The role of haemoglobin mass on VO2max following normobaric 'live high-train low' in endurance-trained athletes

It remains unclear by which mechanism 'live high-train low' (LHTL) altitude training increases exercise performance. Haematological and skeletal muscle adaptations have both been proposed. To test the hypotheses that (i) LHTL improves maximal oxygen uptake (VO(2)max) and (ii) this improvement is related to hypoxia-induced increases in total haemoglobin mass (Hb(mass)) and not to improved maximal oxidative capacity of skeletal muscle, we determined VO(2)max before LHTL and after LHTL, before and after the altitude-induced increases in Hb(mass) (measured by carbon-monoxide rebreathing) had been abolished by isovolumic haemodilution. We obtained skeletal muscle biopsies to quantify mitochondrial oxidative capacity and efficiency. Sixteen endurance-trained athletes were assigned (double-blinded, placebo controlled) to ≥16 h/day over 4 weeks to normoxia (placebo, n=6) or normobaric hypoxia equivalent to 3000 m altitude (LHTL, n=10). Four-week LHTL did not increase VO(2)max, irrespective of treatment (LHTL: 1.5%; placebo: 2.0%). Hb(mass) was slightly increased (4.6%) in 5 (of 10) LHTL subjects but this was not accompanied by a concurrent increase in VO(2)max. In the subjects demonstrating an increase in Hb(mass), isovolumic haemodilution elicited a 5.8% decrease in VO(2)max. Cycling efficiency was altered neither with time nor by LHTL. Neither maximal capacity of oxidative phosphorylation nor mitochondrial efficiency was modified by time or LHTL. The present results suggest that LHTL has no positive effect on VO(2)max in endurance-trained athletes because (i) muscle maximal oxidative capacity is not improved following LHTL and (ii) erythrocyte volume expansion after LHTL, if any, is too small to alter O(2) transport.     

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.     

Acute hypoxia decreases cardiac response to catecholamines in exercising humans

Cardiac chronotropic response to adrenergic activity at rest and exercise has been studied in 8 sea-level natives on the first two days of exposure to high altitude hypoxia (3823 m, 473 mmHg). Maximal O2 uptake (VO2max) was determined at low altitude (day 0:D0) and high altitude (day 2:D2). Submaximal exercise tests were performed at low altitude (day 1:D1) and high altitude (days 3 and 4: D3, D4). Plasma venous norepinephrine (NE) and epinephrine (E) concentrations were determined at rest and at the end of submaximal exercise. From D0 to D2, maximal heart rate decreased by 7% (p less than 0.01), and VO2max decreased by 17% (p less than 0.01). During submaximal exercise, plasma NE did not vary significantly (D1: 1.36 +/- 0.57, D3: 1.48 +/- 0.51, D4: 1.31 +/- 0.54 ng.ml-1). In contrast, relative work load decreased at high altitude (% VO2max at D1, D3 and D4 were respectively: 90.2 +/- 6.1, 83.3 +/- 9.8, 76.9 +/- 8.2). Linear relationships were found, both at low and high altitudes, between NE and VO2, NE and % VO2max, and between the increases in NE and heart rate during exercise. Covariance analysis indicates that these relations shifted to the left at high altitude:for the same NE or increase in NE, VO2 or increase in heart rate was lower at high altitude. Variations in E were similar but not significant. We conclude that hypoxia induced a decrease in cardiac chronotropic response to adrenergic activation during submaximal exercise.     

The role of the right ventricle during hypobaric hypoxic exercise: insights from patients after the Fontan operation

OBJECTIVES: The principal objective of this study was to examine the importance of the right ventricle for maximal systemic oxygen transport during exercise at high altitude by studying patients after the Fontan operation. BACKGROUND: High-altitude-induced hypoxia causes a reduction in maximal oxygen uptake. Normal right ventricular pump function may be critical to sustain cardiac output in the face of hypoxic pulmonary vasoconstriction. We hypothesized that patients after the Fontan operation, who lack a functional subpulmonary ventricle, would have a limited exercise capacity at altitude, with an inability to increase cardiac output. METHODS: We measured oxygen uptake (VO2, Douglas bag), cardiac output (Qc, C2H2 rebreathing), heart rate (HR) (ECG), blood pressure (BP) (cuff), and O2 Sat (pulse oximetry) in 11 patients aged 14.5+/-5.2 yr (mean +/- SD) at 4.7+/-1.6 yr after surgery. Data were obtained at rest, at three submaximal steady state workrates, and at peak exercise on a cycle ergometer. All tests were performed at sea level (SL) and at simulated altitude (ALT) of 3048 m (10,000 ft, 522 torr) in a hypobaric chamber. RESULTS: At SL, resting O2 sat was 92.6+/-4%. At ALT, O2 sat decreased to 88.2+/-4.6% (P < 0.05) at rest and decreased further to 80+/-6.3% (P < 0.05) with peak exercise. At SL, VO2 increased from 5.1+/-0.9 mL x kg(-1) x min(-1) at rest to 23.5+/-5.3 mL x kg(-1) x min(-1) at peak exercise and CI (Qc x m(-2)) increased from 3.3+/-0.7 L x m(-2) to 6.2+/-1.2 L x m(-2). VO2 peak, 17.8+/-4 mL x kg(-1) x min(-1) (P < 0.05), and CI peak, 5.0+/-1.5 L x m(-2) (P < 0.05), were both decreased at ALT. Remarkably, the relationship between Qc and VO2 was normal during submaximal exercise at both SL and ALT. However at ALT, stroke volume index (SVI, SV x m(-2)) decreased from 37.7+/-8.6 mL x min(-1) x m2 at rest, to 31.3+/-8.6 mL x min(-1) x m2 at peak exercise (P < 0.05), whereas it did not fall during sea level exercise. CONCLUSIONS: During submaximal exercise at altitude, right ventricular contractile function is not necessary to increase cardiac output appropriately for oxygen uptake. However, normal right ventricular pump function may be necessary to achieve maximal cardiac output during exercise with acute high altitude exposure.     

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.     

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.     

Long-term intermittent hypoxia increases O2-transport capacity but not VO2max

Long-term intermittent hypoxia, characterized by several days or weeks at altitude with periodic stays at sea level, is a frequently occurring pattern of life in mountainous countries demanding a good state of physical performance. The aim of the study was to determine the effects of a typical South American type of long-term intermittent hypoxia on VO2max at altitude and at sea level. We therefore compared an intermittently exposed group of soldiers (IH) who regularly (6 months) performed hypoxic-normoxic cycles of 11 days at 3550 m and 3 days at sea level with a group of soldiers from sea level (SL, control group) at 0 m and in acute hypoxia at 3550 m. VO2max was determined in both groups 1 day after arrival at altitude and at sea level. At altitude, the decrease in VO2max was less pronounced in IH (10.6 +/- 4.2%) than in SL (14.1 +/- 4.7%). However, no significant differences in VO2max were found between the groups either at sea level or at altitude, although arterial oxygen content (Ca(O(2) )) at maximum exercise was elevated (p < 0.001) in IH compared to SL by 11.7% at sea level and by 8.9% at altitude. This higher Ca(O(2) ) mainly resulted from augmented hemoglobin mass (IH: 836 +/- 103 g, SL: 751 +/- 72 g, p < 0.05) and at altitude also from increased arterial O(2)-saturation. In conclusion, acclimatization to long-term intermittent hypoxia substantially increases Ca(O(2) ), but has no beneficial effects on physical performance either at altitude or at sea level.     

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 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.     

Hemoglobin, muscle oxidative capacity, and VO2max in African-American and Caucasian women

PURPOSE: The purpose of this paper was to determine whether differences in hemoglobin (Hb) and muscle aerobic capacity exist between African-American (AA) and Caucasian (CA) premenopausal women and to determine whether Hb and aerobic capacity of the muscle are associated with the racial differences in maximum oxygen uptake (VO2max). METHODS: 43 AA and 46 CA sedentary premenopausal women were subjects. Percent body fat was determined by four-compartment model, leg lean tissue by dual energy x-ray absorptiometry, VO2max during a graded exercise test, aerobic capacity of the calf muscle by 31P magnetic resonance spectroscopy, and serum Hb by the cyanide method. RESULTS: AA women had reduced VO2max (AA 29.3 +/- 3.0 vs CA 33.6 +/- 5.6 mL.kg(-1) bdw(-1).min, P < 0.01), reduced muscle aerobic capacity (AA 24.3 +/- 5.8 vs CA 21.3 +/- 4.8 s, P = 0.01, where lower values indicate higher aerobic capacity), and reduced Hb (AA 11.8 +/- 1.3 vs CA 12.9 +/- 0.8 g.dL(-1), P < 0.01). The racial difference in VO2max persisted whether the values were unadjusted or adjusted for fat-free mass or leg lean tissue. Multiple regression analysis revealed that both Hb and muscle aerobic capacity were related to VO2max after adjusting for each other, race, and either fat-free mass or leg lean tissue. Being AA was associated with reduced VO2max in mL O2.kg leg lean tissue(-1).min(-1) (zero-order simple Pearson-product correlation -0.60, P < 0.01). When multiple regression was used, the correlation between race and VO2max decreased but persisted (-0.40, <0.01) after adjusting for Hb and muscle aerobic capacity. CONCLUSIONS: These data suggest that differences in Hb and aerobic capacity of muscle are related to reduced VO2max in AA women. However, Hb and aerobic capacity of the muscle can only partially explain the racial differences in VO2max.     

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.     

Effect of high-intensity submaximal work, with or without rest, on subsequent VO2max

PURPOSE: In practice, tests of maximal oxygen uptake (.VO2max) are often preceded by a lactate profile, a highly intense but submaximal exercise bout. The .VO2max response to preceding high-intensity submaximal exercise, with or without a rest period, has not been determined. If .VO2max is limited after a lactate profile, exercise-induced hypoxemia (EIH) may explain the deficit. The purposes of this study were to: 1) examine the effects of high-intensity submaximal exercise, with or without rest, on subsequent .VO2max; and 2) evaluate the role of EIH in causing any observed changes. METHODS: Ten healthy, well-trained, male cross-country skiers (age = 20.5 +/- 4.7 yr, height = 181.6 +/- 6.0 cm, mass = 72.1 +/- 5.7 kg) completed three exercise trials: an incremental run to fatigue (MAX), MAX preceded by a high-intensity submaximal run (lactate profile) and a 20-min rest period (discontinuous protocol [DC]), and MAX preceded by a high-intensity submaximal exercise run with no rest (continuous protocol [C]). .VO2max, minute ventilation, and arterial oxygen saturation were measured throughout, and diffusion capacity was evaluated 2 min postexercise.RESULTS No significant between trial differences were observed, although the difference between .VO2max determined during the MAX trial (62.7 +/- 6.7 mL.kg-1.min-1) and during the DC trial (58.3 +/- 4.4 mL.kg-1.min-1) approached significance (P = 0.059). DC .VO2max responses could be separated into two groups: five responders whose .VO2max suffered during the DC trial (decreased >7.5% from MAX) and five nonresponders, whose .VO2max was unaffected by preceding submaximal exercise and a rest period. Responders showed greater aerobic capacity during the MAX trial. CONCLUSION: .VO2max is significantly reduced in approximately 50% of cross-country skiers when a maximal exercise test is preceded by high-intensity submaximal exercise and a 20 min rest period; the role of EIH in causing these reductions is unclear.     

Oxygen consumption in nonexercising muscle after exercise

Little is known about the effect of exercise intensity on post-exercise oxygen consumption in nonexercising muscle. This study examined the effect of exercise intensity on muscle oxygen consumption (VO2mus) in nonexercising forearm flexor muscles (nonexVO2mus) after cycling exercise. Eight healthy male subjects performed 20 min of cycling exercise at 30%, 50%, and 70% of maximal oxygen consumption (%VO2max) on separate days. The nonexVO2mus values at rest, at the end of exercise, and during recovery after exercise were measured by near-infrared spectroscopy. VO2mus was determined using the rate of decrease in oxygenated hemoglobin during arterial occlusion. The nonexVO2mus at the end of exercise significantly increased by 1.3 +/- 0.1, 2.0 +/- 0.3, and 2.2 +/- 0.3-fold over resting values at 30%, 50%, and 70% VO2max, respectively. NonexVO2mus returned to the resting value after 3 - 5 min of recovery and then showed no significant change for 120 min after exercise at all exercise intensities. NonexVO2mus at the end of exercise at 70% VO2max was significantly higher than that after exercise at 30% VO2max. These results show that 20 min of cycling exercise induced an increase in nonexVO2mus and that higher intensity exercise produces a larger increase in nonexVO2mus after exercise.     

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 and ventilatory effects of an external nasal dilator during ergometry

INTRODUCTION: Athletes and coaches have begun to use external nasal dilators with the perception that they enhance performance and make it "easier to breathe." This study was conducted to ascertain whether application of an external nasal dilator would enhance performance, as measured by maximal oxygen uptake (VO2max), maximal ventilation (V(Emax)), maximal work rate (Wr(max)) or ratings of perceived exertion and dyspnea (RPE, RPD). METHODS: Fifteen subjects (F = 10; M = 5: age, 20+/-1.4, mean +/- SD) performed three incremental exercise tests to fatigue on an ergometer at 1-wk intervals in randomized order. One test was conducted without a nasal dilator, using a nose clip and mouthpiece for oxygen uptake and ventilatory measurements (control, C). The other two tests used a Rudolph 8900 breathing mask that included the nose in the breathing circuit and subjects wore either a placebo (P) or the active dilator (A). RPE for total body (20-point scale) and for dyspnea (10-point scale) were also measured on all tests. RESULTS: There were no significant differences in VO2max (mean +/- SD; C = 3.12+/-1.1; P = 3.12 + 1.06; A = 3.04+/-0.94). V(Emax) (C = 117+/-26; P = 125+/-31; A = 122+/-26), Wr(max) (C = 256+/-73; P = 255+/-70; A = 257+/-74), RPE (C = 18.8+/-1.78; P = 18.9+/-1.33; A = 18.9+/-1.22), or RPD (C = 9.1+/-1.58; P = 9.3+/-1.2; A = 9.13+/-1.2) during exercise between any group. CONCLUSION: Thus, it is concluded that an external nose dilator does not enhance performance as measured by VO2max, V(Emax), Wr(max), or perceived performance as measured by RPE and RPD.     

Maximal physiological responses between aquatic and land exercise in overweight women

PURPOSE: To investigate the maximal physiological responses between aquatic and land-based graded exercise tests in overweight women. METHODS: Twenty healthy, overweight (body mass index (BMI) > or = 25 kg.m(-2)), Caucasian women (mean +/- SD; age 48 +/- 7 yr, BMI 30 +/- 4 kg.m(-2)) completed a deep water running (DWR) and treadmill walking (TMW) graded exercise test. Maximal responses during the DWR and TMW graded exercise tests were compared using paired t-tests. Comparisons were made in the incidence of achievement of maximal oxygen consumption (VO2max) criteria between DWR and TMW protocols. Criteria were a plateau in VO2 (change < 2.1 mL.kg.min(-1)), heart rate (HR) equal to or above the age-adjusted maximum, and respiratory exchange ratio (RER) > or = 1.15. RESULTS: Maximal responses for VO2max (22.5 +/- 4.86 vs 27.7 +/- 4.73 mL.kg.min(-1)), HRmax (159 +/- 16 vs 170 +/- 12 bpm), and RER (1.03 +/- 0.06 vs 1.10 +/- 0.06) were significantly lower (P < 0.01) for the DWR test compared with the TMW test, respectively. Achievement of various VO2max criteria was demonstrated more consistently during the TMW test than the DWR test. CONCLUSION: Maximal physiological responses of overweight women to DWR and TMW are significantly different but are comparable with other populations. As the maximal responses for DWR compared with TMW differ, the use of land-based criteria for VO2max is not recommended for a graded DWR exercise test.     

Oxygen consumption, lactate accumulation, and sympathetic response during prolonged exercise under hypoxia

Six men (33 +/- 3 years old) performed 1 h ergocycle exercise (60% VO2 max) at sea level and at a simulated altitude of 3000 m. A similar relative exercise intensity corresponded to a lower absolute work load (139 +/- 4 W) in hypoxic than normoxic (163 +/- 4 W) conditions. Lower oxygen uptake (VO2) with no change in ventilation (VE), respiratory exchange ratio (R), and heart rate (Hr) were observed during exercise under hypoxia compared to normoxia. A slow rise in VO2, after the initial 5 min exercise, was observed in normoxic (+ 230 ml/min) as well as in hypoxic (250 ml/min) conditions that might be, in part, related to oxidative removal of blood lactate. Peak blood lactate concentration reached at 30 min of exercise was similar in normoxia (4.5 +/- 0.4) and in hypoxia (4.7 +/- 0.5). However, while the lactate level decreased during exercise at sea level, it remained elevated throughout exercise in altitude. Blood lactate concentration measured at the end of exercise was significantly (P less than 0.05) higher in hypoxic (4.4 +/- 0.3) than in normoxic (3.2 +/- 0.4) conditions. Catecholamine response to exercise was similar in both conditions. We conclude that during prolonged exercise at a given relative work load, hypoxia does not affect cardiorespiratory and sympathetic responses but tends to increase blood lactate accumulation. Higher blood lactate concentrations during hypoxic exercise seems to reflect alterations in the removal of blood lactate rather than changes in glycolytic flux.     

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 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.     

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.