Author:
Clark Sally A.,Aughey Robert J.,Gore Christopher J.,Hahn Allan G.,Townsend Nathan E.,Kinsman Tahnee A.,Chow Chin-Moi,McKenna Michael J.,Hawley John A.
Abstract
We determined the effect of 20 nights of live high, train low (LHTL) hypoxic exposure on lactate kinetics, monocarboxylate lactate transporter proteins (MCT1 and MCT4), and muscle in vitro buffering capacity (βm) in 29 well-trained cyclists and triathletes. Subjects were divided into one of three groups: 20 consecutive nights of hypoxic exposure (LHTLc), 20 nights of intermittent hypoxic exposure [four 5-night blocks of hypoxia, each interspersed with 2 nights of normoxia (LHTLi)], or control (Con). Rates of lactate appearance (Ra), disappearance (Rd), and oxidation (Rox) were determined from a primed, continuous infusion of l-[U-14C]lactic acid tracer during 90 min of steady-state exercise [60 min at 65% peak O2 uptake (V̇o2 peak) followed by 30 min at 85% V̇o2 peak]. A resting muscle biopsy was taken before and after 20 nights of LHTL for the determination of βm and MCT1 and MCT4 protein abundance. Ra during the first 60 min of exercise was not different between groups. During the last 25 min of exercise at 85% V̇o2 peak, Ra was higher compared with exercise at 65% of V̇o2 peak and was decreased in LHTLc ( P < 0.05) compared with the other groups. Rd followed a similar pattern to Ra. Although Rox was significantly increased during exercise at 85% compared with 65% of V̇o2 peak, there were no differences between the three groups or across trials. There was no effect of hypoxic exposure on βm or MCT1 and MCT4 protein abundance. We conclude that 20 consecutive nights of hypoxia exposure decreased whole body Ra during intense exercise in well-trained athletes. However, muscle markers of lactate metabolism and pH regulation were unchanged by the LHTL intervention.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
49 articles.
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