25 Race training improves skeletal muscle mitochondrial volume density, function, and capacity in Thoroughbreds

Abstract

Racehorses are among the most elite athletes in the equine industry. However, little is known about mitochondrial adaptations to race training. To test the hypothesis that race training increases mitochondrial biogenesis and capacity, gluteus medius samples were collected from Thoroughbred horses (11 geldings, 2 mares) before and after 14 wk of early race training. Horses entered wk 0 at varying levels of fitness, and therefore, were grouped accordingly: 1) galloping on track (n = 5; mean ± SD V200 = 10.6 ± 0.9 m/s); 2) jogging and cantering on track (n = 5; V200 = 9.8 ± 0.6 m/s); and 3) breezed one furlong at sale (n = 3; unknown V200). All horses increased in workload from a 6-furlong canter (7–9 m/s) to a 12-furlong slow gallop (9–11 m/s). Once horses reached proper fitness, fast work was added weekly in the form of a one-furlong fast gallop (11–13 m/s) or 2–3 furlongs breeze (13–15 m/s). There was no difference in fitness level between groups at wk 14 (V200 = 10.9 ± 0.7 m/s; P = 0.6). Muscle mitochondrial capacities were determined by high resolution respirometry, and mitochondrial enzyme activities were determined by colorimetry. Data were analyzed using linear models in SAS v9.4 with repeated measures. Main effects included time, wk 0 fitness level (trt) and the time × trt interaction; horse(trt) was as a random effect. Mitochondrial volume density (citrate synthase activity; CS) and integrative (per mg protein) mitochondrial function (cytochrome c oxidase activity; CCO) increased ( P ≤ 0.05), while intrinsic CCO (relative to CS activity) decreased ( P = 0.005) from wk 0 to 14. Integrative (per mg tissue) oxidative phosphorylation (P) capacities with complex I (P CI ) and complex II (P CI+II ), as well as maximum electron transport capacity (E CI+II ) increased from wk 0 to 14 ( P ≤ 0.05) but none were affected by wk 0 fitness level. Incoming fitness level only affected intrinsic mitochondrial respiration. Horses with intermediate fitness at wk 0 (group 2) had greater intrinsic P CI , P CI+II , E CI+II , and electron transport capacity with CII only (E CII ) at wk 0 than group 1 or 3 ( P ≤ 0.007) but these measures were not different between groups at wk 14. Intrinsic E CII decreased in all horses from wk 0 to 14 ( P = 0.01) but no other intrinsic mitochondrial capacity measure was affected overall by time. The contribution of P CI to total E CI+II tended to decrease ( P = 0.07) and of E CII to total E CI+II decreased ( P < 0.0001) from wk 0 to 14. This is the first report of mitochondrial adaptations to early race training, which may assist in developing precision management programs to enhance performance and well-being in elite racehorses.