Development and characterization of an overtraining animal model.

ABSTRACT

PURPOSE: Development of an endurance training-overtraining protocol for Wistar rats that includes increased workload and is characterized by analyses of performance and biomarkers. METHODS: The running protocol lasted 11 wk 8 wk of daily exercise sessions followed by 3 wk of increasing training frequency (two, three, and four times), with decreasing recovery time between sessions (4, 3, and 2 h) to cause an imbalance between overload and recovery. The performance tests were made before training (T1) and after the 4th (T2), 8th (T3), 9th (T4), 10th (T5), and 11th (T6) training weeks. All rats showed significantly increased performance at T4, at which time eight rats, termed the trained group (Tr), were sacrificed for blood and muscle assays. After T6, two groups were distinguishable by differences in the slope (alpha) of a line fitted to the individual performances at T4, T5, and T6 nonfunctional overreaching (NFOR; alpha < -15.05 kg x m) and functional overreaching (FOR; alpha >or= -15.05 kg x m). RESULTS: Data were presented as mean +/- SD. FOR maintained the performance at T6 similar to Tr at T4 (530.6 +/- 85.3 and 487.5 +/- 61.4 kg x m, respectively). The FOR and the Tr groups showed higher muscle citrate synthase activity (approximately 40%) and plasma glutamine/glutamate ratio (Gm/Ga; 4.5 +/- 1.7 and 4.5 +/- 0.9, respectively) than the sedentary control (CO) group (2.8 +/- 0.5). The NFOR group lost the performance acquired at T4 (407.3 +/- 88.2 kg x m) after T6 (280.5 +/- 93.1 kg x m) and exhibited sustained leukocytosis. NFOR's Gm/Ga (3.1 +/- 0.2) and muscle citrate synthase activity were similar to CO values. CONCLUSIONS: The decline in performance in the NFOR group could be related to the decrease in muscle oxidative capacity. We observed a trend in the Gm/Ga and leukocytosis that is similar to what has been sometimes observed in overtrained humans. This controlled training-overtraining animal model may be useful for seeking causative mechanisms of performance decline.