The physiological functions of the ovary and development of the corpus luteum occur through the activation of endocrine hormones. In this process, estrogen, a reproductive hormone, is secreted in the ovarian follicle and corpus luteum and affects corpus luteum formation and regression. Estrogen controls the synthesis of reproductive hormones by binding to estrogen receptor–α and –β. Estradiol–17β, synthesized in the ovary, regulates the physiological function of the corpus luteum and the angiogenesis signaling pathway. Estrogen controls progesterone synthesis, which is regulated by StAR-transported cholesterol, P450scc-converted pregnenolone in mitochondria, and 3β-HSD-synthesized progesterone in the smooth endoplasmic reticulum. Estrogen secretion is also stimulated by kisspeptin and regulated by gonadotropin-releasing hormone, follicle-stimulating hormone, and luteinizing hormone. Moreover, the formation of the corpus luteum is closely regulated by angiogenesis. VEGF is an important factor in angiogenesis and plays a role in the survival, proliferation, and migration of endothelial cells. Especially, VEGF–A is a key factor in the physiological functions of endothelial cells. VEGF binds VEGFR–2 and affects the signaling pathways of PI3K, Akt, MAPK, and ERK. Also, VEGF binds to HIF–1α, inducing VEGF secretion. Estrogen promotes the activation of HIF–1α, while the activation of mTOR and Akt stimulates VEGF secretion. Therefore, estrogen is a major reproductive hormone in physiological function and the synthesis and secretion of endocrine hormones in the ovary and corpus luteum.

This paper reviews physiological changes in the nervous system of patients with hemiparesis that may contribute to muscle weakness. The discussion includes the important role that alterations in the physiology of motor units, notably changes in firing rates and muscle fiber atrophy, play in the manifestation of muscle weakeness. This role is compared with the lesser role that spasticity of the antagonist muscle group appears to play in determining the weakness of agonist muscles. The contribution of other factors that result in mechanical restraint of the agonist by the antagonist is discussed relative to muscle weakness in patients with hemiparesis. More studies on patients with hemiparesis are required to assess what role muscle strength training should play in rehabiliting patients after a stroke.