Thoroughbred horses susceptible to recurrent exertional rhabdomyolysis have elevated skeletal muscle mitochondrial capacities.

Recurrent exertional rhabdomyolysis (RER) is a skeletal muscle disease that can intermittently impede careers of equine athletes. Manifesting as episodes of muscular stiffness and degeneration, RER causes lost training and competition days. RER is associated with abnormal intracellular calcium (Ca2+) regulation. Calcium released from the sarcoplasmic reticulum to initiate contraction may also be transported into mitochondria, which impacts energy production. RER-susceptible horses exhibit downregulated mitochondrial proteins but upregulated mitochondrial genes. Thus, mitochondrial function may be impacted by Ca2+ irregularities in RER horses. Fourteen race-fit female Thoroughbred horses were used to test the hypothesis that horses that had previously experienced at least 2 exertional rhabdomyolysis episodes (n = 8; means ± SD; 3.1 ± 1.1 yr) would have impaired skeletal muscle mitochondrial capacities compared with control racehorses (n = 6; 3.5 ± 1.4 yr). Gluteus medius samples were analyzed for oxidative phosphorylation (P) and electron transfer (E) capacities via high-resolution respirometry. Contrary to our hypothesis, integrative (per mg) NADH-linked P (PN), maximal P (PNS), maximal E (ENS), and succinate-linked E (ES) tended to be greater (P ≤ 0.1), whereas intrinsic (relative to citrate synthase activity) PN and ES tended to be greater (P ≤ 0.1) and PNS and ENS were greater (P ≤ 0.03) in RER-susceptible compared with control horses. Horses susceptible to RER appeared to have greater skeletal muscle mitochondrial capacities, which might be consequent to aberrant intramuscular Ca2+ handling in vivo. The clinical significance of this finding remains unclear, but further investigation could lead to mitochondrially targeted treatment and management strategies.NEW & NOTEWORTHY High-performing equine athletes may experience episodes of "tying up," classified as recurrent exertional rhabdomyolysis (RER), which intermittently impedes their ability to perform. In this study, horses susceptible to RER had greater skeletal muscle mitochondrial capacities compared with control horses. The differences in mitochondrial function may be a result of the abnormal calcium regulation that is associated with RER.