Response to an aerobic training intervention in young adults depends on ponderal index at birth.

Poor fetal growth is associated with later-life changes in adult body composition and decrements in muscle strength and morphology. Few studies have investigated the association of poor fetal growth with whole-body exercise. The purpose of this study was to investigate the association of poor fetal growth with the maximal oxygen consumption (VO(2)max), lactate levels during exercise and the response to aerobic training. Thirty-six college-aged men and women (aged 20.8 ± 0.3 years), born to term (37-42 weeks gestation), were recruited to participate in an 8-week training program. Participants comprised two groups, high ponderal index (HIGHPI) and low ponderal index (LOWPI) (n = 18/group), identified as falling above and below the 10th percentile of the ponderal index (g/cm(3))-for-gestational age distribution, respectively. The HIGHPI and LOWPI were matched pair-wise on age, sex, body mass index and pre-study physical activity patterns. The LOWPI and HIGHPI did not differ significantly before training, after training or with a change (Δ) in training VO(2)max (l/min or ml/min kg/fat-free mass (FFM)). However, LOWPI had significantly lower pre-training lactate levels at similar levels of relative work output (P = 0.016), and significantly smaller decreases in lactate at a fixed level of absolute work after training (P = 0.044). These differences were independent of pre-training aerobic fitness, the change in fitness with training, diet and fuel substrate choice. The lower lactate of untrained LOWPI subjects during exercise could reflect metabolic reprograming due to intrauterine growth restriction, or could be secondary to muscle morphological and/or fiber-type distribution changes that also associate with poor fetal growth.

Limits on inferring genetic adaptation to high altitude in Himalayan and Andean populations.

Many physiological and anthropological studies have investigated the unique Andean and Himalayan populations that have resided for many hundreds of generations at high altitude (HA). A nonscientific survey of the extant literature reveals a relatively liberal tradition of inferring genetic (evolutionary) adaptation to HA in these groups, often based on limited evidence and/or based on study designs insufficient to fully address the issue. In order to provide some perspective, I review relevant methodological issues that should be considered before evolutionary inference is made. On the whole, this paper takes a conservative stance and cautions against evolutionary inference based on the serious limitations of currently applied research approaches.

Genetic and environmental adaptation in high altitude natives. Conceptual, methodological, and statistical concerns.

A great number of physiological and anthropological studies have investigated Andean and Himalayan populations native to high altitude (HA). A non-scientific survey of the extant literature reveals a relatively liberal tradition of inferring genetic (evolutionary) adaptation to HA in these groups, often based on limited evidence and/or based on study designs insufficient to fully address the issue. Rather than review the evidence for or against genetic adaptation, and in order to provide some perspective, this paper will review relevant conceptual, methodological, and statistical issues that are germane to the study of HA native human groups. In particular, focus will be on the limitations of the most common research approach which bases evolutionary inference on the comparison of phenotypic mean differences between highland and lowland native populations. The migrant study approach is discussed, as is a relatively new approach based on genetic admixture in hybrid populations.

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.

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment.

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial PO(2) (Pa(O(2))) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O(2) uptake (VO(2 max)) = 51 ml. kg(-1). min(-1)]. They were studied in random order (C or R), with a fast VO(2 max) protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% of VO(2 max) (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in VO(2 max) between R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of VO(2 max). At 90% of VO(2 max), Pa(O(2)) was lower during R (mean +/- SE = 94 +/- 2 Torr) than during C (105 +/- 2 Torr, P < 0.0001), as was ventilation (85.2 +/- 3.8 vs. 98.2 +/- 4.4 l/min BTPS, P < 0.0001) and cardiac output (19.1 +/- 0.6 vs. 21.1 +/- 1.0 l/min, P < 0.001). Arterial PCO(2) (32.0 +/- 0.5 vs. 30.0 +/- 0.6 Torr, P < 0.001) and alveolar-arterial O(2) difference (A-aDO(2); 22 +/- 2 vs. 16 +/- 2 Torr, P < 0.0001) were greater during R. Pa(O(2)) and A-aDO(2) were similar between slow and fast. Nadir Pa(O(2)) was

Effect of developmental and ancestral high-altitude exposure on VO(2)peak of Andean and European/North American natives.

Peak oxygen consumption (VO(2)peak) was measured in 150 adult males (18-35 years old) in Bolivia, using a complete migrant study design to partition developmental from ancestral (genetic) effects of high-altitude (HA) exposure. High-altitude natives (HANs, Aymara/Quechua ancestry, n = 75) and low-altitude natives (LANs, European/North American ancestry, n = 75) were studied at high altitude (3,600-3,850 m) and near sea level (420 m). HAN and LAN migrant groups to a nonnative environment were classified as: multigeneration migrants, born and raised in a nonnative environment; child migrants who migrated to the nonnative environment during the period of growth and development (0-18 years old); and adult migrants who migrated after 18 years of age. Variability in VO(2)peak due to high-altitude adaptation was modeled by covariance analysis, adjusting for fat-free mass and physical activity (training) differences between groups. A trend for increased VO(2)peak with increasing developmental high-altitude exposure in migrant groups did not reach statistical significance, but low statistical power may have limited the ability to detect this effect. HANs and LANs born, raised, and tested at high altitude had similar VO(2)peak values, indicating no genetic effect, or an effect much smaller than that reported previously in the literature. There was no functional correlation between forced vital capacity and VO(2)peak, within or across groups. These results do not support the hypothesis that Andean HANs have been selected to express a greater physical work capacity in hypoxia.

Measurement of cardiac output during exercise by open-circuit acetylene uptake.

Noninvasive measurement of cardiac output (QT) is problematic during heavy exercise. We report a new approach that avoids unpleasant rebreathing and resultant changes in alveolar PO(2) or PCO(2) by measuring short-term acetylene (C(2)H(2)) uptake by an open-circuit technique, with application of mass balance for the calculation of QT. The method assumes that alveolar and arterial C(2)H(2) pressures are the same, and we account for C(2)H(2) recirculation by extrapolating end-tidal C(2)H(2) back to breath 1 of the maneuver. We correct for incomplete gas mixing by using He in the inspired mixture. The maneuver involves switching the subject to air containing trace amounts of C(2)H(2) and He; ventilation and pressures of He, C(2)H(2), and CO(2) are measured continuously (the latter by mass spectrometer) for 20-25 breaths. Data from three subjects for whom multiple Fick O(2) measurements of QT were available showed that measurement of QT by the Fick method and by the C(2)H(2) technique was statistically similar from rest to 90% of maximal O(2) consumption (VO(2 max)). Data from 12 active women and 12 elite male athletes at rest and 90% of VO(2 max) fell on a single linear relationship, with O(2) consumption (VO(2)) predicting QT values of 9.13, 15.9, 22.6, and 29.4 l/min at VO(2) of 1, 2, 3, and 4 l/min. Mixed venous PO(2) predicted from C(2)H(2)-determined QT, measured VO(2), and arterial O(2) concentration was approximately 20-25 Torr at 90% of VO(2 max) during air breathing and 10-15 Torr during 13% O(2) breathing. This modification of previous gas uptake methods, to avoid rebreathing, produces reasonable data from rest to heavy exercise in normal subjects.