Overtraining Syndrome, Mitochondrial DNA and ATP Production

Abstract

Overtraining syndrome is characterized by declining performance and inflammation following intense training, leading to health implications. Diagnostic measures determining overtraining syndrome are limited. Overtraining induces a response from oxidative stress biomarkers proportional to load. Circulating free plasma DNA is associated with tissue injury and exercise-induced inflammation. Research indicates that with chronic, excessive training, aerobic or resistance in nature, plasma DNA concentrations increase with load, suggesting a diagnostic use for overtraining-induced exercise inflammation. Reduction in mitochondrial ATP production contributes to reduced endurance and muscle weakness. Increased mitochondrial DNA oxidative damage, along with cumulative DNA damage may explain overall reduction in mitochondrial DNA copy numbers in skeletal muscle. Reduced mitochondrial DNA copy number may contribute to reduced mRNA abundance, resulting in reduced mitochondrial protein synthesis and oxidative enzyme activity, reducing oxidative phosphorylation. Reduction in availability of ATP may contribute to reduction in remodeling, including energy-requiring reactions in muscle. Although regular aerobic exercise may enhance healthy life expectance, overtraining may produce adverse effects, such as reduction in mitochondrial ATP production, causing the hypothalamic center to reduce unplanned physical activities to conserve energy. With ATP production rates expressed per unit of mitochondrial protein, there are persisting overtraining effects, compounded by reduced mitochondrial content and impaired intrinsic activity of mitochondria. An overall decrease in protein expression associated with differing rates of protein synthesis and breakdown,  and protein turnover leads to accumulation of oxidatively damaged dysfunctional proteins. Further research is needed to examine effects of overtraining on mt DNA deletion, content, and oxidative DNA damage biomarkers.