Iron deficiency anemia and steady-state work performance at high altitude

Thirty-seven young adult male highland residents at 3,600-4,100 m in La Paz, Bolivia, performed short-duration cycle ergometry at 60, 80, and 100% of maximal voluntary O2 consumption (VO2max). Three groups of subjects representing the high-altitude population mean hemoglobin (Hb), the 10th percentile Hb, and below the 1st percentile were examined to test the hypothesis that the relationship of exercise performance to Hb concentration is similar to those relationships established at low altitude. Anemic individuals (n = 8) had 23% lower voluntary VO2max and 28% lower maximal work loads compared with controls (n = 17) or marginally anemic subjects (n = 12) although the relationship of VO2 to work load was similar. Anemic individuals maintained significantly higher arterial O2 partial pressures and Hb saturations during heavy exercise (90 +/- 0.5 vs. 85 +/- 0.6%) in conjunction with a greater heart rate up to maximal effort. A significantly decreased erythrocyte 2,3-diphosphoglycerate (2,3-DPG)-to-Hb molar ratio (0.70 +/- 0.04 vs. 1.12 +/- 0.06), suggestive of a left-shifted dissociation curve in anemics, is in contrast to the expected right-shifted curve. Moderate anemics were similar to controls. Anemic individuals did not differ in arterial lactate concentration from controls at absolute work loads; anemics had significantly lower arterial lactate concentrations at maximal effort than controls with no differences in the work load-to-lactate relationship. In conclusion, O2 transport during exercise at high altitude seems unaffected by the Hb concentrations as low as the 10th percentile of the population mean.(ABSTRACT TRUNCATED AT 250 WORDS)     

Higher arterial oxygen saturation during submaximal exercise in Bolivian Aymara compared to European sojourners and Europeans born and raised at high altitude

Arterial oxygen saturation (SaO(2)) was measured at 3,600-3,850 m by pulse oximetry at rest and during submaximal exercise in three study groups: 1) highland Aymara natives of the Bolivian altiplano (n = 25); 2) lowland European/North American sojourners to the highlands with at least 2 months of acclimatization time to 3,600 m (n = 27); and 3) subjects of European ancestry born and raised at 3,600 m (n = 22). Aymara subjects maintained approximately 1 percentage point higher SaO(2) during submaximal work up to 70% of their maximal work capacity, and showed a smaller rate of decline in SaO(2) with increasing work compared to both European study groups. The higher-exercise SaO(2) of Aymara compared to Europeans born and raised at 3,600 m suggests genetic adaptation. The two European study groups, who differed by exposure to high altitude during their growth and development period, did not show any significant difference in either resting or exercise SaO(2). This suggests that the developmental mode of adaptation is less important than the genetic mode of adaptation in determining exercise SaO(2). A weak correlation was detected (across study groups only) between the residual forced vital capacity (FVC) and the residual SaO(2) measured at the highest level of submaximal work output (P = 0.024, R = 0.26). While firm conclusions based on this correlation are problematic, it is suggested that a part of the higher SaO(2) observed in Aymara natives is due to a larger lung volume and pulmonary diffusion capacity for oxygen. Results from this study are compared to similar studies conducted with Tibetan natives, and are interpreted in light of recent quantitative genetic analyses conducted in both the Andes and Himalayas.     

Determinants of maximal O(2) uptake in rats selectively bred for endurance running capacity.

O(2) transport during maximal exercise was studied in rats bred for extremes of exercise endurance, to determine whether maximal O(2) uptake (VO(2 max)) was different in high- (HCR) and low-capacity runners (LCR) and, if so, which were the phenotypes responsible for the difference. VO(2 max) was determined in five HCR and six LCR female rats by use of a progressive treadmill exercise protocol at inspired PO(2) of approximately 145 (normoxia) and approximately 70 Torr (hypoxia). Normoxic VO(2 max) (in ml. min(-1). kg(-1)) was 64.4 +/- 0.4 and 57.6 +/- 1.5 (P < 0.05), whereas VO(2 max) in hypoxia was 42.7 +/- 0.8 and 35.3 +/- 1.5 (P < 0.05) in HCR and LCR, respectively. Lack of significant differences between HCR and LCR in alveolar ventilation, alveolar-to-arterial PO(2) difference, or lung O(2) diffusing capacity indicated that neither ventilation nor efficacy of gas exchange contributed to the difference in VO(2 max) between groups. Maximal rate of blood O(2) convection (cardiac output times arterial blood O(2) content) was also similar in both groups. The major difference observed was in capillary-to-tissue O(2) transfer: both the O(2) extraction ratio (0.81 +/- 0.002 in HCR, 0.74 +/- 0.009 in LCR, P < 0.001) and the tissue diffusion capacity (1.18 +/- 0.09 in HCR and 0.92 +/- 0.05 ml. min(-1). kg(-1). Torr(-1) in LCR, P < 0.01) were significantly higher in HCR. The data indicate that selective breeding for exercise endurance resulted in higher VO(2 max) mostly associated with a higher transfer of O(2) at the tissue level.     

Acute vs. chronic effects of elevated hemoglobin O(2) affinity on O(2) transport in maximal exercise.

These studies were conducted to compare the effects on systemic O(2) transport of chronically vs. acutely increased Hb O(2) affinity. O(2) transport during maximal normoxic and hypoxic [inspired PO(2) (PI(O(2))) = 70 and 55 Torr, respectively] exercise was studied in rats with Hb O(2) affinity that was increased chronically by sodium cyanate (group 1) or acutely by transfusion with blood obtained from cyanate-treated rats (group 2). Group 3 consisted of normal rats. Hb O(2) half-saturation pressure (P(50); Torr) during maximal exercise was approximately 26 in groups 1 and 2 and approximately 46 in group 3. In normoxia, maximal blood O(2) convection (TO(2 max) = cardiac output x arterial blood O(2) content) was similar in all groups, whereas in hypoxia TO(2 max) was significantly higher in groups 1 and 2 than in group 3. Tissue O(2) extraction (arteriovenous O(2) content/arterial O(2) content) was lowest in group 1, intermediate in group 2, and highest in group 3 (P < 0.05) at all exercise PI(O(2)) values. In normoxia, maximal O(2) utilization (VO(2 max)) paralleled O(2) extraction ratio and was lowest in group 1, intermediate in group 2, and highest in group 3 (P < 0.05). In hypoxia, the lower O(2) extraction ratio values of groups 1 and 2 were offset by their higher TO(2 max); accordingly, their differences in VO(2 max) from group 3 were attenuated or reversed. Tissue O(2) transfer capacity (VO(2 max)/mixed venous PO(2)) was lowest in group 1 and comparable in groups 2 and 3. We conclude that lowering Hb P(50) has opposing effects on TO(2 max) and O(2) extraction ratio, with the relative magnitude of these changes, which varies with PI(O(2)), determining VO(2 max). Although the lower O(2) extraction ratio of groups 2 vs. 3 suggests a decrease in tissue PO(2) diffusion gradient secondary to the low P(50), the lower O(2) extraction ratio of groups 1 vs. 2 suggests additional negative effects of sodium cyanate and/or chronically low Hb P(50) on tissue O(2) transfer.     

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

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

Exercise-induced hypoxemia in athletes: Role of inadequate hyperventilation

These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (PaO2) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO2max) range = 65-77 ml.kg-1.min-1] performed a normoxic graded exercise test on a cycle ergometer to VO2max at sea level. During incremental exercise at VO2max, 5 of the 12 subjects had ideal alveolar to arterial PO2 gradients (PA-aO2) of above 5 kPa (range 5-5.7) and a decline from resting PaO2 (delta PaO2) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise PA-aO2 of 4.0-4.3 kPa with delta PaO2 of 0.4-1.3 kPa while the remaining 3 subjects had PA-aO2 of 4.3-5 kPa with delta PaO2 between 1.7 and 2.0 kPa. The correlation between PAO2 and PaO2 at VO2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption vs PaO2 and arterial partial pressure of carbon dioxide vs PaO2 at VO2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.     

A new approach to assessing maximal aerobic power in children: the Odense School Child Study

In two experiments maximal aerobic power (VO2max) calculated from maximal mechanical power (Wmax) was evaluated in 39 children aged 9-11 years. A maximal multi-stage cycle ergometer exercise test was used with an increase in work load every 3 min. In the first experiment oxygen consumption was measured in 18 children during each of the prescribed work loads and a correction factor was calculated to estimate VO2max using the equation VO2max = 12.Wmax + 5.weight. An appropriate increase in work rate based on height was determined for boys (0.16 W.cm-1) and girls (0.15 W.cm-1) respectively. In the second experiment 21 children performed a maximal cycle ergometer exercise test twice. In addition to the procedure in the first experiment a similar exercise test was performed, but without measurement of oxygen uptake. Calculated VO2max correlated significantly (p less than 0.01) with those values measured in both boys (r = 0.90) and girls (r = 0.95) respectively, and the standard error of estimation for VO2max (calculated) on VO2max (measured) was less than 3.2%. Two expressions of relative work load (%VO2max and %Wmax) were established and found to be closely correlated. The relative work load in %VO2max could be predicted from the relative work load in %Wmax with an average standard error of 3.8%. The data demonstrate that calculated VO2max based on a maximal multi-stage exercise test provides an accurate and valid estimate of VO2max.     

Maximal aerobic capacity across age in healthy Hispanic and Caucasian women.

We tested the hypothesis that the age-related decline in maximal aerobic capacity, as measured by maximal oxygen uptake (VO(2 max)), is greater in Hispanic than in Caucasian women. We studied 146 healthy sedentary women aged 20-75 yr: 53 Hispanic (primarily of Mexican descent) and 93 Caucasian (non-Hispanic white). The groups did not differ in mean age, body mass, percent body fat, estimated physical activity-related energy expenditure, or education-based socioeconomic status (SES). During maximal exercise, respiratory exchange ratio, rating of perceived exertion, and percent predicted maximal heart rate were similar across age and ethnicity, suggesting equivalent maximum voluntary efforts in all subjects. VO(2 max) (ml x kg(-1) x min(-1)) was inversely related to age (P < 0.01) in Caucasian (r =-0.68) and Hispanic (r = -0.61) women. The absolute rate of decline in VO(2 max) with age was the same in the two groups (-0.31 ml x kg(-1) x min(-1) x yr(-1)). The relative rate of decline (% from age 25 yr) also was similar in the Caucasian (-9.0%) and Hispanic (-9.2%) women. When subjects of all ages were pooled, mean levels of VO(2 max) were similar in the two groups (approximately 28 ml x kg(-1) x min(-1)). These results, the first to our knowledge in Hispanics, indicate that mean levels of VO(2 max), as well as the rate of decline in VO(2 max) with age, are similar in healthy sedentary Hispanic and Caucasian women of similar SES. Thus it does not appear that Hispanic ethnicity per se modulates maximal aerobic capacity in this population.     

Living and training in moderate hypoxia does not improve VO2 max more than living and training in normoxia.

The objective of these experiments was to determine whether living and training in moderate hypoxia (MHx) confers an advantage on maximal normoxic exercise capacity compared with living and training in normoxia. Rats were acclimatized to and trained in MHx [inspired PO2 (PI(O2)) = 110 Torr] for 10 wk (HTH). Rats living in normoxia trained under normoxic conditions (NTN) at the same absolute work rate: 30 m/min on a 10 degrees incline, 1 h/day, 5 days/wk. At the end of training, rats exercised maximally in normoxia. Training increased maximal O2 consumption (VO2 max) in NTN and HTH above normoxic (NS) and hypoxic (HS) sedentary controls. However, VO2 max and O2 transport variables were not significantly different between NTN and HTH: VO2 max 86.6 +/- 1.5 vs. 86.8 +/- 1.1 ml x min(-1) x kg(-1); maximal cardiac output 456 +/- 7 vs. 443 +/- 12 ml x min(-1) x kg(-1); tissue blood O2 delivery (cardiac output x arterial O2 content) 95 +/- 2 vs. 96 +/- 2 ml x min(-1) x kg(-1); and O2 extraction ratio (arteriovenous O2 content difference/arterial O2 content) 0.91 +/- 0.01 vs. 0.90 +/- 0.01. Mean pulmonary arterial pressure (Ppa, mmHg) was significantly higher in HS vs. NS (P < 0.05) at rest (24.5 +/- 0.8 vs. 18.1 +/- 0.8) and during maximal exercise (32.0 +/- 0.9 vs. 23.8 +/- 0.6). Training in MHx significantly attenuated the degree of pulmonary hypertension, with Ppa being significantly lower at rest (19.3 +/- 0.8) and during maximal exercise (29.2 +/- 0.5) in HTH vs. HS. These data indicate that, despite maintaining equal absolute training intensity levels, acclimatization to and training in MHx does not confer significant advantages over normoxic training. On the other hand, the pulmonary hypertension associated with acclimatization to hypoxia is reduced with hypoxic exercise training.     

Deer mouse aerobic performance across altitudes: effects of developmental history and temperature acclimation

Aerobic physiology at high altitudes has been studied in many animals. Prior work on laboratory-bred deer mice (a species with a wide altitudinal range) showed depression of aerobic capacity at high altitude, even after acclimation. However, wild deer mice show no reduction in thermogenic performance at high altitude, and performance limits seem to be due to physiological and anatomical adjustments to environmental temperature and not to oxygen availability. We asked whether across-altitude performance differences exist in deer mice after accounting for temperature acclimation (approximately 5 degrees and 20 degrees -25 degrees C) and prenatal and neonatal development altitude (340 vs. 3,800 m). We measured maximal thermogenic oxygen consumption (VO2sum) in cold exposure and ran mice on a treadmill to elicit maximal exercise oxygen consumption (VO2max). We found a 10% reduction in VO2max at 3,800 m compared with that at 340 m; thus, the mice were able to compensate for most of the 37% reduction in oxygen availability at the higher altitude. Development altitude did not affect VO2max. There was no effect of test altitude or development altitude on VO2sum in warm-acclimated animals, but both test and development altitude strongly affected VO2sum in cold-acclimated mice, and compensation for hypoxia at 3,800 m was considerably less than that for exercise.     

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

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

The ergogenic effect of recombinant human erythropoietin on VO2max depends on the severity of arterial hypoxemia

Treatment with recombinant human erythropoietin (rhEpo) induces a rise in blood oxygen-carrying capacity (CaO(2)) that unequivocally enhances maximal oxygen uptake (VO(2)max) during exercise in normoxia, but not when exercise is carried out in severe acute hypoxia. This implies that there should be a threshold altitude at which VO(2)max is less dependent on CaO(2). To ascertain which are the mechanisms explaining the interactions between hypoxia, CaO(2) and VO(2)max we measured systemic and leg O(2) transport and utilization during incremental exercise to exhaustion in normoxia and with different degrees of acute hypoxia in eight rhEpo-treated subjects. Following prolonged rhEpo treatment, the gain in systemic VO(2)max observed in normoxia (6-7%) persisted during mild hypoxia (8% at inspired O(2) fraction (F(I)O(2)) of 0.173) and was even larger during moderate hypoxia (14-17% at F(I)O(2) = 0.153-0.134). When hypoxia was further augmented to F(I)O(2) = 0.115, there was no rhEpo-induced enhancement of systemic VO(2)max or peak leg VO(2). The mechanism highlighted by our data is that besides its strong influence on CaO(2), rhEpo was found to enhance leg VO(2)max in normoxia through a preferential redistribution of cardiac output toward the exercising legs, whereas this advantageous effect disappeared during severe hypoxia, leaving augmented CaO(2) alone insufficient for improving peak leg O(2) delivery and VO(2). Finally, that VO(2)max was largely dependent on CaO(2) during moderate hypoxia but became abruptly CaO(2)-independent by slightly increasing the severity of hypoxia could be an indirect evidence of the appearance of central fatigue.     

Continued divergence in VO2max of rats artificially selected for running endurance is mediated by greater convective blood O2 delivery.

We previously showed that after seven generations of artificial selection of rats for running capacity, maximal O2 uptake (VO2max) was 12% greater in high-capacity (HCR) than in low-capacity runners (LCR). This difference was due exclusively to a greater O2 uptake and utilization by skeletal muscle of HCR, without differences between lines in convective O2 delivery to muscle by the cardiopulmonary system (QO2max). The present study in generation 15 (G15) female rats tested the hypothesis that continuing improvement in skeletal muscle O2 transfer must be accompanied by augmentation in QO2max to support VO2max of HCR. Systemic O2 transport was studied during maximal normoxic and hypoxic exercise (inspired PO2 approximately 70 Torr). VO2max divergence between lines increased because of both improvement in HCR and deterioration in LCR: normoxic VO2max was 50% higher in HCR than LCR. The greater VO2max in HCR was accompanied by a 41% increase in QO2max: 96.1 +/- 4.0 in HCR vs. 68.1 +/- 2.5 ml stpd O2 x min(-1) x kg(-1) in LCR (P < 0.01) during normoxia. The greater G15 QO2max of HCR was due to a 48% greater stroke volume than LCR. Although tissue O2 diffusive conductance continued to increase in HCR, tissue O2 extraction was not significantly different from LCR at G15, because of the offsetting effect of greater HCR blood flow on tissue O2 extraction. These results indicate that continuing divergence in VO2max between lines occurs largely as a consequence of changes in the capacity to deliver O2 to the exercising muscle.     

Time to exhaustion and time spent at a high percentage of VO2max in severe intensity domain in children and adults

The aim of the study was to compare time spent at a high percentage of VO2max (>90% of VO2max) (ts90%), time to achieve 90% of VO2max (ta90%), and time to exhaustion (TTE) for exercise in the severe intensity domain in children and adults. Fifteen prepubertal boys (10.3 ± 0.9 years) and 15 men (23.5 ± 3.6 years) performed a maximal graded exercise to determine VO2max, maximal aerobic power (MAP) and power at ventilatory threshold (PVTh). Then, they performed 4 constant load exercises in a random order at PVTh plus 50 and 75% of the difference between MAP and PVTh (PΔ50 and PΔ75) and 100 and 110% of MAP (P100 and P110). VO2max was continuously monitored. The P110 test was used to determine maximal accumulated oxygen deficit (MAOD). No significant difference was found in ta90% between children and adults. ts90% and TTE were not significantly different between children and adults for the exercises at PΔ50 and PΔ75. However, ts90% and TTE during P100 (p < 0.05 and p < 0.01, respectively) and P110 (p < 0.001) exercises were significantly shorter in children. Children had a significantly lower MAOD than adults (34.3 ± 9.4 ml · kg vs. 53.6 ± 11.1 ml · kg). A positive relationship (p < 0.05) was obtained between MAOD and TTE values during the P100 test in children. This study showed that only for intensities at, or higher than MAP, lower ts90% in children was linked to a reduced TTE, compared to adults. Shorter TTE in children can partly be explained by a lower anaerobic capacity (MAOD). These results give precious information about exercise intensity ranges that could be used in children's training sessions. Moreover, they highlight the implication of both aerobic and anaerobic processes in endurance performances in both populations.     

Maximal aerobic capacity for repetitive lifting: comparison with three standard exercise testing modes

A multi-stage, repetitive lifting maximal oxygen uptake (VO2max) test was developed to be used as an occupational research tool which would parallel standard ergometric VO2max testing procedures. The repetitive lifting VO2max test was administered to 18 men using an automatic repetitive lifting device. An intraclass reliability coefficient of 0.91 was obtained with data from repeated tests on seven subjects. Repetitive lifting VO2max test responses were compared to those for treadmill, cycle ergometer and arm crank ergometer. The mean +/- SD repetitive lifting VO2max of 3.20 +/- 0.42 l.min-1 was significantly (p less than 0.01) less than treadmill VO2max (delta = 0.92 l.min-1) and cycle ergometer VO2max (delta = 0.43 l.min-1) and significantly greater than arm crank ergometer VO2max (delta = 0.63 l.min-1). The correlation between repetitive lifting oxygen uptake and power output was r = 0.65. VO2max correlated highly among exercise modes, but maximum power output did not. The efficiency of repetitive lifting exercise was significantly greater than that for arm cranking and less than that for leg cycling. The repetitive lifting VO2max test has an important advantage over treadmill or cycle ergometer tests in the determination of relative repetitive lifting intensities. The individual curves of VO2 vs. power output established during the multi-stage lifting VO2max test can be used to accurately select work loads required to elicit given percentages of maximal oxygen uptake.     

Effects of incomplete pulmonary gas exchange on VO2 max

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)     

高原青少年最大有氧能力的研究

采用自行车递增负荷运动试验,对青海西宁地区(海拔2260m)86名13～16岁男女中学生的最大摄氧量,无氧阈以及血氧饱和度等指标进行了测定。结果表明,高原青少年的最大摄氧量较低,而无氧阈则较高。血氧饱和度随负荷增加逐渐降低,在接近极限负荷时迅速下降,提示高原低氧是限制最大运动能力的主要因素。无氧阈较高说明高原青少年组织细胞利用氧的能力提高,这是对高原低氧环境长期适应的结果。     

Skeletal muscle oxygenation during incremental exercise

The purpose of this study was to investigate the relationship between muscle oxygenation level at exhaustion and maximal oxygen uptake (VO2max) in an incremental cycling exercise. Nine male subjects took part in an incremental exhaustive cycling exercise, and then cuff occlusion was performed. Changes in oxy-(deltaHbO2) and deoxy-(deltaHb) hemoglobin concentrations in the vastus lateralis muscle were measured with a near infrared spectroscopy (NIRS). Muscle oxygenation during incremental exercise was expressed as a percentage (%Moxy) of the maximal range observed during an arterial occlusion as the lower reference point. A systematic decrease was observed in %Moxy with increasing intensity. A significant relationship was observed between %Moxy at exhaustion and VO2max (p < 0.01). We concluded that the one of the limiting factor of VO2max is the muscle oxygen diffusion capacity, and %Moxy during exercise could be one of the indexes of muscle oxygen diffusion capacity.     

Maximal oxygen consumption in relation to subordinate traits in lines of house mice selectively bred for high voluntary wheel running.

We studied relations between maximal O2 consumption (VO2 max) during forced exercise and subordinate traits associated with blood O2 transport and cellular respiration in four lines of mice selectively bred for high voluntary wheel running (S lines) and their four nonselected control (C) lines. Previously, we reported VO2 max of 59 females at three Po2 (hypoxia = 14% O2, normoxia = 21%, hyperoxia = 30%). Here, we test the hypothesis that variation in VO2 max can be explained, in part, by hemoglobin concentration and Po2 necessary to obtain 50% O2 saturation of Hb (an estimate of Hb affinity for O2) of the blood as well as citrate synthase activity and myoglobin concentration of ventricles and gastrocnemius muscle. Statistical analyses controlled for body mass, compared S and C lines, and also considered effects of the mini-muscle phenotype (present only in S lines and resulting from a Mendelian recessive allele), which reduces hindlimb muscle mass while increasing muscle mass-specific aerobic capacity. Although S lines had higher VO2 max than C, subordinate traits showed no statistical differences when the presence of the mini-muscle phenotype was controlled. However, subordinate traits did account for some of the individual variation in VO2 max. Ventricle size was a positive predictor of VO2 max at all three Po2. Blood Hb concentration was a positive predictor of VO2 max in S lines but a negative predictor in C lines, indicating that the physiological underpinnings of VO2 max have been altered by selective breeding. Mice with the mini-muscle phenotype had enlarged ventricles, with higher mass-specific citrate synthase activity and myoglobin concentration, which may account for their higher VO2 max in hypoxia.     

A steady-state model of maximal oxygen and carbon dioxide transport in anuran amphibians

A steady-state model, incorporating pulmonary ventilation, pulmonary diffusion capacity, cardiovascular transport capacity, and tissue diffusion capacity, was developed to describe the maximal O2 and CO2 transport capacity for an anuran amphibian (Bufo). Solution of the model by iterative calculation closely predicted 1) the empirical maximal O2 consumption (VO2max) for Bufo, 2) variation in empirical VO2max for three other genera (Rana, Xenopus, Scaphiopus), and the empirically observed effects on VO2max of 3) hypobaric hypoxia, 4) artificially induced anemia, and 5) beta-blockade of heart rate increment with activity. The model indicates that cardiovascular transport is the rate-limiting step to VO2max in amphibians and that an increase in circulatory O2 transport is a major physiological adaptation for increasing total aerobic capacity. CO2 transport and body fluid PCO2 values were primarily determined by pulmonary ventilatory capacity, and to a lesser extent by cardiovascular transport. The model should be generally applicable to other terrestrial vertebrates.