Metzger C E, Baek K, Swift S N, De Souza M J, Bloomfield S A
Department of Health & Kinesiology, Texas A&M University, College Station, TX, USA.
Department of Pharmacology, College of Dentistry and Research of Oral Science, Gangneung-Wonju National University, Gangwondo, Korea.
Osteoporos Int. 2016 Sep;27(9):2755-2764. doi: 10.1007/s00198-016-3590-y. Epub 2016 Apr 29.
Energy restriction causes bone loss, increasing stress fracture risk. The impact of exercise during energy restriction on bone and endocrine factors is examined. Exercise with energy restriction did not influence endocrine factors, but did mitigate some bone loss seen with energy restriction in sedentary rats.
Chronic dietary energy restriction (ER) leads to bone loss and increased fracture risk. Strictly controlled trials of long-term ER with and without vigorous exercise are required to determine whether exercise loading can counterbalance ER-induced bone loss. The aim of this current project is to elucidate the impact of exercise and ER on bone mass, estrogen status, and metabolic hormones.
Twenty-four virgin female Sprague-Dawley rats (n = 8/group) were divided into three groups-ad libitum fed + exercise (Adlib + EX), 40 % energy restricted + exercise (ER + EX), and 40 % energy restricted + sedentary (ER + SED). Energy availability between ER groups was equal. Treadmill running was performed 4 days/week at 70 % VO2max for 12 weeks.
Fat and lean mass and areal bone mineral density (aBMD) were lower after 12 weeks (p < 0.05) for ER + EX vs Adlib + EX, but ER + EX aBMD was higher than ER + SED (p < 0.0001). Serum leptin and a urinary estrogen metabolite, estrone-1-glucuronide (E1G), were lower at week 12 (p = 0.0002) with ER, with no impact of exercise. Serum insulin-like growth factor I (IGF-I) declined (p = 0.02) from baseline to week 12 in both ER groups. ER + EX exhibited higher cortical volumetric bone mineral density (vBMD) at the midshaft tibia (p = 0.006) vs ER + SED.
Exercise during ER mitigated some, but not all, of the bone loss observed in sedentary ER rats, but had little impact on changes in urinary E1G and serum IGF-I and leptin. These data highlight the importance of both adequate energy intake and the mechanical loading of exercise in maintaining bone mass.
能量限制会导致骨质流失，增加应力性骨折风险。本研究探讨了能量限制期间运动对骨骼和内分泌因子的影响。能量限制与运动相结合并未影响内分泌因子，但确实减轻了久坐不动的大鼠在能量限制时出现的部分骨质流失。
长期饮食能量限制（ER）会导致骨质流失和骨折风险增加。需要进行严格控制的长期ER试验，包括有或没有剧烈运动的情况，以确定运动负荷是否可以抵消ER引起的骨质流失。本项目的目的是阐明运动和ER对骨量、雌激素状态和代谢激素的影响。
将24只未交配的雌性Sprague-Dawley大鼠（每组n = 8只）分为三组：自由进食 + 运动（自由进食 + 运动组）、40%能量限制 + 运动（ER + 运动组）和40%能量限制 + 久坐不动（ER + 久坐组）。ER组之间的能量可利用量相等。每周进行4天跑步机跑步，速度为最大摄氧量的70%，持续12周。
12周后，ER + 运动组的脂肪和瘦体重以及骨面积骨密度（aBMD）低于自由进食 + 运动组（p < 0.05），但ER + 运动组的aBMD高于ER + 久坐组（p < 0.0001）。ER组在第12周时血清瘦素和尿雌激素代谢物雌酮 - 1 - 葡萄糖醛酸苷（E1G）较低（p = 0.0002），运动对此无影响。两个ER组从基线到第12周血清胰岛素样生长因子I（IGF - I）均下降（p = 0.02）。与ER + 久坐组相比，ER + 运动组胫骨中段的皮质骨体积骨密度（vBMD）更高（p = 0.
