A B S T R A C T This study represented an initial attempt, by means of cross-sectional investigation, to determine the effects of chronic exposure to high altitude on pulmonary gas exchange. Single-breath DLco and its components were determined at rest and during muscular work in two groups of healthy, non-smoking, sea level natives who had initiated 1-16 yr of residence at 3,100 m altitude either during physical maturation (at age 10±4 yr) or as adults (at age 26±4 yr). The relative degree of acclimatization achieved in these lowland residents was assessed through their comparison both with normal sea-level values and with two additional groups of short-term sojourners and natives to 3,100 m. DLco at rest and work was significantly elevated above normal and above sojourner values in both groups of resident lowlanders at 3,100 m. The high DLCo in the native to 3,100 m was closely approximated in the younger resident lowlander at rest, but only during exercise in the adult resident lowlander. The high DLco at rest and during exercise in the resident lowlanders was not attributable to differences in Hb concentration or in alveolar lung volume; and was accompanied primarily by an increased estimated Dmco and to a lesser extent by an expanded Vc. The interpretation and implications of these findings were limited by the low quantitative capability of Vc and Dmco estimates and by the cross-sectional nature of the study. Nevertheless, the higher than normal DLco and Dmco in the non-native, long-term resident of 3,100 m was substantial, highly significant statistically, and consistent over a wide range of metabolic rates at rest and work. These data provide, then, a reasonable rationale upon which longitudinal experiments may be based to determine the true effects of chronic hypoxia on pulmonary gas exchange in man.
In healthy human sojourners to 3,100 m we studied exercise-induced shifts in HbO2 dissociation: their regulation in femoral venous blood and their net effect on estimated capillary PO2 (PC-O2) in working skeletal muscle. Prolonged heavy work effected an increase of 10.3 plus or minus 0.9 mmHg in in vivo P50 (7.30 PH-v, 41 degrees C-v, and 45 Pv-CO2); due entirely to the additive effects of increased venous temperature and [H+]. The rightward curve shift during work at 3,000 m, compared to that at 250 m, produced a similar increase in in vivo P50 but a reduced net effect on PC-O2, because Cv-02 at 3,100 m was reduced similar to 2 ml/100 ml to the lower converging portions of the curve. The lower Cv-O2 (and Pv-O2) at 3,100 M was attributable to a small decrease in total systemic blood flow. The net effect of the rightward curve shift during exercise on mean to end-capillary PO2 was positive in most cases (+1 to +8 mmHg PCO2). However, it was shown that the levels of mean to end-capillary PO2 (28-13 mmHg), which would have been obtained during exercise in the absence of any rightward curve shift, were more than adequate to sustain a steady state of aerobic energy production in working skeletal muscle. These data do not support the concept of a significant contribution to oxygen delivery to working skeletal muscle from in vivo shifts in HbO2 dissociation, during either acclimatization to high altitude or during prolonged muscular work.
A good deal of information is available on the influence of hypoxia, or altitude, on physical performance, especially during prolonged exercise (2, 3, 4, 7, 8, 12, 18-22, 29, 33, 34-37, 41, 44, 45, 52). But, more than any other recent event, it was the Olympic Games in Mexico City that aroused so much interest in the problems surrounding altitude and sport performance; Four main questions were, at that time, asked.1. To what extent is performance affected at moderate altitude (about 2,000m -6,600 ft)?2. Can the negative effects be overcome by the processes of adaptation; to what extent can they be overcome; and how long does adaptation take? 3. Can extremely hard training at this altitude lead to any bodily harm?4. Can the performance at sea level be improved by training at altitude?This last question is still of considerable interest as we are constantly confronted with athletes who want to carry out some portion of their training programme at altitude to improve their performance at sea level. The Delivery of EnergyThe two main energy delivering pathways in the resynthesis of adenosine triphosphate (ATP) should here be recalled to mind:1. The breakdown of energy-yielding substrates without the participation of oxygen; that is, the anaerobic energy delivery.2. The degradation of substrates in which oxygen is the ultimate hydrogen acceptor; that is, the aerobic process. Figure 1 shows the shift of anaerobic to aerobic energy delivery in relation to the work time at sea level for individuals with high maximal power for both. For a maximal effort of less than two minutes duration, the anaerobic processes dominate, but for muscular work of more than two minutes duration the energy cost must be defrayed primarily through oxidative processes (29 reduced when the oxygen content in the inspired air, and therefore the oxygen content in the blood, is also red uced.In the following discussion the influence of adaptive mechanisms on the aerobic and anaerobic processes during altitude training must be separated.The values for arterial oxygen saturation, obtained under resting conditions at various altitudes, or using hypoxia-simulating gas mixtures, are reduced relative to those obtained at sea level (Fig. 2) (13,29). The effect of this decreasing arterial oxygen saturation is to reduce the ability to perform prolonged work.There is an actual diminution of the maximal oxygen uptake -or physical working capacity -for some days after arrival in Mexico City (Fig. 4). During residence at Mexico City (2,250m -7,382 ft) there is, however, an improvement as a resuft of various adaptive mechanisms; the maximal capacity as measured at sea level, nevertheless, was not reached even after prolonged residence. The measurements of different research groups show considerable variation in the degree both of diminution and of readjustment that can occur in maximal capacity (2,18,29,44,50,52 As a result of the lower arterial oxygen supply due to breathing a 15.9% hypoxic mixture under the same conditions of exercise, the coronary arterio-v...
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