Hyperventilation-induced hypocapnic alkalosis slows the adaptation of pulmonary O2 uptake during the transition to moderate-intensity exercise

摘要

The effect of voluntary hyperventilation-induced hypocapnic alkalosis (RALK) on pulmonary O2 uptake (V˙o2) kinetics and muscle deoxygenation was examined in young male adults (n = 8) during moderate-intensity exercise. Subjects performed five repetitions of a step-transition in work rate from 20 W cycling to a work rate corresponding to 90% of the estimated lactate threshold during control (CON; , ∼40 mmHg) and during hyperventilation (RALK; , ∼20 mmHg). V˙o2 was measured breath-by-breath and relative concentration changes in muscle deoxy- (ΔHHb), oxy- (ΔO2Hb) and total (ΔHbtot) haemoglobin were measured continuously using near-infrared (NIR) spectroscopy (Hamamatsu, NIRO 300). The time constant for the fundamental, phase 2, V˙o2 response (τV˙o2) was greater (P < 0.05) in RALK (48 ± 11 s) than CON (31 ± 9 s), while τHHb was similar between conditions (RALK, 12 ± 4 s; CON, 11 ± 4 s). The ΔHbtot was lower (P < 0.05) in RALK than CON, prior to (RALK, −3 ± 5 μmol l⁻¹; CON, −1 ± 4 μmol l⁻¹) and at the end (RALK, 1 ± 6 μmol l⁻¹; CON, 5 ± 5 μmol l⁻¹) of moderate-intensity exercise. Although slower adaptation of V˙o2 during RALK may be related to an attenuated activation of PDH (and other enzymes) and provision of oxidizable substrate to the mitochondria (i.e. metabolic inertia), the present findings also suggest a role for a reduction in local muscle perfusion and O2 delivery.