Abstract

Background: According to the theory of mitochondrial aging, oxidative stress plays a major role in aging and age related degenerative diseases. Since oxygen consumption and reactive oxygen species rate increase during aerobic exercise, we hypothesised that heavy aerobic training could lead to enhanced mitochondrial DNA (mtDNA) deletion in postmitotic tissues, leading in turn to premature aging and degenerative diseases.

Methods: Sixty adult male 2 month old Wistar₁₄₈₄₈ rats were divided into six equal groups. Two groups were trained for 3 months by running on a treadmill (5 days/week, incline 6°; group 1: 40 m/min, 20 min/day; group 2: 20 m/min, 40 min/day), while two sedentary groups participated in aerobic exercise only at the end of the study (incline 6°; group 3: 40 m/min; group 4: 20 m/min). To control for physical and physiological parameters, two groups of untrained animals were killed at the beginning (group 6) and end (group 5) of the study. Expand long PCR was used to investigate mtDNA deletion in soleus muscle and a sequencing method was used to confirm the mtDNA deletion break point.

Results: Our results did not show any mtDNA deletion in untrained rats or in those that underwent moderate training (group 2) We only found mtDNA deletion (4.6 kb) in the soleus muscle of heavily trained rats (group 1).

Conclusions: These results demonstrate that one session of aerobic exercise does not cause mtDNA deletion in skeletal muscle. The difference in results between heavy and moderate aerobic training may be due to low work rate or up-regulation of inducible antioxidant systems in moderate training.