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J Appl Physiol 68: 1393-1398, 1990;
8750-7587/90 $5.00
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Journal of Applied Physiology, Vol 68, Issue 4 1393-1398, Copyright © 1990 by American Physiological Society

ARTICLES

Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease

J. M. Hagberg, D. S. King, M. A. Rogers, S. J. Montain, S. M. Jilka, W. M. Kohrt and S. L. Heller
Department of Medicine, Jerry Lewis Neuromuscular Research Center, St. Louis, Missouri.

This study was designed to determine whether patients with McArdle's disease, who do not increase their blood lactate levels during and after maximal exercise, have a slow "lactacid" component to their recovery O2 consumption (VO2) response after high-intensity exercise. VO2 was measured breath by breath during 6 min of rest before exercise, a progressive maximal cycle ergometer test, and 15 min of recovery in five McArdle's patients, six age-matched control subjects, and six maximal O2 consumption- (VO2 max) matched control subjects. The McArdle's patients' ventilatory threshold occurred at the same relative exercise intensity [71 +/- 7% (SD) VO2max] as in the control groups (60 +/- 13 and 70 +/- 10% VO2max) despite no increase and a 20% decrease in the McArdle's patients' arterialized blood lactate and H+ levels, respectively. The recovery VO2 responses of all three groups were better fit by a two-, than a one-, component exponential model, and the parameters of the slow component of the recovery VO2 response were the same in the three groups. The presence of the same slow component of the recovery VO2 response in the McArdle's patients and the control subjects, despite the lack of an increase in blood lactate or H+ levels during maximal exercise and recovery in the patients, provides evidence that this portion of the recovery VO2 response is not the result of a lactacid mechanism. In addition, it appears that the hyperventilation that accompanies high-intensity exercise may be the result of some mechanism other than acidosis or lung CO2 flux.


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