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Does high muscle temperature accentuate skeletal muscle injury from eccentric exercise?

ABSTRACT: Hyperthermia is suspected of accentuating skeletal muscle injury from novel exercise, but this has not been well studied. This study examined if high muscle temperatures alters skeletal muscle injury induced by eccentric exercise (ECC). Eight volunteers (age, 22.5 ± 4.1 year; height, 169.5 ± 10.8 cm; body mass, 76.2 ± 12.6 kg), serving as their own control, and who were not heat acclimatized, completed two elbow flexor ECC trials; in one trial the biceps were heated >40°C (HEAT) and in the other trial there was no heating (NON). HEAT was applied with shortwave diathermy (100 W) for 15 min immediately before the first ECC bout and for 2 min in between each bout. Individuals were followed for 10 days after each ECC session, with a 6-week washout period between arms. The maximal voluntary isometric contraction decreased by 41 ± 17% and 46 ± 20% in the NON and HEAT trials, respectively. Bicep circumference increased by 0.07 ± 0.08 mm (4%, P = 0.04) and relaxed range of motion decreased by 11.5 ± 8.2° (30%, P < 0.001) in both trials. Serum creatine kinase peaked 72-h following ECC (NON: 6289 ± 10407; HEAT: 5486 ± 6229 IU L(-1), 38-fold increase, P < 0.01) as did serum myoglobin (NON: 362 ± 483; HEAT: 355 ± 373 μg L(-1), 13-fold increase, P < 0.03). Plasma HSP 70 was higher (P < 0.02) in HEAT after 120-h of recovery. There were no differences between treatments for plasma HSP27 and interleukins 1β, 6, and 10. The results indicate that >40°C muscle temperature does not alter skeletal muscle injury or functional impairments induced by novel ECC.

SUBMITTER: Castellani JW

PROVIDER: S-EPMC4873630 | biostudies-other | 2016 May

REPOSITORIES: biostudies-other

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Project description:BACKGROUND:In muscular dystrophy and old age, skeletal muscle repair is compromised leading to fibrosis and fatty tissue accumulation. Therefore, therapies that protect skeletal muscle or enhance repair would be valuable medical treatments. Hypoxia-inducible factors (HIFs) regulate gene transcription under conditions of low oxygen, and HIF target genes EPO and VEGF have been associated with muscle protection and repair. We tested the importance of HIF activation following skeletal muscle injury, in both a murine model and human volunteers, using prolyl hydroxylase inhibitors that stabilize and activate HIF. METHODS:Using a mouse eccentric limb injury model, we characterized the protective effects of prolyl hydroxylase inhibitor, GSK1120360A. We then extended these studies to examine the impact of EPO modulation and infiltrating immune cell populations on muscle protection. Finally, we extended this study with an experimental medicine approach using eccentric arm exercise in untrained volunteers to measure the muscle-protective effects of a clinical prolyl hydroxylase inhibitor, daprodustat. RESULTS:GSK1120360A dramatically prevented functional deficits and histological damage, while accelerating recovery after eccentric limb injury in mice. Surprisingly, this effect was independent of EPO, but required myeloid HIF1?-mediated iNOS activity. Treatment of healthy human volunteers with high-dose daprodustat reduced accumulation of circulating damage markers following eccentric arm exercise, although we did not observe any diminution of functional deficits with compound treatment. CONCLUSION:The results of these experiments highlight a novel skeletal muscle protective effect of prolyl hydroxylase inhibition via HIF-mediated expression of iNOS in macrophages. Partial recapitulation of these findings in healthy volunteers suggests elements of consistent pharmacology compared to responses in mice although there are clear differences between these two systems.

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Does high muscle temperature accentuate skeletal muscle injury from eccentric exercise?

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