Enhanced endothelial vasoreactivity in endurance-trained older men.

Using external vascular ultrasound, we measured brachial artery diameter (Diam) at rest, after release of 4 min of limb ischemia, i. e., endothelium-dependent dilation (EDD), and after sublingual nitroglycerin, i.e., non-endothelium-dependent dilation (NonEDD), in 35 healthy men aged 61-83 yr: 12 endurance athletes (A) and 23 controls (C). As anticipated, treadmill exercise maximal oxygen consumption (VO(2 max)) was significantly higher in A than in C (40. 2 +/- 6.6 vs. 27.9 +/- 3.8 ml. kg(-1). min(-1); respectively, P < 0. 0001). With regard to arterial physiology, A had greater EDD (8.9 +/- 4.2 vs. 5.7 +/- 3.5%; P = 0.02) and a tendency for higher NonEDD (13.9 +/- 6.7 vs. 9.7 +/- 4.2%; P = 0.07) compared with C. By multiple linear regression analysis in the combined sample of older men, only baseline Diam (beta = -2.0, where beta is the regression coefficient; P = 0.005) and VO(2 max) (beta = 0.23; P = 0.003) were independent predictors of EDD; similarly, only Diam (beta = -4.0; P = 0.003) and VO(2 max) (beta = 0.27; P = 0.01) predicted NonEDD. Thus endurance-trained older men demonstrate both augmented EDD and NonEDD, consistent with a generalized enhanced vasodilator responsiveness, compared with their sedentary age peers.     

Decline in VO2max with aging in master athletes and sedentary men

Fifteen well-trained master endurance athletes [62.0 +/- 2.3 (SE) yr] and 14 sedentary control subjects (61.4 +/- 1.4 yr) were reevaluated after an average follow-up period of approximately 8 yr to obtain information regarding the effects of physical activity on the age-related decline in maximal O2 uptake capacity (VO2max). The master athletes had been training for 10.2 +/- 2.9 yr before initial testing and continued to train during the follow-up period. The sedentary subjects' VO2max declined by an average of 3.3 ml.kg-1.min-1 (33.9 +/- 1.7 vs. 30.6 +/- 1.6, P less than 0.001) over the course of the study, a decline of 12% per decade. In these subjects maximal heart rate declined 8 beats/min (171 vs. 163) and maximal O2 pulse decreased from 0.20 to 0.18 ml.kg-1.beat (P less than 0.05). The master athletes' VO2 max decreased by an average of 2.2 ml.kg-1.min-1 (54.0 +/- 1.7 vs. 51.8 +/- 1.8, P less than 0.05), a 5.5% decline per decade. The master athletes' maximal heart rate was unchanged (171 +/- 3 beats/min) and their maximal O2 pulse decreased from 0.32 to 0.30 ml.kg-1.beat (P less than 0.05). These findings provide evidence that the age-related decrease in VO2max of master athletes who continue to engage in regular vigorous endurance exercise training is approximately one-half the rate of decline seen in age-matched sedentary subjects. Furthermore our results suggest that endurance exercise training may reduce the rate of decline in maximal heart rate that typically occurs as an individual ages.     

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.     

Comparison of body water turnover in endurance runners and age-matched sedentary men

This study compared the body water turnover in endurance athletes and age-matched sedentary men. Eight competitive endurance athletes (20.8+/-1.9 yr) and age-matched eight sedentary men (21.6+/-2.5 yr) participated in this study. Total body water and body water turnover were measured using the deuterium (D(2)O) dilution technique. Urine samples were obtained every day for 10 days after oral administration of D(2)O. The day-by-day concentrations were used to calculate the biological half-life of D(2)O and body water turnover. Maximal oxygen uptake (VO(2max)) and oxygen uptake corresponding to ventilatory threshold (VO(2VT)) as an index of aerobic capacity were determined during a graded exercise test. Both VO(2max) and VO(2VT) were higher in the exercise group than in the sedentary group (P<0.05). The biological half-life of D(2)O was significantly shorter in the exercise group than in the sedentary group (5.89+/-0.81 days vs. 7.52+/-0.77 days, P<0.05), and the percentage of the body water turnover was significantly higher in the exercise group than in the sedentary group (11.99+/-1.96% vs. 9.39+/-1.21%, P<0.05). The body water turnover was correlated with VO(2max) and VO(2VT), respectively (P<0.05). Based on these findings, this study speculates that a level of physical activity may induce a body water turnover higher in the healthy state, since the better trained subjects have a higher body water turnover.     

Physiological factors associated with the lower maximal oxygen consumption of master runners

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.     

Lactate threshold and distance-running performance in young and older endurance athletes

Many well-trained elite older runners have performances comparable to those of much younger nonelite runners. We sought to determine whether the physiological determinants of endurance performance in two groups of such athletes were the same. Eight master athletes (age 56 +/- 5 yr) were matched on the basis of 10-km performance and training to younger runners (age 25 +/- 3 yr). The master athletes had a 9% lower maximum O2 uptake (VO2max) (P less than 0.05) than the matched young runners, despite the similarity in their performance. Running economy was not different between these groups. However, the master athletes attained a 2.5-mM blood lactate level during steady-state exercise at a higher percentage of their VO2max (P less than 0.05), although both groups attained this lactate level at the same running speed and VO2. Thus, despite having significantly lower VO2max values, the older athletes were able to perform as well as the younger runners because they were able to work closer to their VO2max for the duration of the race.     

Early onset of pulmonary gas exchange disturbance during progressive exercise in healthy active men.

Some recent studies of competitive athletes have shown exercise-induced hypoxemia to begin in submaximal exercise. We examined the role of ventilatory factors in the submaximal exercise gas exchange disturbance (GED) of healthy men involved in regular work-related exercise but not in competitive activities. From the 38 national mountain rescue workers evaluated (36 +/- 1 yr), 14 were classified as GED and were compared with 14 subjects matched for age, height, weight, and maximal oxygen uptake (VO2 max; 3.61 +/- 0.12 l/min) and showing a normal response (N). Mean arterial PO2 was already lower than N (P = 0.05) at 40% VO2 max and continued to fall until VO2 max (GED: 80.2 +/- 1.6 vs. N: 91.7 +/- 1.3 Torr). A parallel upward shift in the alveolar-arterial oxygen difference vs. %VO2 max relationship was observed in GED compared with N from the onset throughout the incremental protocol. At submaximal intensities, ideal alveolar PO2, tidal volume, respiratory frequency, and dead space-to-tidal volume ratio were identical between groups. As per the higher arterial PCO2 of GED at VO2 max, subjects with an exaggerated submaximal alveolar-arterial oxygen difference also showed a relative maximal hypoventilation. Results thus suggest the existence of a common denominator that contributes to the GED of submaximal exercise and affects the maximal ventilatory response.     

Impact of exercise training on insulin sensitivity, physical fitness, and muscle oxidative capacity in first-degree relatives of type 2 diabetic patients

First-degree relatives of type 2 diabetic patients (offspring) are often characterized by insulin resistance and reduced physical fitness (VO2 max). We determined the response of healthy first-degree relatives to a standardized 10-wk exercise program compared with an age-, sex-, and body mass index-matched control group. Improvements in VO2 max (14.1 +/- 11.3 and 16.1 +/- 14.2%; both P < 0.001) and insulin sensitivity (0.6 +/- 1.4 and 1.0 +/- 2.1 mg x kg(-1) x min(-1); both P < 0.05) were comparable in offspring and control subjects. However, VO2 max and insulin sensitivity in offspring were not related at baseline as in the controls (r = 0.009, P = 0.96 vs. r = 0.67, P = 0.002). Likewise, in offspring, exercise-induced changes in VO2 max did not correlate with changes in insulin sensitivity as opposed to controls (r = 0.06, P = 0.76 vs. r = 0.57, P = 0.01). Skeletal muscle oxidative capacity tended to be lower in offspring at baseline but improved equally in both offspring and controls in response to exercise training (delta citrate synthase enzyme activity 26 vs. 20%, and delta cyclooxygenase enzyme activity 25 vs. 23%. Skeletal muscle fiber morphology and capillary density were comparable between groups at baseline and did not change significantly with exercise training. In conclusion, this study shows that first-degree relatives of type 2 diabetic patients respond normally to endurance exercise in terms of changes in VO2 max and insulin sensitivity. However, the lack of a correlation between the VO2 max and insulin sensitivity in the first-degree relatives of type 2 diabetic patients indicates that skeletal muscle adaptations are dissociated from the improvement in VO2 max. This could indicate that, in first-degree relatives, improvement of insulin sensitivity is dissociated from muscle mitochondrial functions.     

Sex differences in endurance capacity and metabolic response to prolonged, heavy exercise

In order to test for possible sex differences in endurance capacity, groups of young, physically active women (n = 6) and men (n = 7) performed bicycle ergometer exercise at 80% and 90% of their maximal oxygen uptakes (VO2 max). The groups were matched for age and physical activity habits. At 80% VO2 max the women performed significantly longer (P less than 0.05), 53.8 +/- 12.7 min vs 36.8 +/- 12.2 min, respectively (means +/- SD). Mid-exercise and terminal respiratory exchange ratio (R) values were significantly lower in women, suggesting a later occurrence of muscle glycogen depletion as a factor in their enhanced endurance. At 90% VO2 max the endurance times were similar for men and women, 21.2 +/- 10.3 min and 22.0 +/- 5.0 min, respectively. The blood lactate levels reached in these experiments were only marginally lower (mean differences 1.5 to 2 mmol X l-1) than those obtained at VO2 max, suggesting high lactate levels as a factor in exhaustion. The changes in body weight during the 80% experiments and the degree of hemoconcentration were not significantly different between men and women.     

Histochemical and enzymatic characteristics of skeletal muscle in master athletes

Many older athletes are capable of endurance performances equal to those of young runners who have higher maximal O2 uptakes (VO2max). To determine whether this is a result of differences in skeletal muscle characteristics, gastrocnemius muscle biopsy samples were obtained from eight master athletes [aged 63 +/- 6 (SD) yr] and eight young (aged 26 +/- 3 yr) runners. The young runners were matched with the master athletes for 10-km running performance and for their volume, pace, and type of training. Despite similar 10-km run times, VO2max was 11% lower (P less than 0.05) in the master athletes. Fiber type distribution did not differ between groups, with both groups having 60% type I and very few type IIb fibers. Succinate dehydrogenase and beta-hydroxyacyl-CoA dehydrogenase activities, however, were 31 and 24% higher in the master athletes compared with the matched young runners, whereas lactate dehydrogenase activity was 46% lower (all P less than 0.05). The capillary-to-fiber ratio was also greater in the master athletes; however, capillary density was similar in the two groups, because of the master athletes' 34% larger (P less than 0.05) type I fibers. These differences in skeletal muscle characteristics may explain the master athletes' ability to perform as well as some young runners despite having a lower VO2max.     

Cardiovascular responses to lower body negative pressure in trained and untrained older men.

To determine whether aerobic conditioning alters the orthostatic responses of older subjects, cardiovascular performance was monitored during graded lower body negative pressure in nine highly trained male senior athletes (A) aged 59-73 yr [maximum O2 uptake (VO2 max) = 52.4 +/- 1.7 ml.kg-1 x min-1] and nine age-matched control subjects (C) (VO2 max = 31.0 +/- 2.9 ml.kg-1 x min-1). Cardiac volumes were determined from gated blood pool scintigrams by use of 99mTc-labeled erythrocytes. During lower body negative pressure (0 to -50 mmHg), left ventricular end-diastolic and end-systolic volume indexes and stroke volume index decreased in both groups while heart rate increased. The decreases in cardiac volumes and mean arterial pressure and the increase in heart rate between 0 and -50 mmHg were significantly less in A than in C. For example, end-diastolic volume index decreased by 32 +/- 4 ml in C vs. 14 +/- 2 ml in A (P < 0.01), mean arterial pressure declined 7 +/- 5 mmHg in C and increased by 5 +/- 3 mmHg in A (P < 0.05), and heart rate increased 13 +/- 3 beats/min in C and 7 +/- 1 beats/min in A (P < 0.05). These data suggest that increased VO2 max among older men is associated with improved orthostatic responses.     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity.

This study investigates whether a 6-wk intermittent hypoxia training (IHT), designed to avoid reductions in training loads and intensities, improves the endurance performance capacity of competitive distance runners. Eighteen athletes were randomly assigned to train in normoxia [Nor group; n = 9; maximal oxygen uptake (VO2 max) = 61.5 +/- 1.1 ml x kg(-1) x min(-1)] or intermittently in hypoxia (Hyp group; n = 9; VO2 max = 64.2 +/- 1.2 ml x kg(-1) x min(-1)). Into their usual normoxic training schedule, athletes included two weekly high-intensity (second ventilatory threshold) and moderate-duration (24-40 min) training sessions, performed either in normoxia [inspired O2 fraction (FiO2) = 20.9%] or in normobaric hypoxia (FiO2) = 14.5%). Before and after training, all athletes realized 1) a normoxic and hypoxic incremental test to determine VO2 max and ventilatory thresholds (first and second ventilatory threshold), and 2) an all-out test at the pretraining minimal velocity eliciting VO2 max to determine their time to exhaustion (T(lim)) and the parameters of O2 uptake (VO2) kinetics. Only the Hyp group significantly improved VO2 max (+5% at both FiO2, P < 0.05), without changes in blood O2-carrying capacity. Moreover, T(lim) lengthened in the Hyp group only (+35%, P < 0.001), without significant modifications of VO2 kinetics. Despite similar training load, the Nor group displayed no such improvements, with unchanged VO2 max (+1%, nonsignificant), T(lim) (+10%, nonsignificant), and VO2 kinetics. In addition, T(lim) improvements in the Hyp group were not correlated with concomitant modifications of other parameters, including VO2 max or VO2 kinetics. The present IHT model, involving specific high-intensity and moderate-duration hypoxic sessions, may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations, resulting in increased endurance performance capacity.     

Oxygen uptake kinetics during treadmill running in boys and men.

The purpose of this study was to compare the kinetics of the oxygen uptake (VO(2)) response of boys to men during treadmill running using a three-phase exponential modeling procedure. Eight boys (11-12 yr) and eight men (21-36 yr) completed an incremental treadmill test to determine lactate threshold (LT) and maximum VO(2). Subsequently, the subjects exercised for 6 min at two different running speeds corresponding to 80% of VO(2) at LT (moderate exercise) and 50% of the difference between VO(2) at LT and maximum VO(2) (heavy exercise). For moderate exercise, the time constant for the primary response was not significantly different between boys [10.2 +/- 1.0 (SE) s] and men (14.7 +/- 2.8 s). The gain of the primary response was significantly greater in boys than men (239.1 +/- 7.5 vs. 167.7 +/- 5.4 ml. kg(-1). km(-1); P < 0.05). For heavy exercise, the VO(2) on-kinetics were significantly faster in boys than men (primary response time constant = 14.9 +/- 1.1 vs. 19.0 +/- 1.6 s; P < 0.05), and the primary gain was significantly greater in boys than men (209.8 +/- 4.3 vs. 167.2 +/- 4.6 ml. kg(-1). km(-1); P < 0.05). The amplitude of the VO(2) slow component was significantly smaller in boys than men (19 +/- 19 vs. 289 +/- 40 ml/min; P < 0.05). The VO(2) responses at the onset of moderate and heavy treadmill exercise are different between boys and men, with a tendency for boys to have faster on-kinetics and a greater initial increase in VO(2) for a given increase in running speed.     

Fat energy use and plasma lipid changes associated with exercise intensity and temperature

The effect of 60 min of exercise at two intensities (50 and 60% VO2max) and temperatures (0 and 22 degrees C) on changes (delta) in plasma lipids [triglycerides (TG), glycerol (GLY), total cholesterol (TC), and HDL-cholesterol (HDL-C)] was examined. Subjects were 10 men aged 27 +/- 7 years (VO2max = 3.81 +/- 0.45 1 min, % fat = 12.2% +/- 7.1%). VO2 and respiratory exchange ratio results indicated that total energy and fat energy use were similar at the two temperatures. Changes in plasma volume (%delta PV) were different (P less than 0.05) at the two temperatures (22 degrees C: -2.3% vs 0 degrees C: 1.1%). Combining the data at each temperature revealed that the increases in concentrations were greater (P less than 0.05) at 22 degrees C (delta TG = 0.22, delta GLY = 0.20, delta TC = 0.14, delta HDL-C = 0.05 mmol l-1) vs 0 degrees C (delta TG = 0.10, delta GLY = 0.12, delta TC = 0.05, delta HDL-C = 0.02 mmol l-1). Combining the data for each intensity revealed that the increases in concentration were greater (P less than 0.05) at 60% VO2max for delta TG and delta HDL-C. The 60% VO2max/22 degrees C bout produced greater changes (P less than 0.05) than all other bouts for delta TC and delta HDL-C (0.21 and 0.08 mmol l-1, respectively). Only delta TG and delta GLY were greater at 22 degrees C when adjusted for %delta PV. These metabolic and plasma lipid results indicate that cold exposure does not act synergistically with exercise to further stimulate fat metabolism.     

Endurance training in older men and women II. Blood lactate response to submaximal exercise

Seven men and four women (age 63 +/- 2 yr, mean +/- SD, range 61-67 yr) participated in a 12-mo endurance training program to determine the effects of low-intensity (LI) and high-intensity (HI) training on the blood lactate response to submaximal exercise in older individuals. Maximal oxygen uptake (VO2max), blood lactate, O2 uptake (VO2), heart rate (HR), ventilation (VE), and respiratory exchange ratio (R) during three submaximal exercise bouts (65-90% VO2max) were determined before training, after 6 mo of LI training, and after an additional 6 mo of HI training. VO2max (ml X kg-1 X min-1) was increased 12% after LI training (P less than 0.05), while HI training induced a further increase of 18% (P less than 0.01). Lactate, HR, VE, and R were significantly lower (P less than 0.05) at the same absolute work rates after LI training, while HI training induced further but smaller reductions in these parameters (P greater than 0.05). In general, at the same relative work rates (ie., % of VO2max) after training, lactate was lower or unchanged, HR and R were unchanged, and VO2 and VE were higher. These findings indicate that LI training in older individuals results in adaptations in the response to submaximal exercise that are similar to those observed in younger populations and that additional higher intensity training results in further but less-marked changes.     

Angiotensin II type 1 receptor blockade corrects cutaneous nitric oxide deficit in postural tachycardia syndrome

Low-flow postural tachycardia syndrome (POTS) is associated with increased plasma angiotensin II (ANG II) and reduced neuronal nitric oxide (NO), which decreases NO-dependent vasodilation. We tested whether the ANG II type 1 receptor (AT(1)R) antagonist losartan would improve NO-dependent vasodilation in POTS patients. Furthermore, if the action of ANG II is dependent on NO, then the NO synthase inhibitor nitro-L-arginine (NLA) would reverse this improvement. We used local heating of the skin of the left calf to 42 degrees C and laser-Doppler flowmetry to assess NO-dependent conductance [percent maximum cutaneous vascular conductance (%CVC(max))] in 12 low-flow POTS patients aged 22.5 +/- 0.8 yr and in 15 control subjects aged 22.0 +/- 1.3 yr. After measuring the baseline local heating response at three separate sites, we perfused individual intradermal microdialysis catheters at those sites with 2 microg/l losartan, 10 mM NLA, or losartan + NLA. The predrug heat response was reduced in POTS, particularly the plateau phase reflecting NO-dependent vasodilation (50 +/- 5 vs. 91 +/- 7 %CVC(max); P < 0.001 vs. control). Losartan increased baseline flow in both POTS and control subjects (from 6 +/- 1 to 21 +/- 3 vs. from 10 +/- 1 to 21 +/- 2 %CVC(max); P < 0.05 compared with predrug). The baseline increase was blunted by NLA. Losartan increased the POTS heat response to equal the control subject response (79 +/- 7 vs. 88 +/- 6 %CVC(max); P = 0.48). NLA decreased both POTS and control subject heat responses to similar conductances (38 +/- 4 vs. 38 +/- 3 %CVC(max); P < 0.05 compared with predrug). The addition of NLA to losartan reduced POTS and control subject conductances compared with losartan alone (48 +/- 3 vs. 53 +/- 2 %CVC(max)). The data suggest that the reduction in cutaneous NO-dependent vasodilation in low-flow POTS is corrected by AT(1)R blockade.     

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)     

Oxygen uptake kinetics and time to exhaustion in cycling and running: a comparison between trained and untrained subjects

The objective of the present study was to compare pulmonary gas exchange kinetics (VO2 kinetics) and time to exhaustion (Tlim) between trained and untrained individuals during severe exercise performed on a cycle ergometer and treadmill. Eleven untrained males in running (UR) and cycling (UC), nine endurance cyclists (EC), and seven endurance runners (ER) were submitted to the following tests on separate days: (i) incremental test for determination of maximal oxygen uptake (VO2max) and the intensity associated with the achievement of VO2max (IVO2max) on a mechanical braked cycle ergometer (EC and UC) and on a treadmill (ER and UR); (ii) all-out exercise bout performed at IVO2max to determine the time to exhaustion at IVO2max (Tlim) and the time constant of oxygen uptake kinetics (tau). The tau was significantly faster in trained group, both in cycling (EC = 28.2 +/- 4.7s; UC = 63.8 +/- 25.0s) and in running (ER = 28.5 +/- 8.5s; UR = 59.3 +/- 12.0s). Tlim of untrained was significantly lower in cycling (EC = 384.4 +/- 66.6s vs. UC; 311.1 +/- 105.7 s) and higher in running (ER = 309.2 +/- 176.6 s vs. UR = 439.8 +/- 104.2 s). We conclude that the VO2 kinetic response at the onset of severe exercise, carried out at the same relative intensity is sensitive to endurance training, irrespective of the exercise type. The endurance training seems to differently influence Tlim during exercise at IVO2max in running and cycling.     

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.