Evidence for an inadequate hyperventilation inducing arterial hypoxemia at submaximal exercise in all highly trained endurance athletes

PURPOSE: The majority of highly trained endurance athletes with a maximal oxygen uptake greater than 60 mL x min(-1) x kg(-1) develop exercise-induced hypoxemia (EIH). Yet some of them apparently do not. The pathophysiology of EIH seems to be multifactorial, and one explanatory hypothesis is a relative hypoventilation. Nevertheless, conflicting results have been reported concerning its contribution to EIH. The aim of this study was to compare the cardiorespiratory responses to maximal exercise of highly trained endurance athletes demonstrating the same aerobic capacity without EIH (N athletes) and with EIH (H athletes). METHODS: Ten N athletes and twelve H athletes performed an incremental exercise test. Measurements of arterial blood gases and cardiorespiratory parameters were performed at rest and during exercise. RESULTS: All athletes presented a significant decrease in PaO2 (P < 0.05) from rest up to 80% VO2max associated with an increase in PaCO2, both findings consistent with a relative hypoventilation. Then the H athletes, who had a greater training volume per week and a higher second ventilatory threshold than the N athletes (respectively, 17 +/- 1.1 vs 13.1 +/- 0.7 h x wk(-1); 91.8 +/- 1.7 vs 86.1 +/- 1.8% VO2max), presented a continuous PaO2 decrease up to VO2max. This was associated with a widening (Ai-a)DO2. CONCLUSION: This study showed that a relative hypoventilation, probably induced by a high level of endurance training, induced hypoxemia in all athletes. However, a nonventilatory mechanism, perhaps related to the volume of training, seemed to affect gas exchanges beyond the second ventilatory threshold in the H athletes, thereby enhancing EIH.     

Measuring and predicting maximal aerobic power in international-level intermittent sport athletes

AIM: The purpose of this study was to measure actual VO2max during the multi-stage fitness test (MSFT) and to compare this with predicted values obtained using previously established, commonly used methods. We also wanted to determine a new and more accurate regression equation for the prediction of VO2max in intermittent sport athletes. METHODS: Twenty-six, elite, male, intermittent sport athletes performed the MSFT with oxygen uptake (VO2) and heart rate (HR) measured throughout. Paired t-tests were used to compare measured VO2max with predicted VO2max. Linear regression was used to determine the equation for the prediction of VO2max from the total number of shuttles completed. RESULTS: There were no differences between the two methods of predicting VO2max, however, both predicted values (53.6+/-3.9 and 51.3+/-4 mL x kg(-1) x min(-1)) were significantly lower (9.3% and 13.2%, respectively) than measured VO2max (59.1+/-6.6 mL x kg(-1) x min(-1), P < 0.001). Correlations between measured and predicted VO2max were similar for both prediction methods (r = 0.61, P = 0.013 and r = 0.68 and P = 0.004). We present a new prediction equation [Y (VO2max, mL x kg(-1) x min(-1)) = 0.38 x total number of shuttles completed +25.98] (where R = 0.69; R2 = 0.48; SEE = 4.9 mL x kg(-1) x min(-1); SEE% = 8.3) which provides a more valid method of predicting actual max in intermittent sport athletes. CONCLUSIONS: A new regression equation to predict VO2max in intermittent sport athletes has been established. Whilst some error in predicting VO2max still exists, the new equation will provide coaches and sport-scientists with a more suitable equation with which to predict VO2max in intermittent sport athletes.     

Short-term overtraining: effects on performance, circulatory responses, and heart rate variability

PURPOSE AND METHODS: Nine elite canoeists were investigated concerning changes in performance, heart rate variability (HRV), and blood-chemical parameters over a 6-d training camp. The training regimen consisted of cross-country skiing and strength training, in total 13.0+/-1.6 h, corresponding to a 50% increase in training load. RESULTS: Time to exhaustion (RunT) decreased from 19.1+/-1.0 to 18.0+/-1.2 min (P < 0.05). VO2max and max lactate (La(max)) both decreased significantly (P < 0.05) over the training period (4.99+/-0.97 to 4.74+/-0.98 L x min(-1) and from 10.08+/-1.25 to 8.98+/-1.03 mmol x L(-1) respectively). Heart rates (HR) decreased significantly at all workloads. Plasma volume increased by 7+/-7% (P < 0.05). Resting cortisol, decreased from 677+/-244 to 492+/-222 nmol x L(-1) (P < 0.05), whereas resting levels of adrenaline and noradrenaline remained unchanged. The change between tests in RunT correlated significantly with the change in HRmax (r = 0.79; P = 0.01). There were no group changes in high or low frequency HRV, neither at rest nor following a tilt. CONCLUSIONS: The reduced maximal performance indicates a state of fatigue/overreaching and peripheral factors are suggested to limit performance even though HRmax and La(max) both were reduced. The reduced submaximal heart rates are probably a result of increased plasma volume. HRV in this group didn't seem to be affected by short-term overtraining.     

Short-arm (1.9 m) +2.2 Gz acceleration: isotonic exercise load-O2 uptake relationship

BACKGROUND: The deconditioning syndrome from prolonged bed rest (BR) or spaceflight includes decreases in maximal oxygen uptake (VO2max), muscular strength and endurance, and orthostatic tolerance. In addition to exercise training as a countermeasure, +Gz (head-to-foot) acceleration training on 1.8-2.0 m centrifuges can ameliorate the orthostatic and acceleration intolerances induced by BR and immersion deconditioning. PURPOSE: Study A was designed to determine the magnitude and linearity of the heart rate (HR) response to human-powered centrifuge (HPC) acceleration with supine exercise vs. passive (no exercise) acceleration. Study B was designed to test the hypothesis that moderate +Gz acceleration during exercise will not affect the respective normal linear relationships between exercise load and VO2max, HR, and pulmonary ventilation (VEBTPS). Study C: To determine if these physiological responses from the HPC runs (exercise + on-platform acceleration) will be similar to those from the exercise + off-platform acceleration responses. METHODS: In Study A, four men and two women (31-62 yr) were tested supine during exercise + acceleration and only passive acceleration at 100% [maximal acceleration (rpm) = Amax] and at 25%, 50%, and 75% of Amax. In Studies B and C, seven men (33+/-SD 7 yr) exercised supine on the HPC that has two opposing on-platform exercise stations. A VO2max test and submaximal exercise runs occurred under three conditions: (EX) exercise (on-platform cycle at 42%, 61%, 89% and 100% VO2max) with no acceleration; (HPC) exercise + acceleration via the chain drive at 25%,50%, and 100% Gzmax (35%, 72% and 100% VO2max); and (EXA) exercise (on-platform cycle at 42%, 61%, 89%, and 100% VO2max) with acceleration performed via the off-platform cycle operator at +2.2+/-0.2 Gz [50% of max (rpm) G]. RESULTS: Study A: Mean (+/-SE) Amax was 43.7+/-1.3 rpm (mean = +3.9+/-0.2, range = 3.3 to 4.9 Gz). Amax run time for exercise +acceleration was 50-70 s, and 40-70 s for passive acceleration. Regression of X HR on Gz levels indicated explained variances (r2) of 0.88 (exercise) and 0.96 (passive). The mean exercise HR of 107+/-4 (25%), to 189+/-13 (100%) bpm were 43-50 bpm higher (p < 0.05) than comparable passive HR of 64+/-2 to 142+/-22 bpm, respectively. Study B: There were no significant differences in VO2, HR or VEBTPS at the submaximal or maximal levels between the EX and EXA runs. Mean (+/-SE) VO2max for EX was 2.86+/-0.12 L x min(-1)(35+/-2 ml x min(-1) x kg(-1)) and for EXA was 3.09+/-0.14 L x min(-1) (37+/-2 ml-min(-1) x kg(-1)). Study C: There were no significant differences in the essentially linear relationships between the HPC and EXA data for VO2 (p = 0.45), HR (p < 0.08), VEBTPS (p = 0.28), or the RE (p = 0.15) when the exercise load was % VO2max. CONCLUSION: Addition of + 2.2 Gz acceleration does not significantly influence levels of oxygen uptake, heart rate, or pulmonary ventilation during submaximal or maximal cycle ergometer leg exercise on a short-arm centrifuge.     

Physiological responses during submaximal interval swimming training: Effects of interval duration

The aim of the present study was to determine the time sustained near VO2max in two interval training (IT) swimming sessions comprising 4x400 m (IT(4x400)) or 16x100 (IT(16xl00)). Elite swimmers (Mean+/-SD age 18+/-2 yrs; body mass 66.9+/-6.5 kg: swim VO2max 55.7+/-5.8 ml.kg(-1).min(-1)) completed three experimental sessions at a 50-m indoor pool over a one week period. The first test comprised a 5 x 200-m incremental test to exhaustion for determination of the pulmonary ventilation threshold (VT, m.s(-1)), VO2max, the velocity associated with VO2max (VO2max, m(s(-1)) and maximum heart rate (HR(max), b.min(-1)). The remaining two tests involved the IT(4x400) and IT(16xl00) performed in a randomised order. The two IT sessions where completed at a velocity representing 25% of the difference between the VT and the VO2max (delta25%) and in the same work to rest ratio. During the IT sessions VO2 as well as HR were measured. The duration (s) >90% VO2max, also the duration (s) >90% HR(max), were not significantly different in the IT(16x100) and IT(4x400). However, limits of agreement (LIM(AG)) analysis demonstrated considerable individual variation in the time >90% VO2max (mean difference +/-2SD = 222+/-819 s) and the time >90% HRmax (mean difference +/-2SD = 61+/-758 s) between the two IT sessions. This factor deserves further research to establish the characteristics of those athletes which influence the physiological responses in IT of short or longer duration repetitions.     

Enhanced cardiovascular hemodynamics in endurance-trained postmenopausal women athletes

PURPOSE: We sought to determine whether older women athletes who had habitually performed vigorous endurance exercise training had higher stroke volumes and cardiac outputs than sedentary postmenopausal women during maximal exercise. METHODS: Seventeen endurance-trained, postmenopausal women athletes (age 65 +/- 4 yr; VO2max 2.11 +/- 0.31 L x min(-1), 38.3 mL x kg(-1) x min(-1)) and 14 sedentary, postmenopausal women (age 63 +/- 5 yr; VO2max 1.41 +/- 0.22 L x min(-1), 23.7 +/- 3.5 mL x kg(-1) x min(-1)) performed maximal treadmill exercise while cardiac output (via acetylene rebreathing) and other cardiovascular hemodynamics were measured. Approximately half of the subjects in each group were on hormone replacement therapy (HRT). RESULTS: The greater VO2max of the athletes was the result of a greater cardiac output (12.8 +/- 1.6 vs. 9.3 +/- 1.4 L x min(-1)) resulting from their significantly larger stroke volume (80 +/- 10 vs 57 +/- 10 mL) at maximal exercise. There were no significant differences in maximal cardiac output or maximal stroke volume related to HRT status in the sedentary women or athletes. CONCLUSIONS: These data indicate that endurance-trained, competitive, postmenopausal women have higher stroke volumes and cardiac outputs during maximal exercise, than their sedentary peers. However, these data suggest that HRT may not affect maximal CV function in sedentary or endurance-trained postmenopausal women.     

Ventilatory threshold and maximal oxygen uptake during cycling and running in female triathletes

Maximal oxygen uptake (VO2max) and the ventilatory threshold (Tvent) were measured during cycle ergometry (CE) and treadmill running (TR) in a group of 10 highly trained female triathletes. Tvent was defined as the VO2 at which the ventilatory equivalent for oxygen increased without a marked rise in the ventilatory equivalent for carbon dioxide. Female triathletes achieved a significantly higher mean (+/- SE) relative VO2max for running (63.6 +/- 1.2 ml.kg-1.min-1) than for cycling (59.9 +/- 1.3 ml.kg-1.min-1). When oxygen uptake measured at the ventilatory threshold was expressed as a percent of VO2max, the mean value obtained for TR (74.0 +/- 2.0% of VO2max) was significantly greater than the value obtained for CE (62.7 +/- 2.1% of VO2max). This occurred even though the total training time and intensity were similar for the two modes of exercise. Female triathletes had average running and cycling VO2max values that compared favorably with maximal oxygen uptake values previously reported for elite female runners and cyclists, respectively. However, mean running and cycling Tvent values (VO2 Tvent as%VO2max) were lower than recently reported values for single-sport athletes. The physiological variability between the triathletes studied and single-sport athletes may be attributed in part to differences in training distance or intensity, and/or to variations in the number of years of intense training in a specific mode of exercise. It was concluded that these triathletes were well-trained in both running and cycling, but not to the same extent as female athletes who only train and compete in running or cycling.     

Erythropoiesis and performance after two weeks of living high and training low in well trained triathletes

The purpose of our study was to evaluate hematologic acclimatization during 2 weeks of intensive normoxic training with regeneration at moderate altitude (living high-training low, LHTL) and its effects on sea-level performance in well trained athletes compared to another group of equally trained athletes under control conditions (living low - training low, CONTROL). Twenty-one triathletes were ascribed either to LHTL (n = 11; age: 23.0 +/- 4.3 yrs; VO 2 max: 62.5 +/- 9.7 [ml x min -1 x kg -1]) living at 1956 m of altitude or to CONTROL (n = 10; age: 18.7 +/- 5.6 yrs; VO 2 max: 60.5 +/- 6.7 ml x min -1 x kg -1) living at 800 m. Both groups performed an equal training schedule at 800 m. VO 2 max, endurance performance, erythropoietin in serum, hemoglobin mass (Hb tot, CO-rebreathing method) and hematological quantities were measured. A tendency to improved performance in LHTL after the camp was not significant (p < 0.07). Erythropoietin concentration increased temporarily in LHTL (Delta 14.3 +/- 8.7 mU x ml -1; p < 0.012). Hb tot remained unchanged in LHTL whereas was slightly decreased from 12.5 +/- 1.3 to 11.9 +/- 1.3g x kg -1 in CONTROL (p < 0.01). As the reticulocyte number tended to higher values in LHTL than in CONTROL, it seems that a moderate stimulation of erythropoiesis during regeneration at altitude served as a compensation for an exercise-induced destruction of red cells.     

Effect of work duration on physiological and rating scale of perceived exertion responses during self-paced interval training

This study compared running velocity, physiological responses, and perceived exertion during self-paced interval training bouts differing only in work bout duration. Twelve well-trained runners (nine males, three females, 28+/-5 years, VO2 max 65+/-6 mL min(-1) kg(-1)) performed preliminary testing followed by four "high-intensity" interval sessions (Latin squares, 1 session week(-1) over 4 weeks) consisting of 24 x 1, 12 x 2, 6 x 4, or 4 x 6-min running bouts with a 1:1 work-to-rest interval (total session duration 48 min). The average running velocity decreased (93%, 88%, 86%, 84% vVO2 max, P < 0.01) with increasing work duration. Peak VO2 averaged about 92+/-4% of VO2 max for 2-, 4-, and 6-min intervals compared with only 82+/-5% for 1-min bouts (P < 0.001). Six of 12 athletes achieved their highest average VO2 and heart rate during 4-min intervals. The average RPEpeak (rating scale of perceived exertion) was approximately 17+/-1 for all four interval sessions. RPE increased by 2-4 U during an interval training session. The mean lactate concentration was similar across sessions (4.3+/-1.1-4.6+/-1.5 mmol L(-1)). Under self-paced conditions, well-trained runners perform "high-intensity" intervals at an RPE of approximately 17, independent of interval duration. The optimal interval duration for eliciting a high physiological load is 3-5 min under these training conditions. Increases in RPE during an interval bout are not associated with increasing blood lactate concentration.     

Cardiovascular responses to facial cooling are age and fitness dependent.

PURPOSE: Aging of the cardiovascular system may be altered by differences in physical fitness. We investigated the cardiovascular responses to brief periods of facial cooling (5 degrees C) in 20 healthy men differing in age and aerobic fitness (VO2max). METHODS: Facial cooling was administered at rest in the supine position during 60-s quiet breathing to 6 fit young (FY; VO2max = 75.8 +/- 18 mL x kg(-1) x min(-1); 29 +/- 7 yr), 6 sedentary young (SY; VO2max = 36.0 +/- 2.2 mL x kg(-1) x min(-1); 27 +/- 3 yr), 6 fit old (FO; VO2max = 56.1 +/- 4.0 mL x kg(-1) x min(-1); 54 +/- 5 yr), and 6 sedentary old (SO; VO2max = 29.6 +/- 5.0 mL x kg(-1) x min(-1); 62 +/- 2 yr) volunteers. The following were measured before and after facial cooling: heart rate (HR), mean arterial blood pressure (MAP), pressure-rate product (PRP), and M-mode echocardiographically determined left ventricular internal dimensions, peak circumferential shortening (peak V(CF)), and ejection fraction (EF). RESULTS: Facial cooling produced a statistically significant bradycardia in all groups except for the SO whereas MAP was increased in the young groups but unchanged in the older groups. Pressure-rate product was significantly reduced in the FY, unchanged in the SY and FO, and significantly increased in the SO group. None of the groups showed a change in left ventricular dimensions, whereas only the SO group showed an increase in peak V(CF) (P < 0.05). CONCLUSIONS: These data suggest that endurance training and fitness level do not significantly alter cardiovascular responses to facial cooling in young men or physically fit older men. However, in older subjects, a sedentary lifestyle appears to be associated with an absent facial cooling reflex bradycardia, an increased PRP, and contractility (peak V(CF)).     

Autonomic recovery after exercise in trained athletes: intensity and duration effects

PURPOSE: To investigate the effects of training intensity and duration, through a range representative of training in endurance athletes, on acute recovery of autonomic nervous system (ANS) balance after exercise. METHODS: Nine highly trained (HT) male runners (VO2max 72 +/- 5 mL.kg.min(-1), 14 +/- 3 training hours per week) and eight trained (T) male subjects (VO2max 60 +/- 5 mL.kg.min(-1), 7 +/- 1 training hours per week) completed preliminary testing to determine ventilatory thresholds (VT1, VT2) and VO2max. HT performed four intensity-controlled training sessions: 60 min and 120 min below VT1; 60 min with 30 min between VT1 and VT2 (threshold); and 60 min above VT2 (6 x 3 min at 96% VO2max, 2 min of recovery). T also completed the interval session to compare ANS recovery between HT and T. Supine heart rate variability (HRV) was quantified at regular intervals through 4 h of recovery. RESULTS: When HT ran 60 or 120 min below VT1, HRV returned to pretraining values within 5-10 min. However, training at threshold (2.7 +/- 0.4 mM) or above VT2 (7.1 +/- 0.7 mM) induced a significant, but essentially identical, delay of HRV recovery (return to baseline by approximately 30 min). In T, HRV recovery was significantly slower, with HRV returning to baseline by >or=90 min after the same interval session. CONCLUSIONS: In the highly trained endurance athlete, exercise for 相似文献   

Comparison of physiological strain and muscular performance of athletes during two intermittent running exercises at the velocity associated with VO2max

The purpose of this study was to examine physiological strain and muscular performance responses of well trained athletes during two intermittent running exercise protocols at the velocity associated with VO2max. Ten national level middle-distance runners (VO2max 69.4+/-5.1; mean+/-SD) performed in random order two 28 min treadmill running exercises: 14 bouts of 60 s runs with 60 s rest (IR60) and 7 bouts of 120 s runs with 120 s rest between each run (IR120). During IR120 peak oxygen uptake (12%), peak heart rate (3%) and peak blood lactate (79%) were significantly higher than during IR60 (P< 0.001) and almost the same as in the VO2max test. In IR120 the relative aerobic energy release calculated on the basis of the accumulated oxygen deficit during the running bouts was significantly higher than in IR60 (81.5+/-2.7 vs. 70.2+/-2.6%, P<0.001) likewise the sum oxygen consumption during the 14 min running (P< 0.001), while during the 14 min recovery it was as much lower (P < 0.001). There were no changes either during or between the IR60 and IR120 protocols with regard to the muscular performance parameters, stride length or height of maximal vertical jumps. In conclusion, during intermittent running at the velocity associated with VO2max doubling the duration of work and rest bouts from 60 s to 120s increased the physiological strain of well trained athletes to the same level as at exhaustion in the VO2max test but the muscular performance variables were not influenced.     

Degree of arterial desaturation in normoxia influences VO2max decline in mild hypoxia.

PURPOSE: Elite endurance athletes display varying degrees of pulmonary gas exchange limitations during maximal normoxic exercise and many demonstrate reduced arterial O2 saturations (SaO2) at VO2max--a condition referred to as exercise induced arterial hypoxemia (EIH). We asked whether mild hypoxia would cause significant declines in SaO2 and VO2max in EIH athletes while non-EIH athletes would be unaffected. METHODS: Nineteen highly trained males were divided into EIH (N = 8) or Non-EIH (N = 6) groups based on SaO2 at VO2max (EIH <90%, Non-EIH >92%). Athletes with intermediate SaO2 values (N = 5) were only included in correlational analyses. Two randomized incremental treadmill tests to exhaustion were completed--one in normoxia, one in mild hypoxia (FIO2 = 0.187; approximately 1,000 m). RESULTS: EIH subjects demonstrated a significant decline in VO2max from normoxia to mild hypoxia (71.1+/-5.3 vs. 68.1+/-5.0 mL x kg(-1) min(-1), P<0.01), whereas the non-EIH group did not show a significant deltaVO2max (67.2+/-7.6 vs. 66.2+/-8.4 mL x kg(-1) x min(-1)). For all 19 athletes, SaO2 during maximal exercise in normoxia correlated with the change in VO2max from normoxia to mild hypoxia (r = -0.54, P<0.05). However, the change in SaO2 and arterial O2 content from normoxia to mild hypoxia was equal for both EIH and Non-EIH (deltaSaO2 = 5.2% for both groups), bringing into question the mechanism by which changes in SaO2 affect VO2max in mild hypoxia. CONCLUSIONS: We conclude that athletes who display reduced measures of SaO2 during maximal exercise in normoxia are more susceptible to declines in VO2max in mild hypoxia compared with normoxemic athletes.     

Heart rate variability during night sleep and after awakening in overtrained athletes

PURPOSE: This study was conducted to test the hypothesis of autonomic imbalance in overtrained athletes during sleep and after awakening with analyses of heart rate variability (HRV) and nocturnal urine stress hormones. METHODS: We examined 12 athletes diagnosed to be severely overtrained (OA, 6 men and 6 women, mean age (+/-SD) 25 +/- 7 yr) and 12 control athletes (CA, 6 men and 6 women, mean age 24 +/- 5 yr). Overtraining diagnosis was further supported by higher perceived stress in OA than in CA (24.8 +/- 10.8 vs 15.3 +/- 5.5, P < 0.05). HRV was analyzed with time and frequency domain methods from RR intervals (RRI) recorded during sleep and after awakening. Nocturnal urine stress hormones were analyzed by liquid chromatography. RESULTS: No differences were found in HRV or stress hormones during night sleep. After awakening, the standard deviation of RRI (84 +/- 31 vs 116 +/- 41 ms, P < 0.05) and low-frequency power of RRI (2153 +/- 2232 vs 4286 +/- 2904 ms, P < 0.05) were lower in OA than in CA. From sleep to after awakening, the coefficient of variation of RRI decreased more in OA than in CA (from 11.8 +/- 3.3 to 7.7 +/- 2.5%, P < 0.001 vs from 11.9 +/- 1.8 to 10.0 +/- 2.5%, P < 0.01, respectively, interaction P < 0.05). CONCLUSION: The present findings suggest that in OA, cardiac autonomic modulation is at the level of control athletes during sleep, but the parasympathetic cardiac modulation is slightly diminished after awakening. Further investigations should concentrate on autonomic responses to different challenges, such as awakening in the present study.     

The changes in running performance and maximal oxygen uptake after long-term training in elite athletes

AIM: The relationship between VO2max (mL x kg(-1) x min(-1)) and running performance has been assessed in cross-sectional studies. Follow-up studies of the long-term effects of running training on the changes in performance and VO2max have not been undertaken. METHODS: Twenty-five male endurance-trained (MET) and 8 female endurance-trained (FET) athletes were tracked over 4 years. In each event the athletes were divided into Class A, including half the number of athletes with the best performances, and Class B. VO2max, examined at the end of the competitive season, and the best performance was chosen each year. RESULTS: After 3 years of training, in MET and FET athletes the performance improved by 1.77% and 0.69% (P<0.01 and P=0.579), respectively. In Class A runners, training resulted in non-significant increase in performance (-0.04%) (P=0.982) and in Class B runners, performance increased by 3.16% (P=0.001). In all groups VO(2max) remained essentially unchanged. Longitudinal changes in the VO2max were not related with the changes in running performance in any group. CONCLUSIONS: This study show than in older runners with more years of training, heavy training does not produce improvements in running performance neither changes in the VO2max. It is possible that these elite athletes have reached the plateau in their performance; although unlikely, some improvement in training techniques may happen and break the present limit. In younger runners with less years of training, heavy training produce improvements in running performance without changes in the VO2max. These athletes that had not attained his biological limits at the beginning of study improved the performance in competition and it is quite probable that this improvement be due to training. The changes in performance were not related to changes in VO2max. Consequently, another physiological or psychological variables must be studied by longitudinal form to explain the variability of performance in competition.     

Cardiovascular responses to head-up tilt after an endurance exercise program

The cardiovascular responses to 10 min of orthostasis were assessed before and after an aerobic exercise program. Five men and five women (18-25 years old) exercised for 7 weeks, four times per week, for 50 min per session at 70% of maximal heart rate (HR). Before and after the exercise program, maximal aerobic power (VO2max) was determined, and HR, systolic (SBP), diastolic (DBP), and pulse (PP) blood pressures were measured each minute during 5 min of supine rest, 10 min of foot-supported 70 degree head-up tilt (HUT), and 5 min of supine rest. Orthostatic tolerance was not determined. Calf compliance was measured in five of the subjects before and after the program as the change in leg volume at occluding pressures of 20, 40, 60, 80, and 100 mm Hg. Following the program, VO2max increased by 8.7% (p = 0.012), while decreases were noted in resting HR (9.4%, p = 0.041), SBP (5.0%, p less than 0.0005), and DBP (14.2%, p less than 0.0005). Despite a greater HR increase during HUT (7.1 beat.min-1, p = 0.034), SBP decreased by 3.4 mm Hg during HUT after the exercise program (p = 0.008). No differences were noted in the changes in DBP, MAP, or PP upon tilting (p greater than 0.05). After the program, the amount of fluid pooled in the calf at high occluding pressures (80 and 100 mm Hg) increased by 0.96 +/- 0.24 and 1.10 +/- 0.33 ml.100 ml tissue-1 (X +/- S.E.M., p = 0.017 and p = 0.028, respectively). We suggest that control of blood pressure during 10 min of orthostasis may be altered by endurance exercise training.     

Basophil releasability in young highly trained and older athletes

PURPOSE: Exercise-induced hypoxemia in highly trained athletes is associated with an increase in histamine release during exercise. The cells most implicated in blood histamine release are basophils. The aim of this study was to determine whether high-level endurance training induces modifications in histamine releasability from human basophils. METHODS: Seven young highly trained athletes (YA) [aged 26.1+/-1.3 yr (mean +/- SEM)] and seven master athletes (MA) (64.4+/-4.1 yr), all known to develop exercise-induced hypoxemia, were respectively compared with seven young untrained men (YC) (23.0+/-1.5 yr) and seven older untrained men (OC) (61.6+/-1.3 yr). During an incremental exhaustive exercise, blood samples for measurement of anti-IgE-induced histamine release from leukocytes were drawn at rest, VO2max, and recovery. RESULTS: Basophils from "leukocyte-rich" supernatant in YA and MA showed significantly higher histamine release induced by anti-IgE (1 microg x mL(-1) than, respectively, YC (P<0.01) and OC (P<0.05) at rest, VO2ax (P<0.01), and recovery (P<0.01). Basophils in YA and MA also showed a histamine release induced by anti-IgE that was higher at VO2max than at rest (respectively. P<0.01 and P<0.05), but this change was not found in the control groups. CONCLUSION: In conclusion, the basophils in highly trained endurance athletes, both young and older, showed higher anti-IgE-induced histamine release than those of untrained men. This effect of high-level training seemed to be potentiated by exercise.     

Individual variation in the reduction of heart rate and performance at lactate thresholds in acute normobaric hypoxia

Heart rate monitoring and lactate measurements are used to control exercise intensity during training at moderate altitude although there is some uncertainty about hypoxia-induced changes in these parameters at equivalent submaximal exercise intensities compared to normoxia. To study the influence of acute normobaric hypoxia (FiO2 0.15) on heart rate and performance at the individual anaerobic lactate threshold (IAT), at the 4 mmol x l(-1) threshold (AT) and at an intensity requiring 80 % of VO2max measured in the respective environment, 20 endurance-trained male athletes performed an incremental treadmill test in normoxia and normobaric hypoxia. During exercise in normobaric hypoxia, heart rate and velocity were significantly (p < 0.001) reduced with a wide individual variation at the IAT (range: - 1 to - 17 min(-1), - 0.3 to - 3.5 km x h(-1)), at the AT (- 2 to - 13 min(-1), - 0.2 to - 3.3 km x h(-1)) as well as at an intensity requiring 80 % of VO2max (0 to - 18 min(-1), - 1.1 to - 3.7 km x h(-1)). Relative VO2 at the lactate thresholds expressed as a percentage of VO2max was not significantly different compared to normoxia (86 +/- 6 % vs. 84 +/- 5 %, IAT; 90 +/- 5 % vs. 88 +/- 6 %, AT), but also showed a considerable individual variation. In conclusion, heart rate and performance have to be reduced individually to a varying extent during exercise in a hypoxic environment in order to achieve an equivalent intensity compared to exercise in normoxia.     

Effect of longitudinal physical training and water immersion on orthostatic tolerance in men

To test the hypothesis that moderately intense physical training has no effect on orthostasis, orthostatic and fluid-electrolyte-endocrine responses to 60 degrees head-up tilt were compared before and after 6 h of water immersion (34.5 +/- 0.1 degrees C) up to the neck following 6 months of exercise training. During the tilt test the five male subjects (27-42 years) each wore a lower-body positive-pressure suit (MAST-111A antishock trousers). The tilt procedure consisted of a 40-min supine control period (suit deflated), followed by a maximum 90-min tilt period (suit inflated to 50 +/- 5 mm Hg for 30 min, then deflated for 60 min or until presyncope). The mean +/- S.E. pretraining cycle ergometer peak VO2 was 3.20 +/- 0.14 L.min-1 (39 +/- 2 ml.min-1.kg-1), 3.36 +/- 0.27 L.min-1 (42 +/- 4 ml.min-1.kg-1) after 3 months (N.S.), and increased by 18% to 3.78 +/- 0.36 L.min-1 (48 +/- 5 ml.min-1.kg-1, +22%, p less than 0.05) posttraining. During pretraining, water immersion tilt tolerance decreased from 74 +/- 16 min before to 34 +/- 9 min (delta = 40 min, p less than 0.05) after immersion. During posttraining, water immersion tilt tolerance decreased similarly from 74 +/- 16 min preimmersion to 44 +/- 13 min (delta = 30 min, p less than 0.05) postimmersion (74 vs. 74 min, N.S.; 34 vs. 44 min, N.S.).(ABSTRACT TRUNCATED AT 250 WORDS)