调理和生理热疗对犬骨骼肌线粒体耗氧量的影响

Effect of conditioning and physiological hyperthermia on

canine skeletal muscle mitochondrial oxygen consumption

Keywords：cellular respirometry; oxidative phosphorylation; uncoupling.

关键词：细胞呼吸测量； 氧化磷酸化； 解耦

哺乳动物：狗

作者：Michael S Davis 1, Montana R Barrett 1

出版期刊：《JOURNAL OF APPLIED PHYSIOLOGY》 2021/5/2

Abstract：

Exercise often causes skeletal muscle hyperthermia, likely resulting in decreased efficiency of mitochondrial respiration. We hypothesized that athletic conditioning would improve mitochondrial tolerance to hyperthermia. Skeletal muscle biopsies were obtained from six Alaskan sled dogs under light general anesthesia before and after a full season of conditioning and racing, and respiration of permeabilized muscle fibers was measured at 38, 40, 42, and 44°C. There was no effect of temperature on phosphorylating respiration, and athletic conditioning increased maximal phosphorylating respiration by 19%. Leak respiration increased and calculated efficiency of oxidative phosphorylation decreased with increasing incubation temperature, and athletic conditioning resulted in higher leak respiration and lower calculated oxidative phosphorylation efficiency at all temperatures. Conditioning increased skeletal muscle expression of putative mitochondrial leak pathways adenine nucleotide transporter 1 and uncoupling protein 3, both of which were correlated with the magnitude of leak respiration. We conclude that athletic conditioning in elite canine endurance athletes results in increased capacity for mitochondrial proton leak that potentially reduces maximal mitochondrial membrane potential during periods of high oxidative phosphorylation. This effect may provide a mechanistic explanation for previously reported decreases in exercise-induced muscle damage in well-conditioned subjects.NEW & NOTEWORTHY Athletic conditioning is expected to increase exercise capacity through improved function of cardiopulmonary and musculoskeletal tissues. Our finding of decreased calculated efficiency of skeletal muscle mitochondria in one of the premier mammalian athletes suggests that this mandate for improved function may take the form of sacrificing capacity for maximal oxidative phosphorylation to minimize exercise-induced muscle damage caused by mitochondrial oxidative stress.

文章摘要：

运动经常导致骨骼肌过热，可能导致线粒体呼吸效率降低。我们假设运动调节会提高线粒体对高热的耐受性。在整个赛季的调理和比赛前后，在轻度全身麻醉下对六只阿拉斯加雪橇犬进行骨骼肌活检，并在 38、40、42 和 44°C 下测量透化肌肉纤维的呼吸。温度对磷酸化呼吸没有影响，运动调节使最大磷酸化呼吸增加了 19%。随着培养温度的升高，漏气呼吸增加，氧化磷酸化计算效率降低，运动调节导致所有温度下漏气呼吸增加，氧化磷酸化计算效率降低。调理增加了假定的线粒体泄漏途径腺嘌呤核苷酸转运蛋白 1 和解偶联蛋白 3 的骨骼肌表达，这两者都与泄漏呼吸的幅度相关。我们得出结论，精英犬耐力运动员的运动调节导致线粒体质子泄漏能力增加，这可能会降低高氧化磷酸化期间的最大线粒体膜电位。这种效应可能为先前报道的运动引起的肌肉损伤减少的良好条件受试者提供机械解释。新的和值得注意的运动调节有望通过改善心肺和肌肉骨骼组织的功能来增加运动能力。我们在一位主要哺乳动物运动员中发现骨骼肌线粒体的计算效率降低，这表明这种改善功能的任务可能采取牺牲最大氧化磷酸化能力的形式，以尽量减少由线粒体氧化应激引起的运动引起的肌肉损伤。

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