Passive heat stress induces mitochondrial adaptations in skeletal muscle

Abstract

The mitochondria are central to skeletal muscle metabolic health. Impaired mitochondrial function is associated with various muscle pathologies, including insulin resistance and muscle atrophy. As a result, continuous efforts are made to find ways to improve mitochondrial health in the context of disuse and disease. While exercise is known to cause robust improvements in mitochondrial health, not all individuals are able to exercise. This creates a need for alternate interventions which elicit some of the same benefits as exercise. Passive heating (i.e., application of heat in the absence of muscle contractions) is one potential intervention which has been shown to increase mitochondrial enzyme content and activity, and to improve mitochondrial respiration. Associated with increases in mitochondrial content and/or function, passive heating can also improve insulin sensitivity in the context of type II diabetes and preserve muscle mass in the face of limb disuse. This area of research remains in its infancy, with many questions yet to be answered about how to maximize the benefits of passive heating and elucidate the mechanisms by which heat stress affects muscle mitochondria.

Graphical Abstract

Keywords:

• Heat
• skeletal muscle
• mitochondria
• atrophy
• thermal
• physiological effects of hyperthermia (i.e.,
• perfusion effects
• hypoxia
• pH
• metabolism
• microenvironment
• redox)
• heat shock response (i.e.
• HSP
• chaperones
• thermotolerance)

Acknowledgements

The graphical abstract and Figure 3 were created using BioRender.com

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by an Interdisciplinary Research Award from Brigham Young University.