Arterial haemoglobin oxygen saturation is affected by F1O2 at submaximal running velocities in elite athletes

This study was conducted to determine whether arterial desaturation would occur at submaximal workloads in highly trained endurance athletes and whether saturation is affected by the fraction of oxygen in inspired air (F(I)O2). Six highly trained endurance athletes (5 women and 1 man, aged 25+/-4 yr, VO2max 71.3+/-5.0 ml x kg(-1) x min(-1)) ran 4x4 min on a treadmill in normoxia (F(I)O2 0.209), hypoxia (F(I)O2 0.155) and hyperoxia (F(I)O2 0.293) in a randomized order. The running velocities corresponded to 50, 60, 70 and 80% of their normoxic maximal oxygen uptake (VO2max). In hypoxia, the arterial haemoglobin oxygen saturation percentage (SpO2%) was significantly lower than in hyperoxia and normoxia throughout the test, and the difference became more evident with increasing running intensity. In hyperoxia, the SpO2% was significantly higher than in normoxia at 70% running intensity as well as during recovery. The lowest values of SpO2% were 94.0+/-3.8% (P<0.05, compared with rest) in hyperoxia, 91.0+/-3.6% (P<0.001) in normoxia and 72.8+/-10.2% (P<0.001) in hypoxia. Although the SpO2% varied with the F(I)O2, the VO2 was very similar between the trials, but the blood lactate concentration was elevated in hypoxia and decreased in hyperoxia at the 70% and 80% workloads. In conclusion, elite endurance athletes may show an F(I)O2-dependent limitation for arterial O2 saturation even at submaximal running intensities. In hyperoxia and normoxia, the desaturation is partly transient, but in hypoxia the desaturation worsens parallel with the increase in exercise intensity.     

Effect of exercise-induced arterial O2 desaturation on VO2max in women

PURPOSE: We have recently reported that many healthy habitually active women experience exercise induced arterial hypoxemia (EIAH). We questioned whether EIAH affected VO2max in this population and whether the effect was similar to that reported in men. METHODS: Twenty-five healthy young women with widely varying fitness levels (VO2max, 56.7 +/- 1.5 mL x kg(-1) x min(-1); range: 41-70 mL x kg(-1) x min(-1)) and normal resting lung function performed two randomized incremental treadmill tests to VO2max (FIO2: 0.21 or 0.26) during the follicular phase of their menstrual cycle. Arterial blood samples were taken at rest and near the end of each workload during the normoxic test. RESULTS: During room air breathing at VO2max, SaO2 decreased to 91.8 +/- 0.4% (range 87-95%). With 0.26 FIO2, SaO2, at VO2max remained near resting levels and averaged 96.8 +/- 0.1% (range 96-98%). When arterial O2 desaturation was prevented via increased FIO2, VO2max increased in 22 of the 25 subjects and in proportion to the degree of arterial O2 desaturation experienced in normoxia (r = 0.88). The improvement in VO2max when systemic normoxia was maintained averaged 6.3 +/- 0.3% (range 0 to +15%) and the slope of the relationship was approximately 2% increase in VO2max for every 1% decrement in the arterial oxygen saturation below resting values. About 75% of the increase in VO2max resulted from an increase in VO2 at a fixed maximal work rate and exercise duration, and the remainder resulted from an increase in maximal work rate. CONCLUSIONS: These data demonstrate that even small amounts of EIAH (i.e., >3% delta SaO2 below rest) have a significant detrimental effect on VO2max in habitually active women with a wide range of VO2max. In combination with our previous findings documenting EIAH in females, we propose that inadequate pulmonary structure/function in many habitually active women serves as a primary limiting factor in maximal O2 transport and utilization during maximal exercise.     

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.     

The oxygen uptake response of sprint- vs. endurance-trained runners to severe intensity running.

We compared the oxygen uptake (VO2) response of sprint- and endurance-trained runners for an exhaustive square wave run lasting approximately 2 minutes. Six sprinters and six middle- and long-distance runners each performed two exhaustive square wave runs lasting approximately 2 min and two exhaustive ramp tests. VO2 was determined breath-by-breath (QP9000; Morgan Medical, Rainham, UK) and averaged across the two repeats of each test; for the square wave test, the averaged VO2 response (excluding the first 15 s) was then modelled using a monoexponential function. Both VO2peak for the ramp test (67.5+/-3.3 vs. 54.5+/-8.5 mlxkg(-1)xmin(-1); P= 0.006) and the asymptotic VO2 for the square wave run (59.6+/-2.7 vs. 50.7+/-4.6 mlxkg(-1)xmin(-1); P= 0.002) were higher for the endurance than for the sprint group. However, as a percentage of VO2peak, this asymptotic VO2 did not differ between the groups (90.1+/-3.2% (endurance) vs. 96.2+/-9.0% (sprint); P= 0.145). Across all 12 subjects, the %VO2peak attained in the square wave run was negatively correlated with VO2peak (Pearson's r= -0.811, P= 0.001). We conclude that VO2max is more important than training history as a determinant of the %VO2max attained in exhaustive square wave running lasting approximately 2 min.     

Influence of acute moderate hypoxia on time to exhaustion at vVO2max in unacclimatized runners

Eight unacclimatized long-distance runners performed, on a level treadmill, an incremental test to determine the maximal oxygen uptake (VO2max) and the minimal velocity eliciting VO2max (vVO2max) in normoxia (N) and acute moderate hypoxia (H) corresponding to an altitude of 2,400 m (PIO 2 of 109 mmHg). Afterwards, on separate days, they performed two all-out constant velocity runs at vO2 max in a random order (one in N and the other in H). The decrease in VO2max between N and H showed a great degree of variability amongst subjects as VO2max decreased by 8.9 +/- 4 ml x min(-1) x kg)(-1) in H vs. N conditions (-15.3 +/- 6.3 % with a range from -7.9 % to -23.8 %). This decrease in VO2max was proportional to the value of VO2max (VO2max vs. delta VO2max N-H, r = 0.75, p = 0.03). The time run at vVO2max was not affected by hypoxia (483 +/- 122 vs. 506 +/- 148 s, in N and H, respectively, p = 0.37). However, the greater the decrease in vVO2max during hypoxia, the greater the runners increased their time to exhaustion at vVO2max (vVO2max N-H vs. tlim @vVO2max N-H, r = -0.75, p = 0.03). In conclusion, this study showed that there was a positive association between the extent of decrease in vVO2max, and the increase in run time at vVO2max in hypoxia.     

Effect of endurance training on the VO2-work rate relationship in normoxia and hypoxia

PURPOSE: We postulated that the relationship between VO2 and work rate (VO2-WR relationship) during incremental exercise is dependent on O2 availability, and that training-induced adaptations alter this relationship. We therefore studied the effect of endurance training on VO2 response during incremental exercise in normoxia and hypoxia (FIO2=0.134). METHODS: Before and after training (6 d.wk, 4 wk), eight subjects performed incremental exercises under normoxia and hypoxia and one constant-work rate exercise in normoxia at 80% of pretraining VO2max. The slopes of the VO2-WR relationship during incremental exercise were calculated using all the points (whole slope) or only points before the lactate threshold (pre-LT slope). The difference between VO2max measured and VO2max expected from the pre-LT slope (DeltaVO2) was determined, as was the difference between VO2 at minute 10 and VO2 at minute 4 during the constant-work rate exercise (DeltaVO2(10'-4')). RESULTS: In normoxia, training induced a significant decrease in the whole slope (11.0+/-1.0 vs 9.9+/-0.4 mL.min.W, P<0.05). In hypoxia, training induced a significant increase in the pre-LT slope (8.7+/-1.2 vs 9.8+/-0.7 mL.min.W; P<0.05) and the whole slope (8.5+/-1.2 vs 9.4+/-0.5 mL.min.W; P<0.05). A significant correlation between the decrease of DeltaVO2 and the decrease of DeltaVO2(10'-4') with training was found in normoxia (P<0.01, r=0.79). CONCLUSIONS: Taken together, these results indicate that adaptations induced by endurance training are associated with more efficient incremental and constant-workload exercise performed in normoxia. Moreover, training contributes to improved O2 delivery during moderate exercise performed in hypoxia, and to enhanced near-maximal exercise tolerance.     

The influence of acute hypoxia on the prediction of maximal oxygen uptake using multi-stage shuttle run test

BACKGROUND: The purpose of this study was to investigate changes in predicted maximal oxygen uptake (VO(2max)) by the multistage shuttle run test (MSSR) and several physiological parameters in MSSR under normoxia and two hypoxic conditions and the influences of acute hypoxia on these changes in MSSR. METHODS: Experimental design: six college long distance runners (LR), seven college rugby athletes (RG) and eight untrained college males (UM) performed incremental running test on the treadmill and MSSR in 17.5% (HYP(17.5%)) and 15.5% (HYP(15.5%)) of oxygen concentration and normoxia (NOR(20.9%)). Measures: VO(2max) was measured by the treadmill protocol and predicted by MSSR. Maximal heart rate (HR(max)) and maximal blood lactate concentration (BLa(max)) were recorded at the termination of each test. RESULTS: Significant correlation was observed between measured VO2(max) by the treadmill protocol (57.2+/-8.3 ml x kg(-1) x min(-1)) and predicted VO(2max) in NOR(20.9%) (54.6+/-8.0 ml x kg(-1) x min(-1)) (r=0.80, p<0.05). Also strong correlations in predicted VO(2max) between NOR(20.9%) and HYP(17.5%) (51.1+/-8.0 ml x kg(-1) x min(-1)) (r=0.90, p<0.05) and between NOR(20.9%) and HYP(15.5%) (48.1+/-7.3 ml x kg(-1) x min(-1)) (r=0.82, p<0.05) were observed. CONCLUSIONS: The results show that although MSSR underpredicts VO(2max), it is effective to evaluate aerobic power and can detect the influence of oxygen concentration on aerobic power. The specific movement of MSSR may affect the performance of LR but MSSR can describe the influence of hypoxia on the performance of LR compared to normoxia. Thus MSSR can be used to evaluate the influence of hypoxia or altitude on aerobic power as a field test.     

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 exercise intensity on relationship between VO2max and cardiac output

PURPOSE: The purpose of this study was to determine whether the maximal oxygen uptake (VO2max) is attained with the same central and peripheral factors according to the exercise intensity. METHODS: Nine well-trained males performed an incremental exercise test on a cycle ergometer to determine the maximal power associated with VO2max (pVO2max) and maximal cardiac output (Qmax). Two days later, they performed two continuous cycling exercises at 100% (tlim100 = 5 min 12 s +/- 2 min 25 s) and at an intermediate work rate between the lactate threshold and pVO2max (tlimDelta50 +/- 12 min 6 s +/- 3 min 5 s). Heart rate and stroke volume (SV) were measured (by impedance) continuously during all tests. Cardiac output (Q) and arterial-venous O2 difference (a-vO2 diff) were calculated using standard equations. RESULTS: Repeated measures ANOVA indicated that: 1) maximal heart rate, VE, blood lactate, and VO2 (VO2max) were not different between the three exercises but Q was lower in tlimDelta50 than in the incremental test (24.4 +/- 3.6 L x min(-1) vs 28.4 +/- 4.1 L x min(-1); P < 0.05) due to a lower SV (143 +/- 27 mL x beat(-1) vs 179 +/- 34 mL x beat(-1); P < 0.05), and 2) maximal values of a-vO2 diff were not significantly different between all the exercise protocols but reduced later in tlimDelta50 compared with tlim100 (6 min 58 s +/- 4 min 29 s vs 3 min 6 s +/- 1 min 3 s, P = 0.05). This reduction in a-vO2 diff was correlated with the arterial oxygen desaturation (SaO2 = -15.3 +/- 3.9%) in tlimDelta50 (r = -0.74, P = 0.05). CONCLUSION: VO2max was not attained with the same central and peripheral factors in exhaustive exercises, and tlimDelta50 did not elicit the maximal Q. This might be taken into account if the training aim is to enhance the central factors of VO2max using exercise intensities eliciting VO2max but not necessarily Qmax.     

Effect of acute hypoxia on maximal oxygen uptake and maximal performance during leg and upper-body exercise in Nordic combined skiers

We examined the effect of normobaric hypoxia (3200 m) on maximal oxygen uptake (VO2max) and maximal power output (Pmax) during leg and upper-body exercise to identify functional and structural correlates of the variability in the decrement of VO2max (DeltaVO2max) and of maximal power output (DeltaPmax). Seven well trained male Nordic combined skiers performed incremental exercise tests to exhaustion on a cycle ergometer (leg exercise) and on a custom built doublepoling ergometer for cross-country skiing (upper-body exercise). Tests were carried out in normoxia (560 m) and normobaric hypoxia (3200 m); biopsies were taken from m. deltoideus. DeltaVO2max was not significantly different between leg (-9.1+/-4.9%) and upper-body exercise (-7.9+/-5.8%). By contrast, Pmax was significantly more reduced during leg exercise (-17.3+/-3.3%) than during upper-body exercise (-9.6+/-6.4%, p<0.05). Correlation analysis did not reveal any significant relationship between leg and upper-body exercise neither for DeltaVO2max nor for DeltaPmax. Furthermore, no relationship was observed between individual DeltaVO2max and DeltaPmax. Analysis of structural data of m. deltoideus revealed a significant correlation between capillary density and DeltaPmax (R=-0.80, p=0.03), as well as between volume density of mitochondria and DeltaPmax (R=-0.75, p=0.05). In conclusion, it seems that VO2max and Pmax are differently affected by hypoxia. The ability to tolerate hypoxia is a characteristic of the individual depending in part on the exercise mode. We present evidence that athletes with a high capillarity and a high muscular oxidative capacity are more sensitive to hypoxia.     

Effect of acute hypoxia on maximal exercise in trained and sedentary women

PURPOSE: The purpose of this study was to determine the physiological responses of sedentary and endurance-trained female subjects during maximal exercise at different levels of acute hypoxia. METHODS: Fourteen women who were sea level residents were divided into two groups according to their level of fitness: 1) endurance-trained women (TW) (N = 7), VO(2max) = 56.3 +/- 4.7 mL.kg(-1).min(-1); and 2) sedentary women (SW) (N = 7), VO(2max) = 34.8 +/- 5.6 mL.kg(-1).min(-1). Subjects performed four maximal cycle ergometer tests in normoxia and under hypoxic conditions (F(I)O(2) = 0.187, 0.154, and 0.117, corresponding to altitudes of 1000, 2500, and 4500 m, respectively). RESULTS: VO(2max) decreased significantly by 3.6 +/- 2.1, 14 +/- 2.5, and 27.4 +/- 3.6% in TW, and by 5 +/- 4, 9.4 +/- 6.4, and 18.7 +/- 7% in SW at 1000, 2500, and 4500 m, respectively. The drop of VO(2max) (DeltaVO(2max)) was greater in TW at and above 2500 m. Arterial O2 saturation (SpO(2)) at maximal exercise was lower in TW at every altitude (1000 m: 90.9 +/- 1.9 vs 94.6 +/- 1.4%; 2500 m: 82.8 +/- 2.8 vs 90.0 +/- 2.1%; 4500 m: 65.0 +/- 4.7 vs 73.6 +/- 4.5%). Maximal heart rate decreased significantly from 1000 m in the two groups. SpO(2) was correlated to DeltaVO(2max) at 4500 m (r = -0.81, P < 0.01) and 2500 m (r = -0.81, P < 0.01), but not below. Furthermore, we noted a relationship between SpO(2) and O2 pulse (VO(2)/HR) at every F(I)O(2). CONCLUSION: These results demonstrate that endurance-trained women show a greater decrement in VO(2max) at high altitudes. This could be explained mainly by a higher arterial desaturation, which is largely caused, according to our results, by diffusion limitation.     

Oxygen uptake response during maximal cycling in hyperoxia, normoxia and hypoxia

BACKGROUND: Oxygen uptake (VO2) on-kinetics is decelerated in acute hypoxia and accelerated in hyperoxia in comparison with normoxia during submaximal exercise. However, the effects of fraction of oxygen in inspired air (FIO2) on VO2 kinetics during maximal exercise are unknown. HYPOTHESIS: The effects of FIO2 on VO2 on-kinetics during maximal exercise are similar to submaximal exercise. METHODS: There were 11 endurance athletes who were studied during maximal 7-min cycle ergometer exercise in hyperoxia (FIO2 0.325), hypoxia (FIO2 0.166) and normoxia (FIO2 0.209). The individual VO2 data were fit to a curve by using a three exponential model. RESULTS: In hypoxia, VO2 on-response amplitude during Phase 2 (approximately 20-100 s from the beginning of exercise) was lower (p < 0.05) when compared with hyperoxia; time constant of VO2 Phase 3 (beyond approximately 100 s after beginning of exercise) was shorter (p < 0.05) when compared with hyperoxia; and mean response time (MRT, O-63%) for VO2peak was shorter (p < 0.05) when compared with normoxia and hyperoxia. VO2peak was higher in hyperoxia (4.80 +/- 0.48 L x min(-1), p < 0.05) and lower in hypoxia (4.03 +/- 0.46 L x min(-1), p < 0.05) than in normoxia (4.36 +/- 0.44 L x min(-1)). CONCLUSIONS: Moderate hypoxia or hyperoxia do not affect VO2 time constants at the onset of maximal exercise. However, MRT for VO2peak is shortened in hypoxia. It is suggested that the differences in VO2peak and power output during the latter half of the test and the point that FIO2 was modified only moderately might explain most of the discrepancy with the previous studies.     

Lung function, arterial saturation and oxygen uptake in elite cross country skiers: influence of exercise mode

Arterial desaturation during exercise is common in endurance-trained athletes, a phenomenon often more pronounced when the muscle mass engaged in the exercise is large. With this background, the present study monitored seven international-level cross country skiers performing on a treadmill while running (RUN), double poling (DP; upper body exercise) and diagonal skiing (DIA; arm and leg exercise). Static and dynamic lung function tests were performed and oxygen uptake was measured during submaximal and maximal exercise. Lung function variables (including the diffusion capacity) were only 5-20% higher than reported in sedentary men. Vital capacity was considerably lower than expected from the skiers' maximal oxygen uptake (VO(2max)), but the maximal ventilation followed a linear relationship with VO(2max). None or only a mild desaturation was observed in DP, RUN and DIA. Blood lactate concentration was slightly higher in DIA than in DP but not different from RUN. In DIA, VO(2max) was 6.23 +/- 0.47 L/min (mean +/- SD), which was 3.8% and 13.9% higher than in RUN and DP, respectively, with similar peak heart rates for the three exercise modes. No relationships were present either between the degree of desaturation and pulmonary functions tests, or with peak oxygen uptakes. The low blood lactate accumulation during the exhaustive efforts contributed to the arterial oxygen saturation being mild in spite of the very high oxygen uptake observed in these skiers.     

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.     

Muscle glycogen depletion alters oxygen uptake kinetics during heavy exercise

PURPOSE: To test the hypothesis that muscle fiber recruitment patterns influence the oxygen uptake (VO2) kinetic response, constant-load exercise was performed after glycogen depletion of specific fiber pools. METHODS: After validation of protocols for the selective depletion of Type I and II muscle fibers, 19 subjects performed square-wave exercise at 80% VT (moderate) and at 50% of the difference between VT and VO2max (heavy) without any prior depleting exercise (CON), after HIGH (10 x 1-min exercise bouts at 120% VO2max), and after LOW (3 h of exercise at 30% VO2max) exercise. RESULTS: Differences in VO2 kinetic parameters were only observed in heavy exercise AFTER HIGH: the VO2 primary component was higher (1.75 +/- 0.12 L x min) compared with CON (1.65 +/- 0.11 L x min, P < 0.05), and the VO2 slow component was lower (0.18 +/- 0.03 L x min) compared with CON (0.24 +/- 0.04 L x min, P < 0.05). CONCLUSIONS: The results indicate that the VO2 response to heavy constant-load exercise can be altered by depletion of glycogen in the Type II muscle fibers, lending support to the theory that muscle fiber recruitment influences both the VO2 primary and slow component amplitudes during heavy intensity exercise.     

The long-acting phosphodiesterase inhibitor tadalafil does not influence athletes' VO2max, aerobic, and anaerobic thresholds in normoxia

Whereas experimental studies showed that in healthy trained subjects, the phosphodiesterase-5 inhibitor (PDE-5i) sildenafil improves exercise capacity in hypoxia and not in normoxia, no studies on the effects of the long half-life PDE-5i tadalafil exist. In order to evaluate whether tadalafil influences functional parameters and performance during a maximal exercise test in normoxia, we studied 14 healthy male athletes in a double-blind cross-over protocol. Each athlete performed two tests on a cycle ergometer, both after placebo or tadalafil (at therapeutic dose: 20 mg) administration. Oxygen consumption (VO2), blood lactate, respiratory exchange ratio, rate of perceived exertion, arterial blood pressure (BP), heart frequency (HR) and oxygen pulse (VO2/HR) were evaluated before exercise, at individual ventilatory and anaerobic thresholds (IVT and IAT), at VO2max and during recovery. Compared to placebo, a single tadalafil administration significantly reduced systolic BP before and after exercise (p < 0.05), decreased VO2/HR at IVT (13.3 +/- 1.8 vs. 14.5 +/- 2.1 mL . beat (-1); p = 0.03), but did not modify individual VO2max, IVT, or IAT. In healthy athletes, 20 mg of tadalafil does not substantially influence physical fitness-related parameters, exercise tolerance, and cardiopulmonary responses to maximal exercise in normoxia; it remains to be verified if higher doses/prolonged use influence health and/or sport performance in field conditions.     

Maximal oxygen uptake as a parametric measure of cardiorespiratory capacity

INTRODUCTION: Maximal oxygen uptake (.VO2max) was defined by Hill and Lupton in 1923 as the oxygen uptake attained during maximal exercise intensity that could not be increased despite further increases in exercise workload, thereby defining the limits of the cardiorespiratory system. This concept has recently been disputed because of the lack of published data reporting an unequivocal plateau in .VO2 during incremental exercise. PURPOSE: The purpose of this investigation was to test the hypothesis that there is no significant difference between the .VO2max obtained during incremental exercise and a subsequent supramaximal exercise test in competitive middle-distance runners. We sought to determine conclusively whether .VO2 attains a maximal value that subsequently plateaus or decreases with further increases in exercise intensity. METHODS: Fifty-two subjects (36 men, 16 women) performed three series of incremental exercise tests while measuring .VO2 using the Douglas bag method. On the day after each incremental test, the subjects returned for a supramaximal test, during which they ran at 8% grade with the speed chosen individually to exhaust the subject between 2 and 4 min. .VO2 at supramaximal exercise intensities (30% above incremental .VO2max) was measured continuously. RESULTS: .VO2max measured during the incremental test (63.3 +/- 6.3 mL.kg(-1).min(-1); mean +/- SD) was indistinguishable from the .VO2max during the supramaximal test (62.9 +/- 6.2, N = 156; P = 0.77) despite a sufficient duration of exercise to demonstrate a plateau in .VO2 during continuous supramaximal exercise. These data provide strong support for the hypothesis that there is indeed a peak and subsequent plateau in .VO2 during maximal exercise intensity. CONCLUSIONS: .VO2max is a valid index measuring the limits of the cardiorespiratory systems' ability to transport oxygen from the air to the tissues at a given level of physical conditioning and oxygen availability.     

Time spent at VO2max: a methodological issue

This study was designed to propose a standardised procedure to determine the time spent at VO2max (tVO2max) based on the VO2max of the day (i. e. the VO2max value measured the day of the test). Ten male subjects first performed a graded field test, followed by a continuous running exercise to exhaustion, at the velocity of the Université de Montréal Track Test (V(UMTT)) plus 1 km x h(-1) (V(UMTT)(+1)). The second test consisted of an exhaustive run at 100 % of V(UMTT), followed by a V(UMTT)(+1) test. Different methods were used to compare time spent at VO2max, based on the VO2max of the graded field test, and time spent at VO2max, based on the VO2max of the day, during an exhaustive run at 100 % of V(UMTT). Results have shown that V(UMTT)(+1) tests were of sufficient intensity and duration to identify the VO2max of the day. Time spent at VO2max ranged from 25 +/- 53 s to 139 +/- 76 s according to the method used. However, the tVO2max method based on the sum of each value higher than 95 % of VO2max of the day appeared more robust than methods based on the time to exhaustion minus time to reach VO2 reference value, or the method based on the sum of values higher than VO2max minus 2.1 ml x kg(-1) x min(-1).     

Exercise performance in hypoxia after novel erythropoiesis stimulating protein treatment

Maximal aerobic power at high altitude (<4000 m) does not increase with altitude acclimatization. In order to investigate the isolated effects of increased arterial oxygen content (CaO2) on maximal oxygen uptake (VO2max) in hypoxia, we studied 10 subjects during exercise in acute exposure to 12.6% O2 before and after novel erythropoiesis stimulating protein (NESP) induced increases in CaO2. Over a period of 1 month, weekly NESP treatment increased resting hemoglobin (Hb) from 13.8+/-0.9 to 16.2+/-0.5 g/dL, hematocrit from 42.1+/-0.6% to 49.0+/-1.5%, and CaO2 from 189.7+/-3.0 to 218.6+/-5.7 mL/L. At maximal exercise CaO2 was increased from 172.3+/-3.7 to 191.5+/-3.8 mL/L with NESP treatment, and although maximal heart rate was similar in both conditions (178.4+/-2.6 and 180.9+/-2.5 b.p.m.) VO2max remained unaltered, the values being 3.12+/-2.0 and 3.12+/-2.0, before and after NESP treatment, respectively. NESP-injections in human subjects causes Hb and accordingly CaO2 to increase both in normoxia and hypoxia. Despite increases in CaO2 at maximal exercise in hypoxia VO2max is not increased.     

Oxygen uptake and heart rate responses during hypoxic exercise in children and adults

Control of ventilation and heart rate during exercise appears to undergo maturation, while aerobic metabolism (VO2) may not. Since we had previously found that hypoxia during exercise produced different ventilatory responses in children (C) compared to adults (A), we hypothesized that VO2 and heart rate kinetics during exercise would show similar maturational responses to hypoxia. To test this hypothesis, we examined the responses during progressive (ramp) and constant work rate tests in children and adults breathing either room air or hypoxic gas (FiO2 = 0.15). When corrected for body weight, children and adults had similar values for lactic acidosis threshold (LAT) (C: 29.1 +/- 5.0 ml.min-1.kg-1; A: 27.9 +/- 4.3) and VO2max (C: 40.7 +/- 8.6 ml.min-1.kg-1; A: 45.2 +/- 6.7) during normoxia. Hypoxia significantly lowered LAT (C: 27.5 +/- 5.4 ml.min-1.kg-1; A: 23.2 +/- 3.8; both P less than 0.05) and VO2max (C: 37.7 +/- 8.3 ml.min-1.kg-1; A: 40.1 +/- 5.3; both P less than 0.05) in both children and adults. Metabolic efficiency (delta VO2/delta work rate) and the VO2-heart rate relationship (delta VO2/delta HR/kg) were similar in the two groups and unaffected by hypoxia. During the constant work rate exercise, VO2 kinetics (time constant during phase 2 of the response (pi 1) and the O2 deficit) were similar between children and adults and were significantly slowed by hypoxia, consistent with current understanding of the control of oxidative metabolism. Finally, heart rate was increased at rest and during exercise with hypoxia, while the time to reach 75% of the end-exercise response was delayed significantly, in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)