Ventilation's role in the decline in V-over-dot-O2 and SaO2 in acute hypoxic exercise

The role of ventilation in the response in aerobic capacity and arterial oxygen saturation (SaO(2)) to acute hypoxic exercise was studied in 13 healthy active men divided into two groups based on their normoxic maximal exercise (V) over dot(E)/(V) over dotO(2), (LOW less than or equal to 27.7; HIGH greater than or equal to 30.2) and PAO(2) estimates (LOW less than or equal to 107 mm Hg; HIGH greater than or equal to 110 mm Hg). Groups performed two incremental progressive maximal cycle exercise ((V) over dot O-2max) 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 ((V) over dot (E),(V) over dot(E)/(V) over dot O-2, and (V) over dot(E)/(V) over dot CO2) during both normoxic and hypoxic exercise (P less than or equal to 0.05). During maximal hypoxic exercise, LOW had a greater decline in both (V) over dot (2max) (21.6 mL.kg(-1).min(-1) vs 16.6 mL.kg(-1).min(-1)) and SaO(2) (31.9% vs 22.1%). Modest but significant correlations were identified between normoxic (V) over dot(E)/(V) over dot(2), and the decline in both (V) over dot(2 max) (r = -0.62) and SaO(2) (r = -0.60). No correlations were identified between rHVR and any ventilatory response or SaO(2). 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.