, extended session of heavy exercise would be effective in inducing adaptations in energy metabolism during exercise in the absence of increases in oxidative potential. Ten healthy males [maximal aerobic power (VO(2 peak)) = 43.4 +/- 2.2 (SE) ml x kg(-1) x min(-1)] participated in a 16-h training session involving cycling for 6 min each hour at approximately 90% of maximal oxygen consumption. Measurements of metabolic changes were made on tissue extracted from the vastus lateralis during a two-stage standardized submaximal cycle protocol before (Pre) and 36-48 h after (Post) the training session. At Pre, creatine phosphate (PCr) declined (P < 0.05) by 32% from 0 to 3 min and then remained stable until 20 min of exercise at 60% VO(2 peak) before declining (P < 0.05) by a further 35% during 20 min of exercise at 75% VO(2 peak). Muscle lactate (mmol/kg dry wt) progressively increased (P < 0.05) from 4.59 +/- 0.64 at 0 min to 17.8 +/- 2.7 and 30.9 +/- 5.3 at 3 and 40 min, respectively, whereas muscle glycogen (mmol glucosyl units/kg dry wt) declined (P < 0.05) from a rest value of 360 +/- 24 to 276 +/- 31 and 178 +/- 36 at similar time points. During exercise after the training session, PCr and glycogen were not as depressed (P < 0.05), and increases in muscle lactate were blunted (P < 0.05). All of these changes occurred in the absence of increases in oxidative potential as measured by the maximal activities of citrate synthase and malate dehydrogenase. These findings are consistent with other studies, namely, that muscle metabolic adaptations to regular exercise are an early adaptive event that occurs before increases in oxidative potential.     

Influence of priming exercise on pulmonary O2 uptake kinetics during transitions to high-intensity exercise from an elevated baseline.

It has been suggested that the slower O2 uptake (VO2) kinetics observed when exercise is initiated from an elevated baseline metabolic rate are linked to an impairment of muscle O2 delivery. We hypothesized that "priming" exercise would significantly reduce the phase II time constant (tau) during subsequent severe-intensity cycle exercise initiated from an elevated baseline metabolic rate. Seven healthy men completed exercise transitions to 70% of the difference between gas exchange threshold (GET) and peak VO2 from a moderate-intensity baseline (90% GET) on three occasions in each of the "unprimed" and "primed" conditions. Pulmonary gas exchange, heart rate, and the electromyogram of m. vastus lateralis were measured during all tests. The phase II VO2 kinetics were slower when severe exercise was initiated from a baseline of moderate exercise compared with unloaded pedaling (mean+/-SD tau, 42+/-15 vs. 33+/-8 s; P<0.05), but were not accelerated by priming exercise (42+/-17 s; P>0.05). The amplitude of the VO2 slow component and the change in electromyogram from minutes 2 to 6 were both significantly reduced following priming exercise (VO2 slow component: from 0.47+/-0.09 to 0.27+/-0.13 l/min; change in integrated electromyogram between 2 and 6 min: from 51+/-35 to 26+/-43% of baseline; P<0.05 for both comparisons). These results indicate that the slower phase II VO2 kinetics observed during transitions to severe exercise from an elevated baseline are not altered by priming exercise, but that the reduced VO2 slow component may be linked to changes in muscle fiber activation.     

Effects of previous exercise on the ventilatory determination of the aerobic threshold

To study the effects of previous submaximal exercise on the ventilatory determination of the Aerobic Threshold (AeT), 16 men were subjected to three maximal exercise tests (standard test = ST, retest = RT, and test with previous exercise = TPE ) on a cycle ergometer. The protocol for the three tests consisted of 3 min pedalling against 25 W, followed by increments of 25 W every minute until volitional fatigue. TPE was preceded by 10 min cycling at a power output corresponding to the AeT as determined in ST, followed by a recovery period pedalling against 25 W until VO2 returned to values consistent with the initial VO2 response to 25 W. AeT was determined from the gas exchange curves (ventilatory equivalent for O2, fraction of expired O2, excess of VCO2, ventilation, and respiratory gas exchange ratio) printed every 30 s. The results showed good ST X RT reliability (r = 0.89). TPE showed significantly higher AeT values (2.548 +/- 0.44 1 X min-1) when compared with ST (2.049 +/- 0.331 X min-1) and RT (2.083 +/- 0.30 1 X min-1). There were no significant differences for the sub-threshold respiratory gas exchange ratios among the trials. The sub-threshold VO2 response showed significantly higher values for TPE at power outputs above 50 W. It was concluded that the performance of previous exercise can increase the value for the ventilatory determination of the AeT due to a faster sub-threshold VO2 response.