Cates Brittany E, Dillard Bryce M, Foster Brittany R, Patterson Shawnee V, Spivey Thomas P, Combs Eric B, Bowen Robert S
Laboratory of Applied and Exercise Endocrinology, Pilgram Marpeck School of STEM, Truett McConnell University, Cleveland, Georgia.
Physiol Rep. 2018 Jun;6(11):e13730. doi: 10.14814/phy2.13730. Epub 2018 Jun 4.
Physical inactivity is a leading cause of hypokinetic diseases - obesity, heart disease, diabetes, and certain types of cancers. Increased city walkability, better access to fitness facilities, and remediation of socioeconomic barriers prove successful for limited populations within the confines of stringently controlled environments; however, these strategies fail to reverse the ever-increasing physical inactivity epidemic on a global scale indicating the existence of other unidentified factors. These purported biological factors remain critical targets to understand the regulation of this complex phenotype. An estrogenic mechanism that incompletely or slowly adjusts physical activity levels following reintroduction of estrogenic compounds to surgically gonadectomized mice has been postulated to exist. Currently, this mechanism remains scrutinized due to concerns that elevated estrogen levels induce urinary bladder distension. The distension of the urinary bladder may mechanically disrupt physical activity, masking any physiological effects estrogen has on physical activity. The purpose of this study was to evaluate the effects of estrogen on physical activity levels while employing dose-related strategies to alleviate distension in mice. Wheel running data were collected under normal physiological conditions, following removal of endogenous sex steroids via orchidectomy, and during estrogen replacement at various doses (0%, 10%, 50% or 100% estrogen-containing implants) to induce varying degrees of urinary bladder distension. Wheel running distance (P = 0.005) and duration (P = 0.006) decreased after orchidectomy, but slowly increased following estrogen replacement. During the study, wheel running did not return to the levels observed in physiologically intact mice. Significant distension was not observed between estrogen treatment groups indicating that a slow-responding estrogen effect exists in male mice that prevents wheel running from returning to normal levels immediately following steroid reintroduction. The limited increase in wheel running during estrogen treatment following orchidectomy is not an artifact of induced urinary bladder distension.
缺乏身体活动是运动不足相关疾病（肥胖、心脏病、糖尿病和某些类型的癌症）的主要原因。在严格控制的环境范围内，提高城市的步行便利性、改善健身设施的可及性以及消除社会经济障碍，已被证明对有限的人群是成功的；然而，这些策略未能在全球范围内扭转日益严重的身体活动不足的流行趋势，这表明存在其他未被识别的因素。这些所谓的生物学因素仍然是理解这种复杂表型调节的关键靶点。据推测，存在一种雌激素机制，在给手术去势的小鼠重新引入雌激素化合物后，该机制会不完全或缓慢地调节身体活动水平。目前，由于担心雌激素水平升高会导致膀胱扩张，这种机制仍在受到审查。膀胱扩张可能会机械性地干扰身体活动，掩盖雌激素对身体活动的任何生理影响。本研究的目的是在采用剂量相关策略减轻小鼠膀胱扩张的同时，评估雌激素对身体活动水平的影响。在正常生理条件下、通过睾丸切除去除内源性性类固醇后以及在给予不同剂量（含0%、10%、50%或100%雌激素的植入物）的雌激素替代以诱导不同程度的膀胱扩张期间，收集轮转运动数据。睾丸切除后，轮转运动距离（P = 0.005）和持续时间（P = 0.006）下降，但在雌激素替代后缓慢增加。在研究期间，轮转运动未恢复到生理完整小鼠所观察到的水平。雌激素治疗组之间未观察到明显的扩张，这表明雄性小鼠中存在一种反应缓慢的雌激素效应，阻止了在重新引入类固醇后轮转运动立即恢复到正常水平。睾丸切除后雌激素治疗期间轮转运动的有限增加不是诱导膀胱扩张的假象。
