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Novel Pilot Study Reveals that Heat Therapy Increases Muscle Mitochondrial Quality Control and Respiratory Efficiency in Healthy Human Subjects
Author(s) -
Von Schulze Alex,
Fuller Kelly NZ,
McCoin Colin,
Fernandez Clara Amat,
Thyfault John,
Geiger Paige
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.699.1
Subject(s) - mitophagy , skeletal muscle , medicine , endocrinology , insulin resistance , citrate synthase , mitochondrion , respiratory system , carnitine , basal (medicine) , biology , insulin , autophagy , biochemistry , enzyme , apoptosis
Immense focus has been placed on novel treatment strategies to prevent or reverse insulin resistance and type 2 diabetes (T2D). We have shown that heat therapy (HT) in rodents protects against high‐fat diet induced skeletal muscle insulin resistance and impaired glucose homeostasis. However, it remains unknown whether this effect can be translated to humans. The purpose of this pilot study was to determine if HT via hot water immersion was well tolerated in humans and altered mitochondrial metabolism in skeletal muscle. Healthy male and female participants (n=5/sex) underwent one bout of HT increasing core temperature to 38.5°C for 1h. Muscle biopsies were taken one week prior and 24h post HT to determine whether HT impacted mitochondrial respiratory capacity and mitochondrial quality control via autophagy. HT was well tolerated in all subjects and resulted in acute increases in heart rate and reductions in systolic and diastolic blood pressure. HT did not significantly alter maximal mitochondrial respiratory capacity at basal, state3, state3S, or uncoupled states with either palmitoyl‐carnitine + palmitoyl‐CoA (palmitate) or pyruvate + glutamate + malate (PGM) as substrates. However, HT tended to improve respiratory efficiency as indicated by a reduced coupling control ratio (basal/state3) for PGM. Of interest, this improved efficiency and maintenance of mitochondrial respiratory capacity occurred despite HT‐induced reductions in mitochondrial content as inferred by citrate synthase activity. We believe this reduction in muscle mitochondrial content occured as a result of mitophagy ‐ the targeted degradation of damaged mitochondria. Our hypothesis is supported by the observed reductions (or degradation) of the autophagy/mitophagy related protein, microtubule‐associated Proteins 1A/1B light chain 3B‐ phosphatidylethanolamine (LC3II). For the first time, our data suggest that HT increases mitochondrial quality control (via enhanced autophagy/mitophagy) and enhances respiratory efficiency in human skeletal muscle. These data provide promising results for further analysis in metabolically impaired obese subjects. Support or Funding Information NIH P30GM122731; Madison and Lila Self Graduate Fellowship (The University of Kansas) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .