Hyperventilation‐induced hypocapnic alkalosis slows the adaptation of pulmonary O2 uptake during the transition to moderate‐intensity exercise
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abstract
The effect of voluntary hyperventilation‐induced hypocapnic alkalosis (RALK) on pulmonary O2 uptake () 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). 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, response (τ) 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 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.
