The Influence of Localized Heat Therapy on Redox Signaling in Skeletal Muscle

Reactive oxygen species (ROS) have been identified as crucial signaling molecules in skeletal muscle adaptations to exercise and signal for protective pathways within the myofiber. Pathological heat stress studies in animals demonstrate the ability of heat to increase ROS production in skeletal muscle. Limited data on the influence of therapeutic heat on ROS production and redox signaling in human skeletal muscle exists in the literature. The purpose of this study was to assess ROS production and redox signaling in human skeletal muscle following an acute, therapeutic bout of heat treatment. We hypothesized that heat would create an oxidized environment within muscle and activate redox-sensitive pathways. 18 healthy, untrained participants (8 females, 10 males; mean [± SD] age = 20.28 ± 1.53 years, height = 173.33 ± 10.53 cm, mass = 67.18 ± 9.85 kg, body mass index = 22.27 ± 1.82) had one leg randomly assigned to heat treatment while the other served as their own control and received a sham treatment. Participants underwent a single, two-hour session of diathermy on the vastus lateralis of their randomly assigned heat leg. Muscle biopsies of both the heated and unheated (control) vastus lateralis muscles were taken immediately following heat treatment. The ratio of reduced GSH to oxidized GSSG was unchanged from control to heat. Myonuclear accumulation of the redox sensitive regulator of the antioxidant defense system Nrf2 also displayed no significant difference between heat and control samples. qPCR analysis revealed expression of the heat shock gene HSPA1L was significantly increased in heat samples compared to unheated control samples. NQO1 was also elevated. However, the expression of Nrf2 target genes GCLC, GPX1, and HMOX1 was unchanged between control and heat samples. These results indicate that two hours of diathermy treatment does not appear to alter the immediate redox state of skeletal muscle. Mary Lou Fulton Fund College of Life Sciences, Brigham Young University This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.