Multiple variables explain the variability in the decrement in V˙O2max during acute hypobaric hypoxia. Med. Sci. Sports Exerc., Vol. 30, No. 6, pp. 869-879, 1998.
Purpose: We used multiple regression analyses to determine the relationships between the decrement in sea level (SL, 760 Torr) V˙O2max during hypobaric hypoxia (HH) and variables that could alter or be related to the decrement in V˙O2max.
Methods: HH conditions consisted of 682 Torr, 632 Torr, and 566 Torr, and the measured independent variables were SL-V˙O2max, SL lactate threshold (SL-LT), the change in hemoglobin saturation at V˙O2max between 760 and 566 Torr (ΔSaO2max), lean body mass (LBM), and gender. Male (N = 14) and female (N = 14) subjects of varied fitness, training status, and residential altitude (1,640-2,460 m) completed cycle ergometry tests of V˙O2max at each HH condition under randomized and single-blinded conditions.
Results: V˙O2max decreased significantly from 760 Torr after 682 Torr (∼915 m) (3.5 ± 0.9 to 3.4 ± 0.8 L·min−1, P = 0.0003). Across all HH conditions, the slope of the relative decrement in V˙O2max (%V˙O2max) during HH was −9.2%/100 mm Hg (−8.1%/1000 m) with an initial decrease from 100% estimated to occur below 705 Torr (610 m). Step-wise multiple regression revealed that SL-V˙O2max, SL-LT, ΔSaO2max, LBM, and gender each significantly combined to account for 89.03% of the variance in the decrement in V˙O2max (760-566 Torr) (P < 0.001).
Conclusions: Individuals who have a combination of a large SL-V˙O2max, a small SL-LT (V˙O2, L·min−1), greater reductions in ΔSaO2max, a large LBM, and are male have the greatest decrement in V˙O2max during HH. The unique variance explanation afforded by SL-LT, LBM, and gender suggests that issues pertaining to oxygen diffusion within skeletal muscle may add to the explanation of between subjects variability in the decrement in V˙O2max during HH.
Submitted for publication October 1997.
Accepted for publication January 1998.
We acknowledge the generous support provided by David James, M.D. (Director, Cardiopulmonary Laboratory, Pulmonary Division, Veterans Administration Hospital, Albuquerque, NM) for allowing us to use the Poet pulse oximeter and Corval electronically braked cycle ergometer. Gratitude is also expressed to Paul Montner, M.D., for providing validation data of the Poet pulse oximeter from arterial blood during conditions at rest and during incremental exercise to V˙O2max.
Address for correspondence: R. A. Robergs, Ph.D., Johnson Center, B143, The University of New Mexico, Albuquerque, NM 87131. E-mail: firstname.lastname@example.org.