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J Physiol Volume 583, Number 1, 351-364, August 15, 2007 DOI: 10.1113/jphysiol.2007.132837
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SKELETAL MUSCLE AND EXERCISE

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

 Lisa M. K. Chin1,2, Ryan J. Leigh1,2, George J. F. Heigenhauser4, Harry B. Rossiter5, Donald H. Paterson1,2 and John M. Kowalchuk1,2,3

1 Canadian Centre for Activity and Ageing
2 School of Kinesiology, Faculty of Health Sciences
3 Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada, N6A 3K7
4 Department of Medicine, McMaster University, Hamilton, Ontario, Canada, L8S 4K1
5 Institute of Membrane and Systems Biology, Faculty of Biological Sciences, University of Leeds, Leeds LS2 9JT, UK

The effect of voluntary hyperventilation-induced hypocapnic alkalosis (RALK) on pulmonary O2 uptake (Formula ) 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; Formula , ~40 mmHg) and during hyperventilation (RALK; Formula , ~20 mmHg). Formula was measured breath-by-breath and relative concentration changes in muscle deoxy- ({Delta}HHb), oxy- ({Delta}O2Hb) and total ({Delta}Hbtot) haemoglobin were measured continuously using near-infrared (NIR) spectroscopy (Hamamatsu, NIRO 300). The time constant for the fundamental, phase 2, Formula response ({tau}Formula ) was greater (P < 0.05) in RALK (48 ± 11 s) than CON (31 ± 9 s), while {tau}HHb was similar between conditions (RALK, 12 ± 4 s; CON, 11 ± 4 s). The {Delta}Hbtot 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 Formula 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.

(Received 19 March 2007; accepted after revision 13 June 2007; first published online 21 June 2007)
Corresponding author J.M. Kowalchuk: Canadian Centre for Activity and Aging, School of Kinesiology, Faculty of Health Sciences, HSB 411C, University of Western Ontario, London, Ontario, Canada N6A 5B9. Email: jkowalch{at}uwo.ca

L. M. K. Chin and R. J. Leigh contributed equally to this paper.






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