Recovery processes after repeated supramaximal exercise at the altitude of 4,350 m

We tested the hypothesis that prolonged exposure to high altitude would impair the restoration of muscle power during repeated sprints. Seven subjects performed two 20-s Wingate tests (WT1 and WT2) separated by 5 min of recovery, at sea level (N) and after 5-6 days at 4,350 m (H). Mean power output (MPO) and O2 deficit were measured during WT. O2 uptake (VO2) and ventilation (VE) were measured continuously. Blood velocity in the femoral artery (FBV) was recorded by Doppler ultrasound during recovery. Arterialized blood pH and concentrations of bicarbonate ([HCO3-]), venous plasma lactate ([La-]), norepinephrine ([NE]), and epinephrine ([Epi]) were measured before and after WT1 and WT2. MPO decreased between WT1 and WT2 by 6.9% in N (P < 0.05) and by 10.7% in H (P < 0.01). H did not further decrease MPO. O2 deficit decreased between WT1 and WT2 in H only (P < 0.01). Peak VO2 after WT was reduced by 30-40% in H (P < 0.01), but excess postexercise O2 consumption was not significantly lowered in H. During recovery in H compared with N, VE, exercise-induced acidosis, and [NE] were higher, [Epi] tented to be higher, [La-] was not altered, and [HCO3-] and FBV were lower. The similar [La-] accumulation was associated with a higher exercise-induced acidosis and a larger increase in [NE] in H. We concluded from this study that prolonged exposure to high altitude did not significantly impair the restoration of muscle power during repeated sprints, despite a limitation of aerobic processes during early recovery.