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Am J Physiol Regul Integr Comp Physiol 275: R1192-R1201, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 4, R1192-R1201, October 1998

Poor relationship between arterial [lactate] and leg net release during exercise at 4,300 m altitude

George A. Brooks, Eugene E. Wolfel, Gail E. Butterfield, Allen Cymerman, Amy C. Roberts, Robert S. Mazzeo, and John T. Reeves

Department of Integrative Biology, University of California, Berkeley, California 94720; Geriatric Research Educational Clinical Center, Palo Alto Veterans Affairs Medical Center, Palo Alto, California 94304; University of Colorado Health Sciences Center, Denver 80262; University of Colorado, Boulder, Colorado 80309; and United States Army Research Institute for Environmental Medicine, Natick, Massachusetts 01760

We evaluated the hypotheses that on acute exposure to hypobaric hypoxia, sympathetic stimulation leads to augmented muscle lactate production and circulating [lactate] through a beta -adrenergic mechanism and that beta -adrenergic adaptation to chronic hypoxia is responsible for the blunted exercise lactate response after acclimatization to altitude. Five control and 6 beta -blocked men were studied during rest and exercise at sea level (SL), on acute exposure to 4,300 m (A1), and after a 3-wk sojourn at altitude (A2). Exercise was by leg cycling at 49% of SL peak O2 consumption (VO2 peak) (65% of altitude VO2 peak or 87 ± 2.6 W); beta -blockade was by propranolol (80 mg 3× daily), femoral arterial and venous blood was sampled; leg blood flow (Q) was measured by thermodilution, leg lactate net release [&Ldot; = (2) (1-leg Q) venous-arterial concentrationL] was calculated, and vastus lateralis needle biopsies were obtained. Muscle [lactate] increased with exercise and acute altitude exposure but regressed to SL values with acclimatization; beta -blockade had no effect on muscle [lactate]. Arterial [lactate] rose during exercise at SL (0.9 ± 0.1 to 1.5 ± 0.3 mM); exercise at A1 produced the greatest arterial [lactate] (4.4 ± 0.8 mM), and exercise at A2 an intermediate response (2.1 ± 0.6 mM). beta -Blockade reduced circulating [lactate] ~45% during exercise under all altitude conditions. &Ldot; increased transiently at exercise onset but then declined over time under all conditions. Blood and muscle "lactate paradoxes" occurred independent of beta -adrenergic influences, and the hypotheses relating the blood lactate response at altitude to beta -adrenergic mechanisms are rejected. During exercise at altitude, arterial [lactate] is determined by factors in addition to hypoxemia, circulating epinephrine, and net lactate release from active muscle beds.

exertion; environment; blockade; hypoxia; acclimatization; adaptation; epinephrine; norepinephrine


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