Davis 2021 J Appl Physiol

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Davis MS, Barrett MR (2021) Effect of conditioning and physiology hyperthermia on canine skeletal muscle mitochondrial oxygen consumption. J Appl Physiol. 130:1317-1325

» PMID: 33661725 Open Access

Davis Michael S, Barrett Montana R (2021) J Appl Physiol

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 6 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 44C. 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.

Keywords: Uncoupling, oxidative phosphorylation, cellular respirometry

O2k-Network Lab: US OK Stillwater Davis MS


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Stress:Temperature  Organism: Dog  Tissue;cell: Skeletal muscle  Preparation: Permeabilized cells  Enzyme: Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Uncoupling protein  Regulation: Coupling efficiency;uncoupling, Temperature  Coupling state: LEAK, OXPHOS  Pathway: N, S, NS  HRR: Oxygraph-2k