Impact of Hypoxic Exercise Recovery on Skeletal Muscle Glycogen and Gene Expression

骨骼肌 糖原 股外侧肌 最大VO2 缺氧(环境) 肌肉萎缩 医学 基因表达 细胞色素c氧化酶 内科学 基因 内分泌学 生物 化学 线粒体 生物化学 心率 有机化学 氧气 血压
作者
Dustin Slivka,Charles L. Dumke,Walter Hailes,Brent C. Ruby
出处
期刊:High Altitude Medicine & Biology [Mary Ann Liebert]
卷期号:22 (3): 300-307 被引量:2
标识
DOI:10.1089/ham.2021.0028
摘要

Slivka, Dustin, Charles Dumke, Walter Hailes, and Brent Ruby. Impact of hypoxic exercise recovery on skeletal muscle glycogen and gene expression. High Alt Med Biol. 22:300–307, 2021. Background: The impact of altitude during recovery from exercise is largely unknown. The purpose of this study was to determine the acute gene response and muscle glycogen re-synthesis after exercise when exposed to simulated high altitude during recovery. Materials and Methods: Twelve male participants (age, 25 ± 2 years; height, 178 ± 7 cm; weight, 78.8 ± 7.8 kg; VO2peak, 4.25 ± 0.59 l/min; Wpeak 307 ± 44 W; and body fat, 13.1% ± 1.2%) completed two trials (random order), which consisted of cycling for 90 minutes in laboratory conditions and then recovering for 6 hours in laboratory conditions (975 m; normoxia) or at a high simulated altitude (5,000 m; hypoxia). Results: Skeletal muscle biopsies from the vastus lateralis were obtained before exercise, after exercise, and 6 hours after exercise for the measurement of metabolic gene expression and muscle glycogen. Muscle glycogen decreased with exercise (61% ± 13%, p < 0.05) and increased with recovery (78% ± 35%, p < 0.05) with no difference between trials (p > 0.05). Hypoxia-inducible factor (HIF)-1α, HIF-2α, optic atrophy gene 1 (OPA-1), mitofusin 2 (MFN-2), and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) gene expression were suppressed after altitude exposure (p < 0.05), while mitochondrial fission 1 protein (FIS-1), phosphofructokinase (PFK), Cytochrome c oxidase (COX), and hexokinase (HK) were unaffected by altitude exposure (p > 0.05). Conclusions: High-altitude exposure during recovery from exercise inhibits gene expression associated with mitochondrial development without affecting muscle glycogen re-synthesis.
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