Adapatation of VO2 and Muscle Deoxygenation at the Onset of Moderate-Intensity Exercise with Respiratory Alkalosis

Abstract

0437 Following a period of hyperventilation-induced respiratory alkalosis (R-ALK), pulmonary O2 uptake (VO2) kinetics are either not changed (Ward et al., J. Appl. Physiol. 55:742, 1983) or slowed (Hayashi et al., Am. J. Physiol. 277:R1274, 1999) compared to control conditions, while local muscle oxygenation changes have not been examined. PURPOSE: To examine the effect of R-ALK on VO2 kinetics and muscle deoxygenation at the onset of moderate-intensity exercise. METHODS: Young male adults (n = 8) completed 5 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; PETCO2 ∼ 40 mmHg) and following 20 min hyperventilation (R-ALK; PETCO2 ∼20 mmHg). VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively. Changes in muscle deoxy-(HHb), oxy-(HbO2) and total hemoglobin (HbTOT) were measured continuously using near-infrared spectroscopy (NIRS; Hamamatsu, NIRO 300). The adaptation of VO2, HR, and HHb were modelled with a mono-exponential equation using non-linear least-squares regression. RESULTS: During R-ALK, PETCO2 was maintained < 25 mmHg throughout the accommodation and exercise. The phase II VO2 time constant (ô VO2) was longer (P < 0.05) in R-ALK (34 ± 7 s) than CON (27 ± 8 s), while ôHR was similar between conditions (R-ALK, 47 ± 8 s; CON, 38 ± 17 s). Following a delay, the ôHHb was similar between conditions (R-Alk, 7 ± 3 s; Con, 7 ± 4 s), while the HbTOT was lower in R-ALK than CON throughout the accommodation and exercise (end-exercise HbTOT: R-Alk, 1 ± 6 μM; Con, 5 ± 5 μM). CONCLUSION: The slower adaptation of VO2 during R-ALK may be related to a reduction in local muscle perfusion (as seen by a similar HHb and lower HbTOT), although slowed metabolic processes cannot be excluded. Supported by NSERC, Canada.