EXERCISE

Increased muscle mitochondria are largely responsible for the increased resistance to fatigue and health benefits ascribed to exercise training. However, very little attention has been given to the likely benefits of increased brain mitochondria in this regard. We examined the effects of exercise training on markers of both brain and muscle mitochondrial biogenesis in relation to endurance capacity assessed by a treadmill run to fatigue (RTF) in mice. Male ICR mice were assigned to exercise (EX) or sedentary (SED) conditions (n=16-19/gr). EX mice performed 8 weeks of treadmill running for 1 hr/d, 6 d/wk at 25m/min and a 5% incline. Twenty-four hours after the last training bout a subgroup of mice (n=9-11/gr) were sacrificed and brain (brainstem, cerebellum, cortex, frontal lobe, hippocampus, hypothalamus, and midbrain), and muscle (soleus) tissues were isolated for analysis of mRNA expression of peroxisome proliferator-activated receptor gamma coactivator-1-alpha (PGC-1α), Silent Information Regulator T1 (SIRT1), citrate synthase (CS), and mitochondrial DNA (mtDNA) using RT-PCR. A different sub-group of EX and SED mice (n=7-8/gr), performed a treadmill RTF test. Exercise training increased PGC-1α, SIRT1 and CS mRNA and mtDNA, in most brain regions in addition tothe soleus (P<0.05). Mean treadmill RTF increased from 74.0±9.6 min to 126.5±16.1 min following training (P<0.05). These findings suggest that exercise training increases brain mitochondrial biogenesis which may have important implications, not only with regard to fatigue, but also with respect to various central nervous system diseases and age-related dementia that are often characterized by mitochondrial dysfunction.