Relationship between muscle fatigue and oxygen uptake during cycle ergometer exercise with different ramp slope increments.

The surface electromyogram (EMG) from active muscle and oxygen uptake (VO2) were studied simultaneously to examine changes of motor unit (MU) activity during exercise tests with different ramp increments. Six male subjects performed four exhausting cycle exercises with different ramp slopes of 10, 20, 30 and 40 W.min-1 on different days. The EMG signals taken from the vastus lateralis muscle were stored on a digital data recorder and converted to obtain the integrated EMG (iEMG). The VO2 was measured, with 20-s intervals, by the mixing chamber method. A non-linear increase in iEMG against work load was observed for each exercise in all subjects. The break point of the linear relationship of iEMG was determined by the crossing point of the two regression lines (iEMGbp). Significant differences were obtained in the exercise intensities corresponding to maximal oxygen uptake (VO2max) and the iEMGbp between 10 and 30, and 10 and 40 W.min-1 ramp exercises (P < 0.05). However, no significant differences were obtained in VO2max and VO2 corresponding to the iEMGbp during the four ramp exercises. With respect to the relationship between VO2 and exercise intensity during the ramp increments, the VO2-exercise intensity slope showed significant differences only for the upper half (i.e. above iEMGbp). These results demonstrated that the VO2max and VO2 at which a nonlinear increase in iEMG was observed were not varied by the change of ramp slopes but by the exercise intensity corresponding to VO2max and the iEMGbp was varied by the change of ramp slopes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of incomplete pulmonary gas exchange on VO2 max

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation

These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (PaO2) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO2max) range = 65-77 ml.kg-1.min-1] performed a normoxic graded exercise test on a cycle ergometer to VO2max at sea level. During incremental exercise at VO2max, 5 of the 12 subjects had ideal alveolar to arterial PO2 gradients (PA-aO2) of above 5 kPa (range 5-5.7) and a decline from resting PaO2 (delta PaO2) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise PA-aO2 of 4.0-4.3 kPa with delta PaO2 of 0.4-1.3 kPa while the remaining 3 subjects had PA-aO2 of 4.3-5 kPa with delta PaO2 between 1.7 and 2.0 kPa. The correlation between PAO2 and PaO2 at VO2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption vs PaO2 and arterial partial pressure of carbon dioxide vs PaO2 at VO2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.     

The relationship between anaerobic threshold and electromyographic fatigue threshold in college women

The purpose of this study was to investigate the relationship between anaerobic threshold (Th(an)) and muscle fatigue threshold (EMGFT) as estimated from electromyographic (EMG) data taken from the quadriceps muscles (vastus lateralis) during exercise on a cycle ergometer. The subjects in this study were 20 female college students, including highly trained endurance athletes and untrained sedentary individuals, whose fitness levels derived from their maximal oxygen consumption ranged from 24.9 to 62.2 ml.kg-1.min-1. The rate of increase in integrated EMG (iEMG) activity as a function of time (iEMG slope) was calculated at each of four constant power outputs (350, 300, 250, 200 W), sufficiently high to bring about muscle fatigue. The iEMG slopes so obtained were plotted against the exercise intensities imposed, resulting in linear plots which were extrapolated to zero slope to give an intercept on the power axis which was in turn interpreted as the highest exercise intensity sustainable without electromyographic evidence of neuromuscular fatigue (EMGFT). The Th(an) was estimated from gas exchange parameters during an incremental exercise test on the same cycle ergometer. The mean results indicated that oxygen uptake (VO2) at Than was 1.39 l.min-1, SD 0.44 and VO2 at EMGFT was 1.33 l.min-1, SD 0.57. There was no significant difference between these mean values (P greater than 0.05) and there was a highly significant correlation between VO2 at Than and VO2 at EMGFT (r = 0.823, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiorespiratory adaptation with short term training in older men

The purpose of this study was to assess the rate of training-induced cardiorespiratory adaptations in older men [mean (SD), 66.5 (1.2) years]. The eight subjects trained an average of 4.3 (0.3) times each week. The walk/jog training was in two phases with 4 weeks (phase 1) at a speed to elicit 70% of pre-training maximal oxygen consumption (VO2max), and 5 weeks (phase 2) at 80%. Maximal exercise treadmill tests and a standardized submaximal protocol were performed prior to training, at weekly intervals during the training programme, and after training. VO2max (ml.kg-1.min-1) increased significantly over both phases: 6.6% after the first 4 weeks, and an additional 5.2% after the final 5 weeks. The weekly changes in VO2max over phase 1 were well fitted by an exponential association curve (r = 0.75). The half-time for the rate of adaptation was 13.8 days, or 8.3 training sessions. Over phase 2, the change in VO2max did not plateau and a time course could not be determined. Submaximal exercise heart rate (fc) was reduced a significant 10 beats.min-1 after the first 4 weeks, and further 6 beats.min-1 over the final 5 weeks. The fc reductions showed half-times of 9.1 days (phase 1) and 9.8 days (phase 2) (or 5-6 training sessions). The anaerobic ventilation threshold was increased 13.9% over the 9 weeks of training and the respiratory exchange ratio during constant load heavy exercise was significantly reduced; however, these changes could not be described by an exponential time course. Thus, short-term exercise training of older men resulted in significant and rapid cardiorespiratory improvements.     

Lymphocyte proliferation responses after exercise in men: fitness, intensity, and duration effects

This study investigated the effects of intensity and duration of exercise on lymphocyte proliferation as a measure of immunologic function in men of defined fitness. Three fitness groups--low [maximal O2 uptake (VO2max) = 44.9 +/- 1.5 ml O2.kg-1.min-1 and sedentary], moderate (VO2max = 55.2 +/- 1.6 ml O2.kg-1.min-1 and recreationally active), and high (VO2max = 63.3 +/- 1.8 ml O2.kg-1.min-1 and endurance trained)--and a mixed control group (VO2max = 52.4 +/- 2.3 ml O2.kg-1.min-1) participated in the study. Subjects completed four randomly ordered cycle ergometer rides: ride 1, 30 min at 65% VO2max; ride 2, 60 min at 30% VO2max; ride 3, 60 min at 75% VO2max; and ride 4, 120 min at 65% VO2max. Blood samples were obtained at various times before and after the exercise sessions. Lymphocyte responses to the T cell mitogen concanavalin A were determined at each sample time through the incorporation of radiolabeled thymidine [( 3H]TdR). Despite differences in resting levels of [3H]TdR uptake, a consistent depression in mitogenesis was present 2 h after an exercise bout in all fitness groups. The magnitude of the reduction in T cell mitogenesis was not affected by an increase in exercise duration. A trend toward greater reduction was present in the highly fit group when exercise intensity was increased. The reduction in lymphocyte proliferation to the concanavalin A mitogen after exercise was a short-term phenomenon with recovery to resting (preexercise) values 24 h after cessation of the work bout. These data suggest that single sessions of submaximal exercise transiently reduce lymphocyte function in men and that this effect occurs irrespective of subject fitness level.     

Variability of responses across training levels to maximal treadmill exercise

The variability of peak VO2 (ml/min, ml.kg-1.min-1), time on treadmill (TMILLTM), maximal heart rate (HRmax), respiratory exchange ratio at peak VO2 (Rmax), rate of respiration at peak VO2 (FREQ), and exercise-induced changes in plasma lactate concentration (LACDIF) was measured across three maximal treadmill runs in five highly trained, seven moderately trained, and five untrained males. No effect of training level on the variability of any of the parameters was found. Test-retest correlation coefficients for peak VO2 (r = 0.95, run 1 with run 2; r = 0.92, run 1 with run 3; r = 0.92, run 2 with run 3) were similar to previously reported values. Variance component distributions suggested that the underlying physiological mechanisms of response for peak VO2, TMILLTM, and HRmax were different from those of FREQ, Rmax, and LACDIF. Minimum detectable differences for peak VO2 (ml.kg-1.min-1, n = 5, minimum detectable within subject difference, 11.5%; minimum detectable among subject effects, 21.3%) indicated a need for careful attention to research design in future studies.     

Specific alterations of physiological parameters in competitive race walkers

Race walking is the technical and athletic expression of fast walking and it can be considered as a type of endurance performance. The purpose of this study was to examine whether 12 weeks of a specially designed training program results in the further training enhancement of endurance performance and the related physiological parameters in already well-trained race walkers competing at the national and international level. The investigation protocol consisted of determining the maximal oxygen uptake (VO2peak) and related gas exchange values using an automated cardiopulmonary exercise system and of determining blood lactate variables (aerobic threshold - LTAer and the maximal lactate steady state - MLSS) during walking with proper technique at 8, 10, 12 and 14 km·h-1 for 4 minutes without rest in between. Thereafter, the speed on the treadmill was increased by 0.5 km·h-1 every two minutes until exhaustion to determine VO2peak. After 12 weeks of a specially designed endurance training, statistically significant increases in VO2peak (61.8±8.5 mL·kg-1·min-1 pre vs. 66.9±9.5 mL·kg-1·min-1 post training; p<0.05) and blood lactate variables (VO2-LTAer and VO2-MLSS; p<0.05) were noted. The obtained results suggest that the applied training program can improve endurance and race performance in previously well trained race walkers.     

Gas exchange responses to ramp exercise

In the present study, the system of oxygen uptake (VO2) during ramp function exercise protocol can be studied to provide information about the physiological mechanisms underlying the process. The values of maximal oxygen uptake (VO2max) and gas exchange threshold (GET) were reproducibly obtained using ramp test protocol. On the other hand, the determination of VO2/work rate should be restrict to below the exercise intensity of the GET. Therefore, ramp exercise test might be usage for determination of VO2max, GET and/or VO2/work rate (i.e., work efficiency). The data obtained in this study concerning the mean response time (MRT) suggests that the ramp test is not a linear, first-order system. Therefore, the ramp exercise test protocol is recommended for the determination of VO2max, GET and work efficiency, but not for MRT.     

Evidence for altered alpha-adrenoreceptor responsiveness after a single bout of maximal exercise.

We studied hemodynamic responses to alpha- and beta-receptor agonists in eight men to test the hypothesis that adrenoreceptor responsiveness is altered within 24 h of the performance of maximal exercise. Adrenoreceptor responsiveness was tested under two experimental conditions (with and without maximal exercise). Adrenoreceptor tests were performed 24 h after each subject performed graded upright cycle ergometry to volitional exhaustion. The 2 test days (experimental conditions) were separated by at least 1 wk, and the order of exercise and no-exercise conditions was counterbalanced. Steady-state graded infusions of phenylephrine (PE) and isoproterenol (Iso) were used to assess alpha- and beta-adrenoreceptor responsiveness, respectively. Slopes calculated from linear regressions between Iso and PE doses and changes in heart rate, blood pressure, and leg vascular resistance for each subject were used as an index of alpha- and beta-adrenoreceptor responsiveness. The slope of the relationship between heart rate and Iso with maximal exercise was 1773 +/- 164 beats x microm-1x kg-1x min-1 compared with 1987 +/- 142 beats x microg-1x kg-1x min-1 without exercise (P = 0.158), whereas the slopes of the relationship between vascular resistance to Iso were -438 +/- 123 peripheral resistance units (PRU) x microg-1x kg-1x min-1 with maximal exercise and -429 +/- 105 x microg-1x kg-1 x min-1 without exercise (P = 0.904). Maximal exercise was associated with greater (P < 0.05) vascular resistance (15.1 +/- 2.8 PRU x microg-1 kg-1x min-1) and mean arterial blood pressure (15.8 +/- 2.1 mmHg. microg-1x kg-1x min-1) responses to PE infusion compared with no exercise (9.0 +/- 2.0 PRU x microg-1 kg-1 x min-1 and 10.9 +/- 2.0 mmHg. microg-1x kg-1x min-1, respectively). These results provide evidence that a single bout of maximal exercise increases alpha1-adrenoreceptor responsiveness within 24 h without affecting beta-cardiac and vascular adrenoreceptor responses.     

Linear relationship between VO2max and VO2max decrement during exposure to acute hypoxia

The purpose of these experiments is to test the hypothesis that exercise-induced hypoxemia at sea level in highly trained athletes might be exacerbated during acute hypoxia and therefore result in correspondingly larger decrements in maximal O2 uptake (VO2max) compared with less trained individuals. Thirteen healthy male volunteers were divided into two groups according to their level of fitness: 1) trained endurance athletes (T) (n = 7), with a VO2max range of 56-75 ml.kg-1.min-1 and 2) untrained individuals (UT) (n = 6), with a VO2max range of 33-49 ml.kg-1.min-1. Subjects performed two incremental cycle ergometry tests to determine VO2max under hypoxic conditions [14% O2-86% N2, barometric pressure (PB) = 760 Torr] and normoxic conditions (21% O2-79% N2, PB = 760 Torr). Tests were single blind, randomly administered, and separated by at least 72 h. Mean percent oxyhemoglobin saturation (%SaO2) during maximal exercise under hypoxic conditions was significantly (P less than 0.05) lower in the T group (77%) compared with the UT group (86%). Furthermore, the T group exhibited larger decrements (P less than 0.05) in VO2max (normoxic-hypoxic) compared with the UT group. Finally, a significant linear correlation (r = 0.94) existed between normoxic VO2max (ml.kg-1.min-1) and delta VO2max (normoxic-hypoxic). These data suggest that highly T endurance athletes suffer more severe gas exchange impairments during acute exposure to hypoxia than UT individuals, and this may explain a portion of the observed variance in delta VO2max among individuals during acute altitude or hypoxia exposure.     

Endurance training slows down the kinetics of heart rate increase in the transition from moderate to heavier submaximal exercise intensities

To find out whether endurance training influences the kinetics of the increases in heart rate (fc) during exercise driven by the sympathetic nervous system, the changes in the rate of fc adjustment to step increments in exercise intensities from 100 to 150 W were followed in seven healthy, previously sedentary men, subjected to 10-week training. The training programme consisted of 30-min cycle exercise at 50%-70% of maximal oxygen uptake (VO2max) three times a week. Every week during the first 5 weeks of training, and then after the 10th week the subjects underwent the submaximal three-stage exercise test (50, 100 and 150 W) with continuous fc recording. At the completion of the training programme, the subjects' VO2max had increased significantly (39.2 ml.min-1.kg-1, SD 4.7 vs 46 ml.min-1.kg-1, SD 5.6) and the steady-state fc at rest and at all submaximal intensities were significantly reduced. The greatest decrease in steady-state fc was found at 150 W (146 beats.min-1, SD 10 vs 169 beats.min-1, SD 9) but the difference between the steady-state fc at 150 W and that at 100 W (delta fc) did not decrease significantly (26 beats.min-1, SD 7 vs 32 beats.min-1, SD 6). The time constant (tau) of the fc increase from the steady-state at 100 W to steady-state at 150 W increased during training from 99.4 s, SD 6.6 to 123.7 s, SD 22.7 (P less than 0.01) and the acceleration index (A = 0.63.delta fc.tau-1) decreased from 0.20 beats.min-1.s-1, SD 0.05 to 0.14 beats.min-1.s-1, SD 0.04 (P less than 0.02). The major part of the changes in tau and A occurred during the first 4 weeks of training. It was concluded that heart acceleration following incremental exercise intensities slowed down in the early phase of endurance training, most probably due to diminished sympathetic activation.     

Sleep deprivation and cardiorespiratory function. Influence of intermittent submaximal exercise

The effects of 64 h of sleep deprivation upon cardiorespiratory function was studied in 11 young men (VO2max = 55.5 ml kg-1 min-1, STPD). Six subjects engaged in normal sedentary activities, while the others walked on a treadmill at 28% VO2max for one hour in every three; eight weeks later, sleep deprivation was repeated with a crossover of subjects. Immediate post-deprivation measurement of VO2max showed a small but statistically significant decrease (-3.8 ml min-1 kg-1, STPD), with no difference between exercise and control trials. The final decrement in aerobic power was not due to a loss of motivation, as 88% (21 of 24) of post-deprivation tests still showed a plateau of VO2max; in addition, terminal heart rates (198 vs 195 beats min-1), respiratory exchange ratios (1.14 vs 1.15) and blood lactate levels (12.1 vs 11.8 mmol l-1) were not significantly different after sleep deprivation. The decrease in VO2max was associated with a lower VEmax (127 vs 142 l min-1, BTPS) and a substantial haemodilution (13%). Physiological responses to sub-maximal exercise showed persistence of the normal diurnal rhythm in heart rate and oxygen consumption, with no added effects due to sleep deprivation. However, ratings of perceived exertion (Borg scale) increased significantly throughout sleep deprivation. The findings are consistent with a mild respiratory acidosis, secondary to reduced cortical arousal and/or a progressive depletion of tissue glycogen stores which are not altered appreciably by moderate physical activity.     

Cardiac output during exercise in paraplegic subjects

The purpose of this study was to measure the cardiac output using the CO2 rebreathing method during submaximal and maximal arm cranking exercise in six male paraplegic subjects with a high level of spinal cord injury (HP). They were compared with eight able bodied subjects (AB) who were not trained in arm exercise. Maximal O2 consumption (VO2max) was lower in HP (1.11.min, SD 0.1; 17.5 ml.min-1.kg-1, SD 4) than in AB (2.5 l.min-1, SD 0.6; 36.7 ml.min-1.kg, SD 10.7). Maximal cardiac output was similar in the groups (HP, 14 l.min-1, SD 2.6; AB, 16.8 l.min-1, SD 4). The same result was obtained for maximal heart rate (fc,max) (HP, 175 beats.min-1, SD 18; AB, 187 beats.min-1, SD 16) and the maximal stroke volume (HP, 82 ml, SD 13; AB, 91 ml, SD 27). The slopes of the relationship fc/VO2 were higher in HP than AB (P less than 0.025) but when expressed as a %VO2max there were no differences. The results suggest a major alteration of oxygen transport capacity to active muscle mass in paraplegics due to changes in vasomotor regulation below the level of the lesion.     

Metabolism of rats running up and down an incline

The purpose of these experiments was to determine oxygen consumption (VO2) in rats as a function of treadmill speed (10, 20, 30, 40, and 50 m . min-1) as they ran on the level and up and down a 16 degree (17.8%) incline. The slopes of the regression lines relating VO2 (ml O2 . kg-1 . min-1) to running speed (m . min-1) were linear for all three inclines. The regression slope for uphill runners (y = 1.25x + 47.7) was greater than the regression slopes for level (y = 0.88x + 41.2) (P less than 0.025) or downhill (y = 0.68x + 39.7) (P less than 0.005) runners, and the regression slope for level runners was greater than that for downhill runners (P less than 0.10). All VO2 measurements were submaximal. In conclusion, incline has a significant effect on the metabolism of rats running on a motor-driven treadmill.     

Ramp work tests with three different beta-blockers in normal human subjects

The effects of beta-blockade on the responses of oxygen uptake (VO2), heart rate (HR) and blood lactate (La-) were examined during ramp cycle ergometer tests (50 W.min-1 ramp slope) in 8 healthy male volunteers. Each subject took placebo, or one of four different doses of three different beta-blockers (propranolol, metoprolol or oxprenolol) 2 h prior to each test for a total of 15 exercise tests. VO2 was measured breath-by-breath, HR was sampled once per breath, and La- was obtained every minute. Linear regression analysis was applied to VO2 and HR data to obtain the kinetic parameter total lag time (TLT) and a slope value. La- was analyzed by a continuous exponential model with the lactate slope index (LSI) being derived from the individual response curves. Submaximal exercise HR was significantly depressed at the baseline as well as during the ramp tests by beta-blockade. TLT for HR was significantly affected by beta-blockade, with a dose dependent shift from a placebo value of 16 to 26 s with placebo to a value of -40 to -60 s at the highest dose. Slope of HR was significantly depressed relative to placebo. VO2 kinetics assessed by TLT were not significantly affected by beta-blockade. This slope of the VO2 vs work rate relationship was significantly less than placebo only at the highest dose of beta-blocker. The LSI was not significantly affected by beta-blockade. In contrast with the clear impairment of HR response to exercise during beta-blockade, both the VO2 and La- responses appear to be relatively unaffected by beta-blockade during ramp exercise tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Effect of endurance exercise training on ventilatory function in older individuals

To evaluate the effect of endurance training on ventilatory function in older individuals, 1) 14 master athletes (MA) [age 63 +/- 2 yr (mean +/- SD); maximum O2 uptake (VO2max) 52.1 +/- 7.9 ml . kg-1 . min-1] were compared with 14 healthy male sedentary controls (CON) (age 63 +/- 3 yr; VO2max of 27.6 +/- 3.4 ml . kg-1 . min-1), and 2) 11 sedentary healthy men and women, age 63 +/- 2 yr, were reevaluated after 12 mo of endurance training that increased their VO2max 25%. MA had a significantly lower ventilatory response to submaximal exercise at the same O2 uptake (VE/VO2) and greater maximal voluntary ventilation (MVV), maximal exercise ventilation (VEmax), and ratio of VEmax to MVV than CON. Except for MVV, all of these parameters improved significantly in the previously sedentary subjects in response to training. Hypercapnic ventilatory response (HCVR) at rest and the ventilatory equivalent for CO2 (VE/VCO2) during submaximal exercise were similar for MA and CON and unaffected by training. We conclude that the increase in VE/VO2 during submaximal exercise observed with aging can be reversed by endurance training, and that after training, previously sedentary older individuals breathe at the same percentage of MVV during maximal exercise as highly trained athletes of similar age.     

Effect of previous supramaximal work on lacticaemia during supra-anaerobic threshold exercise

Twelve male and female subjects (eight trained, four untrained) exercised for 30 min on a treadmill at an intensity of maximal O2 consumption (% VO2max) 90.0%, SD 4.7 greater than the anaerobic threshold of 4 mmol.l-1 (Than = 83.6% VO2max, SD 8.9). Time-dependent changes in blood lactate concentration [( lab]) during exercise occurred in two phases: the oxygen uptake (VO2) transient phase (from 0 to 4 min) and the VO2 steady-state phase (4-30 min). During the transient phase, [lab] increased markedly (1.30 mmol.l-1.min-1, SD (0.13). During the steady-state phase, [lab] increased slightly (0.02 mmol.l-1.min-1, SD 0.06) and when individual values were considered, it was seen that there were no time-dependent increases in [lab] in half of the subjects. Following hyperlacticaemia (8.8 mmol.l-1, SD 2.0) induced by a previous 2 min of supramaximal exercise (120% VO2max), [lab] decreased during the VO2 transient (-0.118 mmol.l-1.min-1, SD 0.209) and steady-state (-0.088 mmol.l-1.min-1, SD 0.103) phases of 30 min exercise (91.4% VO2max, SD 4.8). In conclusion, it was not possible from the Than to determine the maximal [lab] steady state for each subject. In addition, lactate accumulated during previous supramaximal exercise was eliminated during the VO2 transient phase of exercise performed at an intensity above the Than. This effect is probably largely explained by the reduction in oxygen deficit during the transient phase. Under these conditions, the time-course of changes in [lab] during the VO2 steady state was also affected.