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After effects of chronic hypoxia on VO2 kinetics and on O2 deficit and debt.

Single breath O2 consumption (PB = 730, FI02 = 0.21) was measured at rest, during 10 min cycloergometric exercise at 125 W, and in the following recovery phase in seven subjects before, and 12 days after 6 weeks at 5,200 m or above. Peak blood lactate after exercise (Lâb) was measured. O2 deficits and debts and half times (t1/2) of the VO2 on- and off-kinetics were calculated. Before acclimatization, the VO2 on- and off-responses were close to a single exponential with t1/2 = 30 s. After return to sea level, the VO2 on-response curves were less steep in the initial phase, becoming closer to sigmoid. The t1/2, independent of the shape of the underlying function, was approximately 10 s longer. The VO2 off-responses during the initial 4 min of recovery were the same before and after acclimatization. Average O2 deficit was approximately 320 ml larger after acclimatization: the fast component of O2 debt was similar. Since steady state VO2 and Lâb were the same, the O2 deficit difference can be attributed to a greater utilization of O2 stores. Of these, about 1/3 is explained in terms of increased mixed venous blood O2 stores, due to increased [Hb] (16.6 vs 14.9 g X dl-1), while the remainder is ascribed essentially to increased Mb-bound O2. O2 stores utilization and replenishment is presumed to occur when muscle metabolism is low; as a consequence, while it is clearly detectable from the shape of the initial phase of the VO2 on-response, during recovery it is spread throughout, thus becoming more difficult to appreciate.