Effect of conditioning and physiological hyperthermia on canine skeletal muscle mitochondrial oxygen consumption
| Autor: | Montana R Barrett, Michael S. Davis |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Hyperthermia
medicine.medical_specialty 040301 veterinary sciences Physiology chemistry.chemical_element Oxidative phosphorylation Oxygen Oxidative Phosphorylation 0403 veterinary science 03 medical and health sciences Dogs Oxygen Consumption 0302 clinical medicine Physiology (medical) Internal medicine medicine Animals Muscle Skeletal Chemistry Skeletal muscle 030229 sport sciences 04 agricultural and veterinary sciences Exercise capacity medicine.disease Mitochondria Muscle medicine.anatomical_structure Endocrinology Conditioning |
| Zdroj: | Journal of Applied Physiology. 130:1317-1325 |
| ISSN: | 1522-1601 8750-7587 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|