Impact of Chronic Training on Pituitary Hormone Secretion in Humans

Abstract

The impact of chronic training on pituitary function is best understood by a basic appraisal of the neuroendocrine physiology of any given individual axis and the more complex interactive pathophysiology among axes. Interaxes interactions have received relatively little attention. Even evaluating a single neuroendocrine axis in its dynamic state is a complicated challenge, given combined feedforward and feedback activities among the key control loci within any given axis. For example, in the case of the growth hormone (GH) and insulin-like growth factor 1 (IGF-1) axis, hypothalamic GH-releasing hormone (GHRH) secreted by arcuate nuclei stimulates pituitary GH secretion acutely, whereas the somatostatinergic system originating in the paraventricular nuclei opposes GHRH action. These two neuronal inputs are reciprocally interconnected by intrahypothalamic synapses and common impinging neuromodulator pathways. In addition, secreted GH feeds back on brain GH receptors, stimulating somatostatin secretion and possibly inhibiting GHRH release. Available GH secreted into the bloodstream triggers IGF-1 production in various target tissues, and circulating IGF-1 is capable of inhibiting pituitary GH secretion indirectly and directly. Such feedforward (GHRHs driving GH secretion) and feedback (GHs inhibiting its own secretion, IGF-1 s inhibiting GH secretion, and so forth) dynamic control mechanisms in principle can be modified by the effects of exercise at one or more levels within the axis. Moreover, multiple determinants modulate neuroendocrine responses to training, such as the body composition of the individual, concurrent stress and/or weight loss, gender, diet and energy balance, concomitant drug or hormone use, age, puberty, pregnancy, and/or lactational status.