Vigorous exercise is associated with a suppression of reproductive function in adult females and males. An example is the amenorrhea frequently associated with long-distance runners. We have developed a monkey model in which female monkeys (Macaca fascicularis) that exercise daily on treadmills develop reproductive dysfunction similar to that reported in human athletes. Animals are trained to exercise and to increase their endurance over a period of weeks. Cessation of menstrual cyclicity usually occurs within 6 months of a regimen of daily exercise. Our studies utilize this model to elucidate the physiological mechanisms by which chronic exercise leads to an interruption of normal reproductive function in this representative primate species. One goal is to determine whether metabolic adaptation to vigorous exercise training provides the """"""""signal"""""""" which suppresses the central drive to the reproductive axis. To accomplish this, metabolites are measured during the course of exercise training. Data are then examined to determine whether a metabolic change is closely associated with the onset of reproductive dysfunction. Once a metabolite is identified, we are then reversing the metabolic changes that occur with exercise training to determine whether normal reproductive function is restored. We are also measuring changes in CSF levels of neurotransmitters and neuropeptides throughout vigorous exercise training. Our goal is to identify changes in the activity of central neuronal systems that project onto GnRH neurons and may play a role in causing exercise induced reproductive dysfunction. Once changes are identified, we are using pharmacological approaches to reverse changes in specific neurotransmitter systems and then assessing whether the treatment corrects exercise induced amenorrhea. Information gained in this project has applicability to other 640009ions where metabolic signals have been proposed to be at least partially responsible for the quiescent state of the reproductive axis.
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