Effect of voluntary hyperventilation with supplemental CO2 on pulmonary O2 uptake and leg blood flow kinetics during moderate‐intensity exercise
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New findingsWhat is the central question of this study?Voluntary hyperventilation that induces hypocapnic alkalosis (HYPO) is associated with slowed adaptation of O2 uptake and leg blood flow during moderate exercise; however, it is unknown whether hypocapnia, alkalosis and/or the hyperventilation manoeuvre is related to these observations.What is the main finding and its importance?We included a condition with the same work of breathing as HYPO, but the fall in CO2 was prevented by the addition of higher CO2 to the inspirate (normocapnia). This condition demonstrated that hypocapnia/alkalosis was responsible for the slower leg blood flow response; however, the act of hyperventilation itself also had a role to play in the slower O2 uptake kinetics.Pulmonary O2 uptake () and leg blood flow (LBF) kinetics were examined at the onset of moderate‐intensity exercise, during hyperventilation with and without associated hypocapnic alkalosis. Seven male subjects (25 ± 6 years old; mean ± SD) performed alternate‐leg knee‐extension exercise from baseline to moderate‐intensity exercise (80% of estimated lactate threshold) and completed four to six repetitions for each of the following three conditions: (i) control [CON; end‐tidal partial pressure of CO2 () ∼40 mmHg], i.e. normal breathing with normal inspired CO2 (0.03%); (ii) hypocapnia (HYPO; ∼20 mmHg), i.e. sustained hyperventilation with normal inspired CO2 (0.03%); and (iii) normocapnia (NORMO; ∼40 mmHg), i.e. sustained hyperventilation with elevated inspired CO2 (∼5%). The was measured breath by breath using mass spectrometry and a volume turbine. Femoral artery mean blood velocity was measured by Doppler ultrasound, and LBF was calculated from femoral artery diameter and mean blood velocity. Phase 2 kinetics (τ) was different (P < 0.05) amongst all three conditions (CON, 19 ± 7 s; HYPO, 43 ± 17 s; and NORMO, 30 ± 8 s), while LBF kinetics (τLBF) was slower (P < 0.05) in HYPO (31 ± 9 s) compared with both CON (19 ± 3 s) and NORMO (20 ± 6 s). Similar to previous findings, HYPO was associated with slower and LBF kinetics compared with CON. In the present study, preventing the fall in end‐tidal (NORMO) restored LBF kinetics, but not kinetics, which remained ‘slowed’ relative to CON. These data suggest that the hyperventilation manoeuvre itself (i.e. independent of induced hypocapnic alkalosis) may contribute to the slower kinetics observed during HYPO.
