Excess CO(2) output response during and after short-term intensive exercise in sprinters and long-distance runners

The purpose of the present study was to examine the response of excess CO(2) output to short-term intensive exercise in sprinters (SPR) and long-distance runners (LDR). End-tidal CO(2) pressure (PETCO(2)) increased up to about 20 s postexercise and then returned to the resting level at about 2-3 min postexercise. Thereafter, PETCO(2) remained below the resting level. VCO(2) excess, defined as the difference between VCO(2) and VO(2) was integrated from the start of exercise until PETCO(2) returned to the resting level. This integrated VCO(2) excess was defined as the first phase of CO(2) excess (1st CO(2) excess). The subsequent integrated VCO(2) excess until 10 min postexercise was defined as the second phase of CO(2) excess (2nd CO(2) excess). The ratio of 1st CO(2) excess to the lactate rise from rest to the peak value was significantly lower in SPR than in LDR, whereas 2nd CO(2) excess was significantly greater in SPR than in LDR. The decrease in PETCO(2) at 10 min postexercise was significantly larger in SPR than in LDR. The 2nd CO(2) excess was closely related to the decrease in PETCO(2). The results in the second phase suggest that the difference in the response of excess CO(2) output is derived from the difference in the respiratory chemosensitivity to lactic acid rise.     

The Effects of Caffeine on the Kinetics of O2Uptake, CO2Production and Expiratory Ventilation in Humans During the On-Transient of Moderate and Heavy Intensity Exercise

In order to test the hypothesis that glycogen sparing observed early during exercise following caffeine ingestion was a consequence of tighter metabolic control reflected in faster VO2 kinetics, we examined the effect of caffeine ingestion on oxygen uptake (VO2), carbon dioxide production (VCO2) and expiratory ventilation (VE) kinetics at the onset of both moderate (MOD) and heavy (HVY) intensity exercise. Male subjects (n = 10) were assigned to either a MOD (50% VO2,max, n = 5) or HVY (80% VO2,max, n = 5) exercise condition. Constant-load cycle ergometer exercise was performed as a step function from loadless cycling 1 h after ingestion of either dextrose (placebo, PLAC) or caffeine (CAFF; 6 mg (kg body mass)-1). Alveolar gas exchange was measured breath-by-breath. A 2- or 3-component exponential model, fitted through the entire exercise transient, was used to analyse gas exchange and ventilatory data for the determination of total lag time (TLT: the time taken to attain 63% of the total exponential increase). Caffeine had no effect on TLT for VO2 kinetics at either exercise intensity (MOD: 36 +/- 14 s (PLAC) and 41 +/- 10 s (CAFF); HVY: 99 +/- 30 s (PLAC) and 103 +/- 26 (CAFF) (mean +/- S.D.)). TLT for VE was increased with caffeine at both exercise intensities (MOD: 50 +/- 20 s (PLAC) and 59 +/- 21 s (CAFF); HVY: 168 +/- 35 s (PLAC) and 203 +/- 48 s (CAFF)) and for VCO2 during MOD only (MOD: 47 +/- 14 s (PLAC) and 53 +/- 17 s (CAFF); HVY: 65 +/- 13 s (PLAC) and 69 +/- 17 s (CAFF)). Contrary to our hypothesis, the metabolic effects of caffeine did not alter the on-transient VO2 kinetics in moderate or heavy exercise. VCO2 kinetics were slowed by a reduction in CO2 stores reflected in pre-exercise and exercise endtidal CO2 pressure (PET,CO2) and plasma PCO2 which, we propose, contributed to slowed VE kinetics.     

VE response to VCO2 during exercise is unaffected by exercise training and different exercise limbs

We designed two experiments to investigate the relationship between ventilation (VE) and CO2 output (VCO2) during exercise under the conditions of exercising different limbs, the arms as opposed to the legs (experiment 1), and of different physical training states after undergoing standard exercise training for 90 d (experiment 2). Six healthy young subjects underwent submaximal ramp exercise at an incremental work rate of 15 W/min for the arm and leg, and 11 healthy middle-aged subjects underwent an incremental exercise test at the rate of 30 W/3 min before and after exercise training. We measured pulmonary breath-by-breath VE, VCO2, oxygen uptake (VO2), tidal volume (VT), breathing frequency (bf), and end-tidal O2 and CO2 pressures (PETO2, PETCO2) via a computerized metabolic cart. In experiment 1, arm exercise produced significantly greater VE than did leg exercise at the same work rates, as well as significantly higher VO2, VCO2, and bf. The slopes of the regression lines in the VE-VCO2 relationship were not significantly different: the values were 27.8 +/- 2.1 (SD) during the arm exercise, and 25.3 +/- 3.9 during the leg exercise, with no differences in their intercepts. In experiment 2, the VO2, VCO2, and VE responses at the same work rates were similar in both before and after the 90-d exercise training, whereas the heart rate (HR) and mean blood pressure (MBP) were significantly reduced after training. Exercise training did not alter the VE-VCO2 relationship, the slope of which was 31.9 +/- 4.9 before exercise training and 34.2 +/- 4.4 after exercise training. We concluded that the VE-VCO2 relationship during exercise is unaltered, independent of not only working muscle regions but also exercise training states.     

Immediate CO2 storage capacity at the onset of exercise

The purpose of the present study was to obtain the immediate CO2 storage capacity at the onset of exercise. The CO2 stores at the onset of the exercise were calculated from the difference between the respiratory gas exchange ratio (R) and the metabolic gas exchange ratio (RQ: R obtained at 5.5 min of exercise). The CO2 stores per body weight (CO2 stores/w) were linearly related to the CO2 pressure (P'vCO2) determined by the CO2 rebreathing method (r = 0.713, p less than 0.001), the slope being 0.330 ml/(mmHg X kg). The CO2 stores were then corrected for change in O2 stores with exercise, that defined as total CO2 stores. P'vCO2 was also corrected for the effect of lung-bag volume shrinkage and Haldane effect during CO2 rebreathing, that defined as true PvCO2. The total CO2 stores/w were also related linearly to the true PvCO2 (r = 0.725, p less than 0.001), the slope of the regression line defined as the immediate CO2 storage capacity being 0.650 ml/(mmHg X kg).     

Respiratory compensation point during incremental exercise as related to hypoxic ventilatory chemosensitivity and lactate increase in man

The pulmonary ventilation-O2 uptake (VE-VO2) relationship during incremental exercise has two inflection points: one at a lower VO2, termed the ventilatory threshold (VT); and another at a higher VO2, the respiratory compensation point (RCP). The individuality of RCP was studied in relation to those of the chemosensitivities of the central and peripheral chemoreceptors, which were assessed by resting estimates of hypercapnic ventilatory response (HCVR) and hypoxic ventilatory response (HVR), respectively, and the rate of lactic acid increase during exercise, which was estimated as a slope difference (delta slope) between a lower slope of VCO2-VO2 relationship (VCO2:CO2 output) obtained at work rates below VT and a higher slope at work rates between VT and RCP. Twenty-two male and sixteen female subjects underwent a 1 min incremental exercise test until exhaustion, in which VT, RCP and delta slope were determined. All measures were normalized for body surface area. In the males, the individual difference in RCP was inversely correlated with those of HVR and delta slope (p < 0.05), and in the females, similar tendencies persisted, while the correlation did not reach statistically significant levels (0.05 < p < 0.1). There was no significant correlation between RCP and HCVR in either sex. A multiple linear regression analysis showed that 40 to 50% of the variance of RCP was accounted for by those of HVR and delta slope, both of which were related linearly and additively to RCP, this relation being manifested in the males but not in the females without consideration of the menstrual cycle. These results suggest that the individuality of RCP depends partly on the chemosensitivity of the carotid bodies and the rate of lactic acid increase during incremental exercise.     

Maximal aerobic capacity of Bengali girl athletes of different sports activities

The maximal aerobic capacity (VO2max) and related cardiorespiratory parameters were determined on 67 Bengalee (Indian) girl athletes having nine different sports activities. VO2max was determined with a bicycle ergometer. The highest value for VO2maxl.min-1 was obtained by javelin throwers (1.95), being followed by pentathletes (1.92) and long-distance runners (1.90), whereas the lowest value was achieved by handballers (1.45). When VO2max was expressed in ml.kg-1.min-1, the long-distance runners registered the highest mean value (43.0), which was significantly higher than that of basketballers (34.9), handball players (36.2), badminton players (34.4), and swimmers (36.0). For this measurement, the sprinters (40.0), pentathletes (40.3), javelin throwers (40.0), and jumpers (39.4) did not differ significantly with each other, but each of the groups was significantly superior to basketballers, handballers, badminton players, and swimmers. No significant difference was also found amongst the latter groups. VO2maxl.min-1 was found to be significantly correlated with all the physical characteristics. It was predicted on the basis of age, height, weight, and body surface area using stepwise regression method.     

Peak blood ammonia and lactate after submaximal,maximal and supramaximal exercise in sprinters and long-distance runners

Summary The purpose of this study was to elucidate the difference in peak blood ammonia concentration between sprinters and long-distance runners in submaximal, maximal and supramaximal exercise. Five sprinters and six long-distance runners performed cycle ergometer exercise at 50% maximal, 75% maximal, maximal and supramaximal heart rates. Blood ammonia and lactate were measured at 2.5, 5, 7.5, 10 and 12.5 min after each exercise. Peak blood ammonia concentration at an exercise intensity producing 50% maximal heart rate was found to be significantly higher compared to the basal level in sprinters (P < 0.01) and in long-distance runners (P < 0.01). The peak blood ammonia concentration of sprinters was greater in supramaximal exercise than in maximal exercise (P < 0.05), while there was no significant difference in long-distance runners. The peak blood ammonia content after supramaximal exercise was higher in sprinters compared with long-distance runners (P < 0.01). There was a significant relationship between peak blood ammonia and lactate after exercise in sprinters and in long-distance runners. These results suggest that peak blood ammonia concentration after supramaximal exercise may be increased by the recruitment of fast-twitch muscle fibres and/or by anaerobic training, and that the processes of blood ammonia and lactate production during exercise may be strongly linked in sprinters and long-distance runners.     

Effects of bicarbonate ingestion on the respiratory compensation threshold and maximal exercise performance

Six males performed cycle ergometer exercise on two occasions in random order. Each exercise was preceded by a 2-h period in which matched capsules were administered orally, containing either starch (C) or NaHCO3 (E) in a dose of a 0.2 g.kg-1 body wt; pre-exercise blood pH and [HCO3-] were 7.34 +/- 0.01 and 23.7 +/- 0.5 mM (mean +/- S.E.) for the C study, and 7.41 +/- 0.01 and 28.6 +/- 1.3 mM for the E study (p less than 0.001 and p less than 0.01, respectively). Exercise was continuous and maintained for 10 min at 40% of maximal oxygen uptake (40% VO2max), followed by 15 min at 12 W above the respiratory compensation threshold ([+RCT]) which was determined by the increase of the ventilatory equivalent for carbon dioxide (VE.VCO2(-1)), and for as long as possible at 95% VO2max. Endurance time at 95% VO2max was significantly longer in E than in C (2.98 +/- 0.64 min vs. 2.00 +/- 0.44 min, p less than 0.05). The rate of increase in arterialized venous lactate (LA) was higher in E than in C from rest to exercise at [+RCT], while there was no significant difference in the hydrogen ions ([H+]). Consequently, [H+].LA-1 (nM.mM-1) was significantly lower in E than in C. The change of VE.VCO2(-1) was shifted downward in E compared to C during exercise with the lowest value being observed at the same exercise stage. These results suggest that the respiratory responses to exercise are not affected by the higher level of [HCO3-] induced by NaHCO3 ingestion, and appear to reflect the net change of plasma [HCO3-] or [H+]. Also, induced metabolic acidosis has little effect on [H+] appearance in blood.     

Change point in VCO2 during incremental exercise test: a new method for assessment of human exercise tolerance.

The main purpose of this study was to present a new method to determine the level of power output (PO) at which VCO2 during incremental exercise test (IT) begins to rise non-linearly in relation to power output (PO) - the change point in VCO2 (CP-VCO2). Twenty-two healthy non-smoking men (mean +/- SD: age 22.0 +/- 0.9 years; body mass 74.5 +/- 7.5 kg; height 181 +/- 7 cm; VO2max 3.753 +/- 0.335 l min-1) performed an IT on a cycloergometer. The IT started at a PO of 30 W, followed by gradual increases of 30 W every 3 min. Antecubital venous blood samples were taken at the end of each step and analysed for plasma lactate concentration [La]pl, blood PO2, PCO2 [HCO3-]b and [H+]b. In the detection of the change-point VCO2 (CP-VCO2), a two-phase model was assumed for the 'third-minute-data' of each step of the test. In the first phase, a linear relationship between VCO2 and PO was assumed, whereas in the second, an additional increase in VCO2 was allowed, above the values expected from the linear model. The PO at which the first phase ends is called the change point in VCO2. The identification of the model consists of two steps: testing for the existence of the change point, and estimating its location. Both procedures are based on suitably normalized recursive residuals (see Zoladz et al. 1998a. Eur J Appl Physiol 78, 369-377). In the case of each of our subjects it was possible to detect the CP-VCO2 and the CP-VO2 as described in our model. The PO at the CP-VCO2 amounted to 134 +/- 42 W. The CP- VO2 was detected at 136 +/- 32 W, whereas the PO at the LT amounted to 128 +/- 30 W and corresponded to 49 +/- 11, 49 +/- 8 and 47 +/- 8.6% VO2max, respectively, for the CP-VCO2, CP-VO2 and the LT. The [La]pl at the CP-VCO2 (2.65 +/- 0.76 mmol L-1), at the CP-VO2 (2.53 +/- 0. 56 mmol L-1) and at the LT (2.25 +/- 0.49 mmol L-1) were already significantly higher (P < 0.01, Students t-test) than the value reached at rest (1.86 +/- 0.43 mmol L-1). Our study illustrates that the CP-VCO2 and the CP-VO2 occur at a very similar power output as the LT. We therefore postulate that the CP-VCO2 and the CP-VO2 be applied as an additional criterion to assess human exercise tolerance.     

Lactic acid permeation rate in working gastrocnemii of dogs during metabolic alkalosis and acidosis

In isolated, blood perfused, supramaximally stimulated, isotonically working gastrocnemii of dogs lactic acid (LA) output and O2-consumption (V O2) were measured according to the Fick principle. Simultaneously concentration of muscle tissue was determined at rest and at different times during exercise. In one series of experiments metabolic alkalosis was induced by infusions of THAM of Na bicarbonate. As a result arterial pH increased to about 7.5 and standard [HCO3-1] to 31-35 mmol per 1. In another group of experiments metabolic acidosis was induced by HCl infusions. In these experiments pH decreased to 7.0-7.1 and standard [HO301] to 8-11 mmol per 1. During the first 3-4 min after the onset of exercise LA concentration of muscle tissue rose to 18-19 mumol per g wet weight in both series of experiments. During acidosis the highest average values for LA release from the muscle were about 1.1 mumoles per g per minute. During alkalosis LA permeation rate was nearly three times as high. As a consequence of increased rate of permeation, LA concentration of muscle tissue decreased more rapidly in alkalosis than in acidosis. In both series of experiments work per time and VO2 were practically equal during the first 5-6 min of exercise. Thereafter work per time and VO2 decreased more rapidly in acidosis than in alkalosis, a result which probably is due to higher LA concentration in muscle at this time in acidosis. It is concluded that LA permeation rate across muscle cell membrane is increased by high extracellular HCO3- concentration in combination with low H+ activity and vice versa.     

Ineffective ventilation during exercise in patients with chronic congestive heart failure.

The pathophysiologic mechanisms causing exertional breathlessness in patients with chronic congestive heart failure (CHF) are not fully understood. Therefore, we have studied whether the ventilation in such patients is ineffective during exercise. Thirteen patients with treated chronic CHF (New York Heart Association class II-IV) and eight healthy controls underwent a maximal bicycle ergometer test with continuous analysis of expired air and frequent arterial blood sampling for gas and lactate analysis. All subjects were non-smokers and none had any signs of a pulmonary disease. Peak O2 consumption of the patients was 14.9 +/- 5.3 ml min-1 kg-1 and that of controls 33.6 +/- 7.5 ml min-1 kg-1. In patients with CHF the ratio of pulmonary dead space to tidal volume was significantly elevated at peak exercise compared with that of the controls (0.36 +/- 0.08 vs. 0.20 +/- 0.07, P less than 0.05). The ventilatory equivalent for CO2 (VE:VCO2) was also significantly higher in patients than in controls during exercise (P less than 0.05). Furthermore, both the ventilatory equivalents for CO2 and O2 (VE:VO2) had a significant inverse correlation with peak O2 consumption (P less than 0.001 for VE:VCO2 and P less than 0.05 for VE:VO2), O2 consumption at anaerobic threshold (P less than 0.01) and O2-pulse (P less than 0.001) among the patients. During exercise the arterial PO2 and PCO2 remained normal in patients and controls. These data indicate that in patients with chronic CHF wasted ventilation is pathologically increased during exercise, and this is related to the severity of the disease. Chronic CHF is not associated with decreased ventilatory reserve, hypoxaemia or alveolar hyperventilation. The ineffectiveness of ventilation is probably an important cause of exertional breathlessness in patients with CHF.     

Nine months aerobic fitness induced changes on blood lipids and lipoproteins in untrained subjects versus controls

Regular endurance exercise has favorable effects on cardiovascular risk factors. However, the impact of an exercise-induced change in aerobic fitness on blood lipids is often inconsistent. The purpose of this study was to investigate the effect of nine consecutive months of training on aerobic fitness and blood lipids in untrained adults. Thirty subjects 35-55 years of age (wt: 73.1 +/- 13.6 kg, height 171.1 +/- 9.0 cm, %body fat 24.6 +/- 6.3%, 14 males and 16 females) were randomly assigned to an exercise (EG) (N = 20) and control (CG) (N = 10) group. All subjects completed an incremental treadmill test, anthropometric measurements, and venous blood sample collection before and after the 9 months of exercise. Participants in the exercise group were supervised and adjusted for improvements in running performance, whereas no change was administered for the control group. One-way and multivariate ANOVA was conducted to determine significant differences in means for time and group in selected variables [body mass, % body fat, BMI; VO(2peak), km/h at 2.0 (v-LA2) and 4.0 (v-LA4) mmol l(-1) blood lactate (LA) concentration, km/h of the last load (v-max); TC, LDL-C, HDL-C, TG, Apo B, Apo A-1, and Lp (a)]. Correlation coefficients and multivariate regression analysis was used to determine the association between aerobic fitness and blood lipids. The exercise group improved significantly (P < 0.0001) in VO(2peak), v-LA2, v-LA4, v-max and exhibited a significant decrease in Apo B (P < 0.04) compared to the control group (NS). In 9 months, E achieved 24% increase in VO(2peak) and 18% reduction in Apo B, denoting the impact of cardiovascular fitness on cardiovascular risk.     

Fitness as a determinant of the oxygen uptake/work rate slope in healthy children and children with inflammatory myopathy.

There is evidence that the slope of the change in oxygen uptake accompanying changes in work rate (delta VO2/delta W). during moderate incremental exercise is influenced by fitness (peak VO2). We set out to determine whether delta VO2/delta W was related to fitness in a group of healthy children and in children with juvenile dermatomyositis (JDM), a condition associated with decreased peak VO2. We also hypothesized that delta VO2/delta would be significantly decreased in children with JDM compared to healthy children. METHODS: Twelve children (2 boys) with JDM, mean age 11.6 +/- 3.6 yrs, and 20 healthy children (4 boys), mean age 11.3 +/- 2.9 years, performed an incremental exercise test using a cycle ergometer. delta VO2/delta W below the anaerobic threshold was analyzed using linear regression. Correlations between peak VO2 and delta VO2/delta W were calculated, and differences between the JDM and healthy groups were analyzed using independent t-tests. RESULTS: The delta VO2/delta W was significantly correlated with peak VO2 for children with JDM (r = 0.71, p < 0.01), healthy children (r = 0.53, p < 0.01), and all children combined (r = 0.78, p < 0.001). The delta VO2/delta W (7.4 +/- 1.4 vs. 10.8 +/- 1.2 ml O2.min-1.watt-1) and peak oxygen uptake (VO2peak) (19.2 +/- 5.0 vs. 31.4 +/- 7.2 ml O2.kg-1, min-1) were significantly lower in children with JDM than in healthy children, respectively (all p < or = 0.001). CONCLUSION: Fitness is significantly related to delta VO2/delta W in healthy children and those with JDM. Children with JDM have a significantly lower delta VO2/delta W than healthy children. Further study is needed to identify specific factors influencing delta VO2/delta W.     

Cardiodynamic factors affecting hyperpnea during steady-state exercise in man

In order to know the role of cardiodynamic factors for exercise hyperpnea, ventilation and several cardiorespiratory variables were measured simultaneously in human subjects during exercise. Cardiac output (Q) and mixed venous CO2 content (CVCO2) were determined by a rebreathing method. The correlation coefficients (r) for the relationships between minute expiratory ventilation (VE) and each of end-tidal CO2 tension (PETCO2), Q, CVCO2, CO2 flow into the lung (QCO2, the product of Q and CVCO2), oxygen consumption (VO2), and CO2 output (VCO2) were determined during the steady-state exercise up to 90 W. The correlation was highly significant (r = 0.84-0.99, p less than 0.001) in each case except for PETCO2 (r = 0.13, N.S.). The highest correlation was observed in the VE-VCO2 relationship. It was assume that VCO2 released from the pulmonary capillaries into the alveoli is the most likely stimulus leading to exercise hyperpnea. Arterial CO2 oscillation may be regarded as a potential linkage between VCO2 and VE.     

Oxygen kinetics and debt during recovery from expiratory flow-limited exercise in healthy humans

In healthy subjects expiratory flow limitation (EFL) during exercise can lower O(2) delivery to the working muscles. We hypothesized that if this affects exercise performance it should influence O(2) kinetics at the end of exercise when the O(2) debt is repaid. We performed an incremental exercise test on six healthy males with a Starling resistor in the expiratory line limiting expiratory flow to approximately 1 l s(-1) to determine maximal EFL exercise workload (W (max)). In two more square-wave exercise runs subjects exercised with and without EFL at W (max) for 6 min, while measuring arterial O(2) saturation (% SaO(2)), end-tidal pressure of CO(2) (P (ET)CO(2)) and breath-by-breath O(2) consumption VO2 taking into account changes in O(2) stored in the lungs. Over the last minute of EFL exercise, mean P (ET)CO(2) (54.7 +/- 9.9 mmHg) was significantly higher (P < 0.05) compared to control (41.4 +/- 3.9 mmHg). At the end of EFL exercise %SaO(2) fell significantly by 4 +/- 3%. When exercise stopped, EFL was removed, and we continued to measure VO2. During recovery, there was an immediate step increase in [Formula: see text] so that repayment of EFL O(2) debt started at a higher VO2 than control. Recovery VO2 kinetics after EFL exercise was best characterized by a double-exponential function with fundamental and slow time constants of 27 +/- 11 and 1,020 +/- 305 s, compared to control values of 41 +/- 10 and 1,358 +/- 320 s, respectively. EFL O(2) debt was 52 +/- 22% greater than control (2.19 +/- 0.58 vs. 1.49 +/- 0.38 l). We conclude that EFL exercise increases the O(2) debt and leads to hypoxemia in part due to hypercapnia.     

Acetyl group accumulation and pyruvate dehydrogenase activity in human muscle during incremental exercise.

The changes in the muscle contents of CoASH and carnitine and their acetylated forms, lactate and the active form of pyruvate dehydrogenase complex were studied during incremental dynamic exercise. Eight subjects exercised for 3-4 minutes on a bicycle ergometer at work loads corresponding to 30, 60 and 90% of their VO2max. Muscle samples were obtained by percutaneous needle biopsy technique at rest, at the end of each work period and after 10 minutes of recovery. During the incremental exercise test there was a continuous increase in muscle lactate, from a basal value of 4.5 mmol kg-1 dry weight to 83 mmol kg-1 at the end of the final period. The active form of pyruvate dehydrogenase complex increased from 0.37 mmol acetyl-CoA formed per minute per kilogram wet weight at rest to 0.80 at 30% VO2max, 1.28 and 1.25 at 60 and 90% VO2max, respectively. Both acetyl-CoA and acetylcarnitine increased at the two highest work loads. The increase of acetyl-CoA was from 12.5 mumol kg-1 dry weight at rest to 27.3 after the highest work load and for acetylcarnitine from 6.0 mmol kg-1 dry weight to 15.2. The CoASH and free carnitine contents fell correspondingly. There was a close relationship between acetyl-CoA and acetylcarnitine accumulation in muscle during exercise, with a binding of approximately 500 mol acetyl groups to carnitine for each mole of acetyl-CoA accumulated. The results imply that the carnitine store in muscle functions as a buffer for excess formation of acetyl groups from pyruvate catalyzed by the pyruvate dehydrogenase complex.     

Training profile counts for time-to-exhaustion performance.

The objective of this study was to compare the time to exhaustion (Tlim) at maximal aerobic speed (v.VO2max) in middle- and long-distance runners. Five middle-distance (MDR) and 5 long-distance (LDR) male runners, ages 28 +/- 7 years, were tested running on a treadmill, with the Université de Montréal Track Test (UMTT), on maximal velocity and on time-to-exhaustion track tests. During the laboratory test, cardiorespiratory variables (e.g., HR, .VO2max, .VCO2, .VE) were assessed. Second, running velocity at .VO2max (v.VO2max) during the UMTT was determined and HR values were recorded; also, maximal velocity on a 30-m sprint (V30) and maximal heart rate (HR max) and time to exhaustion were determined on the track. No significant difference was observed between groups during the multistage treadmill test. Significant differences were found between groups for V30 and Tlim, with MDR showing a 23% longer running time than LDR. The results of the present study demonstrated that the training profile of middle-distance and long-distance runners plays a significant role in Tlim performance when v.VO2max is obtained during a test with short-duration stages.     

Metabolism during exercise in young men breathing 4% CO2 (author's transl)]

Fourteen young men (on the average 25 years), well trained (maximal oxygen consumption, VO2 max., between 2.7 to 3.5 1) have been studied at two different levels of exercise: 90 and 140 watts (about 40 and 70% of VO2 max.) in chamber, where the atmosphere was regulated. The subjects performed the exercise after a sojourn of six hours in the chamber, at the same level, either in air or in hypercapnic conditions (FICO2: 0.04; FIO2: 0.21); the order of the exercise tests was determined at random. The rise of total ventilation (VE) during exercise in CO2 atmosphere was particularly related to the increased tidal volume (VT). In spite of the larger increase of VE in hypercapnia, CO2 output (VCO2) and respiratory quotient (R) were lower while PaCO2 was elevated (48 at rest and 54 mmHg during exercise). Oxygen consumption during exercise was the same in both conditions. Values of arterial lactic acid concentration were not different at 90 watts level. On the contrary, at the level of 140 watts, the lactic acid concentration was significantly lower in CO2 atmosphere. The well known changes during exercise of other electrolytes (rise of Na+, K+ and total Ca) was similar in air and in CO2. Only the inorganic phosphorus was higher in CO2 atmosphere at 140 watts.     

Reproducibility of the cycling time to exhaustion at .VO2peak in highly trained cyclists.

The purpose of the present study was to examine, in highly trained cyclists, the reproducibility of cycling time to exhaustion (T(max)) at the power output equal to that attained at peak oxygen uptake (.VO2peak) during a progressive exercise test. Forty-three highly trained male cyclists (M +/- SD; age = 25 +/- 6 yrs; weight = 75 +/- 7 kg; .VO2peak = 64.8 +/- 5.2 ml.kg-1.min-1) performed two T(max) tests one week apart. While the two measures of T(max) were strongly related (r = 0.884; p < 0.001), T(max) from the second test (245 +/- 57 s) was significantly higher than that of the first (237 +/- 57 s; p = 0.047; two-tailed). Within-subject variability in the present study was calculated to be 6 +/- 6%, which was lower than that previously reported for T(max) in sub-elite runners (25%). The mean T(max) was significantly (p < 0.05) related to both the second ventilatory turnpoint (VT(2); r = 0.38) and to .VO2peak (r = 0.34). Despite a relatively low within-subject coefficient of variation, these data demonstrate that the second score in a series of two T(max) tests may be significantly greater than the first. Moreover, the present data show that T(max) in highly trained cyclists is moderately related to VT(2) and .VO2peak.     

Validation of an equation for predicting energy cost of arm ergometry in women

Few studies have examined the validity of metabolic equations for the prediction of energy cost (VO(2)) of arm ergometry in women. Therefore, the purpose of this study was (a) to compare directly measured and predicted VO(2) values using the American College of Sports Medicine (ACSM) equation and (b) to develop and validate a prediction equation for women. A sample of 60 female subjects with mean (+/-SD) age, weight and height 26.5 +/- 14.4 years, 61.5 +/- 7.6 kg, 163.3 +/- 6.0 cm, respectively, was randomly assigned to an equation group (N = 40) and a cross validation group (N = 20). All subjects performed an incremental arm ergometry test (10 W increases every 2 min), until termination criteria were met. Repeated measures ANOVA indicated significant differences between the measured VO(2) and ACSM predicted VO(2) during all the incremental test work rate. Multiple linear regression analysis was used to develop the following upper body exercise VO(2) prediction equation: VO(2)(ml . kg(-1) . min(-1) = 23.461 - (0.272 x Body Weight) + (0.403 x watts) [R(2) = 0.82, SEE = 2.79] Cross validation indicated lower variability using the current prediction equation. An additional independent sample of 13 subjects performed a 30-min steady-state test at 40% of their pre-determined maximal work rate. VO(2) measured during the 30 min steady-state test (was significantly different P < 0.05) from the ACSM prediction at all time intervals. There were no significant differences using the above equation following the 5 min time interval. Therefore, a new equation is proposed as a means of providing a gender-specific energy cost prediction equation.