Ventilation's role in the decline in VO2maxand SaO2in acute hypoxic exercise

GAVIN, TIMOTHY P.; DERCHAK, P. ALEXANDER; STAGER, JOEL M.

Medicine & Science in Sports & Exercise:
Clinical Sciences: Clinically Relevant
Abstract

The role of ventilation in the response in aerobic capacity and arterial oxygen saturation (SaO2) to acute hypoxic exercise was studied in 13 healthy active men divided into two groups based on their normoxic maximal exercise ˙VE/˙VO2 (LOW ≤ 27.7; HIGH ≥ 30.2) and PAO2 estimates (LOW ≤ 107 mm Hg; HIGH ≥ 110 mm Hg). Groups performed two incremental progressive maximal cycle exercise(˙VO2max) tests: normoxia (FIO2 = 20.9%) and acute hypoxia(FIO2 = 13.3%). To evaluate the influence of hypoxic ventilatory drive on ventilation, resting hypoxic ventilatory response (rHVR) was measured. LOW demonstrated lower ventilatory responses (˙VE,˙VE/˙VO2, and ˙VE/˙VCO2) during both normoxic and hypoxic exercise (P ≤ 0.05). During maximal hypoxic exercise, LOW had a greater decline in both ˙VO2max (21.6 mL·kg-1·min-1 vs 16.6 mL·kg-1·min-1) and SaO2 (31.9% vs 22.1%). Modest but significant correlations were identified between normoxic˙VE/˙VO2 and the decline in both ˙VO2max (r =-0.62) and SaO2 (r = -0.60). No correlations were identified between rHVR and any ventilatory response or SaO2. In summary, the results from this study suggest that a low exercise-induced hyperventilatory response is a significant mechanism in the arterial desaturation observed during hypoxic exercise and the decline in aerobic capacity associated with this desaturation. However, the ventilatory response to hypoxic exercise is not dependent upon hypoxic ventilatory drive.

Author Information

Human Performance Laboratory, Department of Kinesiology, Indiana University, Bloomington, IN 47405

Submitted for publication October 1996.

Accepted for publication September 1997.

The authors wish to thank Drs. William F. Brechue, Craig A. Harms, and Russell S. Richardson for their review and comments regarding this manuscript. This study was supported in part by a grant from the Indiana University School of Health, Physical Education, and Recreation (HPER) and in part by a grant from the Graduate School at Indiana University.

Address for correspondence: Timothy P. Gavin, Department of Medicine, University of California, San Diego, LaJolla, CA 920930623. E-mail:tgavin@ucsd.edu.

©1998The American College of Sports Medicine