[Objective] The aim of this investigation was to evaluate bone metabolism responses to acute resistance exercise during the menstrual cycle. [Methods] Subjects were young healthy sedentary women (n=7) with regular menstrual cycles. The subjects performed acute resistance exercise in each phase (follicular and luteal) of the menstrual cycle. Bone metabolism markers (bone formation marker BAP and bone resorption marker ICTP), bone metabolism related hormones (parathyroid hormone, calcitonin, calcium and inorganic phosphorus) and lactate were determined. Blood samples were collected before (Pre) and immediately following the exercise (Post), 1 hour (P1h) and 24 hours (P24h) after the exercise. [Results] BAP significantly increased at Post compared with Pre both in the follicular and luteal phases (p<0.05), but significantly decreased at P1h and P24h in the luteal phase. ICTP significantly increased at Post in the follicular phase (p<0.05) and significantly decreased at P1h and P24h in the luteal phase. The bone metabolism responses in the luteal phase moved to low-bone turnover at P1h and P24h. [Conclusion] The bone metabolism response to acute resistance exercise was different between menstrual phases. These results suggest that bone metabolism is influenced by the menstrual cycle.

In the present review article, we present an overview of beta-adrenoceptor (beta-AR) subtype expression at the mRNA and receptor protein levels in the human detrusor, the in vitro and in vivo bladder function of the beta3-AR, the in vivo effect of beta3-AR agonists on detrusor overactivity in animal models, and the available results of clinical trials of beta3-AR agonists for treating overactive bladder (OAB). There is a predominant expression of beta3-AR mRNA in human bladder, constituting 97% of total beta-AR mRNA. Also, functionally, the relaxant response of human detrusor to catecholamines is mainly mediated through the beta3-ARs. Moreover, the presence of beta1-, beta2-, and beta3-AR mRNAs in the urothelium and suburothelial layer of human bladder has been identified. Stimulation of urothelial beta-ARs results in the release of nitric oxide and an unknown substance inhibiting detrusor contractions from the urothelium. Intravenous application of CL316,243, a selective beta3-AR agonist, in rats selectively inhibits mechano-sensitive Adelta-fiber activity of the primary bladder afferents. A number of selective beta3-AR agonists are currently being evaluated in clinical trials for OAB with promising preliminary results. In conclusion, the beta3-AR agonists are the most notable alternative class of agents to antimuscarinics in the pharmacological treatment of OAB. The beta3-AR agonists act to facilitate bladder storage function probably through at least two mechanisms: first, direct inhibition of the detrusor, and second, inhibition of bladder afferent neurotransduction.
Adrenergic beta-Agonists ; Afferent Pathways ; Animals ; Catecholamines ; Contracts ; Dioxoles ; Humans ; Models, Animal ; Muscarinic Antagonists ; Nitric Oxide ; Rats ; RNA, Messenger ; Urinary Bladder ; Urinary Bladder, Overactive ; Urothelium