Abstract

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 (p = 0.1239). Accumulation of the redox sensitive regulator of the antioxidant defense system Nrf2 to the nucleus additionally displayed no significant difference between heat and control samples (p = 0.6821). qPCR analysis revealed expression of the heat shock gene HSPA1L was significantly increased an average of 504% in heat samples compared to unheated control samples (p = 0.0003). Additional genes analyzed using qPCR showed no significant difference in the expression of Nrf2 target genes GCLC (p = 0.1695), NQO1 (p = 0.8202), and HMOX1 (p = 0.9632) between control and heat samples. Data from RNA sequencing analysis supported findings from qPCR analysis. These results indicate that two hours of diathermy treatment does not appear to alter the redox state of skeletal muscle.

Degree

College and Department

Life Sciences; Exercise Sciences

Rights

https://lib.byu.edu/about/copyright/