Morphofunctional alterations of the nonpregnant murine uterus in response to intense and exhaustive exercise are not related to oxidative stress.

Exercise is a common and noninvasive way to improve human health. In contrast, intense exercise causes damage in various tissues and is usually associated with metabolic changes in organs and tissues. Even though intense exercise is associated with dysfunctions in the female reproductive system, much less is known about the cellular mechanisms underlying its effects particularly on the nonpregnant uterus. We investigated whether the effects of an intense and exhaustive exercise (IEE) program on the isolated C57BL/6 uterine morphology and contractility might be related to increased levels of prooxidation markers. Female mice were submitted to 2 days of IEE. The daily exercise session consisted of a running session until exhaustion, with the treadmill speed set at 85% of each animal's maximum velocity. Training responses were evaluated through two parameters: time to exhaustion and maximum velocity. Absence of exercise-induced hypothalamic-pituitary-adrenal (HPA) axis activation was indirectly evaluated by maintenance of the adrenal gland weight. IEE reduced the thickness of the longitudinal muscular layer by 10%, impaired contractility in response to muscarinic stimulation (increased EC50 and decreased Emax), but showed a strong trend to decreasing the KCl-induced contraction; reduced lipid peroxidation; and did not alter the uterine protein oxidation of exercised animals compared with control. Altogether we provide evidence for the nonpregnant murine uterus being an important target to IEE, leading to morphofunctional alterations which could not be associated with tissue oxidative stress but might well be related with exercise-induced uterine dysfunctions.