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This study compared the ventilation response to an incremental ergometer exercise at two altitudes: 633 mmHg (resident altitude = 1,600 m) and following acute decompression to 455 mmHg (≈4,350 m altitude) in eight male cyclists and runners. At 455 mmHg, the VESTPD at RER <1.0 was significantly lower and the VEBTPS was higher because of higher breathing frequency; at VO2max, both VESTPD and VEBTPS were not significantly different. As percent of VO2max, the VEBTPS was nearly identical and VESTPD was 30% lower throughout the exercise at 455 mmHg. The lower VESTPD at lower pressure differs from two classical studies of acclimatized subjects (Silver Hut and OEII), where VESTPD at submaximal workloads was maintained or increased above that at sea level. The lower VESTPD at 455 mmHg in unacclimatized subjects at submaximal workloads results from acute respiratory alkalosis due to the initial fall in HbO2 (≈0.17 pHa units), reduction in PACO2 (≈5 mmHg) and higher PAO2 throughout the exercise, which are partially pre-established during acclimatization. Regression equations from these studies predict VESTPD from VO2 and P B in unacclimatized and acclimatized subjects. The attainment of ventilatory acclimatization to altitude can be estimated from the measured vs. predicted difference in VESTPD at low workloads after arrival at altitude.

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Physiology International
J.A. Loeppky
R.M. Salgado
A.C. Sheard
D.O. Kuethe
, and
C.M. Mermier


Reports of VO2 response differences between normoxia and hypoxia during incremental exercise do not agree. In this study VO2 and V E were obtained from 15-s averages at identical work rates during continuous incremental cycle exercise in 8 subjects under ambient pressure (633 mmHg ≈1,600 m) and during duplicate tests in acute hypobaric hypoxia (455 mmHg ≈4,350 m), ranging from 49 to 100% of VO2 peak in hypoxia and 42–87% of VO2 peak in normoxia. The average VO2 was 96 mL/min (619 mL) lower at 455 mmHg (n.s. P = 0.15) during ramp exercises. Individual response points were better described by polynomial than linear equations (mL/min/W). The V E was greater in hypoxia, with marked individual variation in the differences which correlated significantly and directly with the VO2 difference between 455 mmHg and 633 mmHg (P = 0.002), likely related to work of breathing (W b ). The greater V E at 455 mmHg resulted from a greater breathing frequency. When a subject's hypoxic ventilatory response is high, the extra work of breathing reduces mechanical efficiency (E). Mean ∆E calculated from individual linear slopes was 27.7 and 30.3% at 633 and 455 mmHg, respectively (n.s.). Gross efficiency (GE) calculated from mean VO2 and work rate and correcting for W b from a V E –VO2 relationship reported previously, gave corresponding values of 20.6 and 21.8 (P = 0.05). Individual variation in V E among individuals overshadows average trends, as also apparent from other reports comparing hypoxia and normoxia during progressive exercise and must be considered in such studies.

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