Aging is associated with decline in physiological function in brain, skeletal muscle and other organs. Our purpose was to influence the brain function and alter age-associated decline with exercise and administration of IGF-1. Therefore we administered IGF-1 during a running exercise protocol to young and old Wistar rats. We intend to follow the possible neurogenesis induced by exercise and/or IGF-1 treatment. We have observed that exercise training without IGF-1 treatment improved brain function measured by the Morris maze test, and the age-associated decline was prevented by exercise training. On the other hand, IGF-1 administration eliminated the beneficial effects of exercise training in the old animals.
Our data indicate that exercise and aging influenced the content of brain derived neurotrophic factor (BDNF). Moreover, the extent of neurogenesis caused by exercise was higher in young group than in the aged. We have also studied the content of silence regulating factor 1 (SIRT1), which has been suggested to be a causative factor of life span at eukaryotes and altering factors of mammals. Our data revealed that SIRT1 levels decreased with aging, and exercise training attenuated this decrease. One of the distinct functions of SIRT1 is controlling the rate of gene expression by histon deacetylation. The content of SIRT4 changed by inverse manner with SIRT1 as a result of aging. SIRT4 is located in mitochondria and it plays a role in cell metabolism. It appears that exercise improves brain function and the concentration of BDNF could play a regulating factor in this beneficial effect. IGF-1 supplementation seems to attenuate the beneficial effects of exercise on function. Moreover, the role of the sirtuin protein family in the aging process confirmed by our study and the regulatory pathways are under intensive investigation.