作者: Johannes D. Veldhuis , Kohji Yoshida
DOI: 10.1007/978-1-62703-314-5_4
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摘要: The impact of chronic training on pituitary function is best understood by a basic appraisal the neuroendocrine physiology any given individual axis and more complex interactive pathophysiology among axes [1–12]. Interaxes interactions have received relatively little attention. Even evaluating single in its dynamic state complicated challenge, combined feedforward feedback activities key control loci within [13, 14]. For example, case growth hormone (GH) insulin-like factor 1 (IGF-1) axis, hypothalamic GH-releasing (GHRH) secreted arcuate nuclei stimulates GH secretion acutely, whereas somatostatinergic system originating paraventricular opposes GHRH action [15]. These two neuronal inputs are reciprocally interconnected intrahypothalamic synapses common impinging neuromodulator pathways [14]. In addition, feeds back brain receptors, stimulating somatostatin possibly inhibiting release. Available into bloodstream triggers IGF-1 production various target tissues, circulating capable indirectly directly (see Fig. 4.1). Such (GHRH’s driving secretion) (GH’s own secretion, IGF-1’s so forth) mechanisms principle can be modified effects exercise at one or levels axis. Moreover, multiple determinants modulate responses to training, such as body composition individual, concurrent stress and/or weight loss, gender, diet energy balance, concomitant drug use, age, puberty, pregnancy, lactational status [16–18].