304. Award Talk: Supporting the Deconditioning-reconditioning Cycle with Antioxidants: Tales from Polo Ponies.

Abstract

Regular exercise training (conditioning) induces physiological adaptations in equine athletes, enhancing physical capacity in equine athletes. However, periods of reduced physical activity (deconditioning) result in partial or complete loss of these conditioning- induced adaptations. Deconditioning is common following injury or the end of a competition season, necessitating an appropriate reconditioning period to re-induce physiological, and thus performance, adaptations. Production of reactive oxygen species (ROS) is necessary for appropriate muscle function, but when redox homeostasis is disturbed, the oxidative stress that results can limit muscle contraction, impact signaling pathways, and ultimately result in cellular damage. Thus, supplementation of antioxidants such as astaxanthin (ASTX) are thought to support the endogenous antioxidant response, improving the physiological adaptations to exercise. To determine the effects of astaxanthin (ASTX) supplementation on oxidative status during a deconditioning- reconditioning cycle, 12 polo ponies were assigned to a control (CON, no supplementation) or supplemented (75 mg ASTX daily orally) group. All horses underwent a 16-wk deconditioning period, with no forced exercise, followed by a 16-wk reconditioning program. Submaximal exercise tests (SET) were performed at the beginning of the study (Baseline), after deconditioning (DECON), and after reconditioning (RECON). Blood samples were collected -30, 0, 15, 30, and 60 min relative to each SET for oxidative status analysis. Muscle biopsy samples were collected 2 wk before (Pre-SET) and 2 h after (Post- SET) each SET for oxidative status and gene expression analyses. Mitochondrial function was analyzed in muscle samples at Pre-SET. Circulating glutathione peroxidase activity was increased (P ≤ 0.02) and oxidative damage to proteins was decreased (P ≤ 0.05) in ASTX. Muscle oxidative status was affected by deconditioning and reconditioning periods (P ≥ 0.05), but not affected by ASTX supplementation (P ≥ 0.09). Gene expression related to mitochondrial biogenesis and respiration was upregulated in ASTX (P ≤ 0.05). Mitochondrial respiratory capacity decreased following deconditioning (P ≤ 0.03) and increased following reconditioning (P ≤ 0.04). While ASTX supplementation can alter circulating oxidative status and muscle gene expression, greater effects on muscle oxidative status and mitochondrial respiration appear to be caused by a deconditioning-reconditioning cycle. Proper reconditioning protocols are critical for inducing and allowing time for adequate physiological adaptations at the cellular level.