Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia.
Am J Physiol Endocrinol Metab. 2012 May 1;302(10):E1221-30. doi: 10.1152/ajpendo.00583.2011. Epub 2012 Feb 21.
We have previously shown that 4 wk of exercise training early in life normalizes the otherwise greatly reduced pancreatic β-cell mass in adult male rats born small. The aim of the current study was to determine whether a similar normalization in adulthood of reduced skeletal muscle mitochondrial biogenesis markers and alterations in skeletal muscle lipids of growth-restricted male rats occurs following early exercise training. Bilateral uterine vessel ligation performed on day 18 of gestation resulted in Restricted offspring born small (P < 0.05) compared with both sham-operated Controls and a sham-operated Reduced litter group. Offspring remained sedentary or underwent treadmill running from 5-9 (early exercise) or 20-24 (later exercise) wk of age. At 24 wk of age, Restricted and Reduced litter offspring had lower (P < 0.05) skeletal muscle peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) protein expression compared with Control offspring. Early exercise training had the expected effect of increasing skeletal muscle markers of mitochondrial biogenesis, but, at this early age (9 wk), there was no deficit in Restricted and Reduced litter skeletal muscle mitochondrial biogenesis. Unlike our previous observations in pancreatic β-cell mass, there was no "reprogramming" effect of early exercise on adult skeletal muscle such that PGC-1α was lower in adult Restricted and Reduced litter offspring irrespective of exercise training. Later exercise training increased mitochondrial biogenesis in all groups. In conclusion, although the response to exercise training remains intact, early exercise training in rats born small does not have a reprogramming effect to prevent deficits in skeletal muscle markers of mitochondrial biogenesis in adulthood.
我们之前已经表明，在生命早期进行 4 周的运动训练可以使出生时体型较小的成年雄性大鼠的胰腺β细胞数量恢复正常，否则这些β细胞数量会大大减少。本研究的目的是确定在生命早期进行运动训练后，是否会使生长受限的雄性大鼠的骨骼肌线粒体生物发生标志物减少和骨骼肌脂质改变在成年期恢复正常。在妊娠第 18 天对子宫双侧血管进行结扎，导致受限后代出生时体型较小（P<0.05），与假手术对照和假手术减少组相比均如此。后代保持久坐或从 5-9 周龄（早期运动）或 20-24 周龄（后期运动）开始进行跑步机跑步。在 24 周龄时，受限和减少组后代的骨骼肌过氧化物酶体增殖物激活受体 γ共激活因子 1α（PGC-1α）蛋白表达低于对照组后代（P<0.05）。早期运动训练对骨骼肌线粒体生物发生标志物有预期的增加作用，但在这个早期年龄（9 周龄），受限和减少组后代的骨骼肌线粒体生物发生并没有缺陷。与我们之前在胰腺β细胞数量方面的观察结果不同，早期运动对成年骨骼肌没有“重编程”效应，因此无论是否进行运动训练，成年受限和减少组后代的 PGC-1α 均较低。后期运动训练增加了所有组的线粒体生物发生。总之，尽管对运动训练的反应仍然完好无损，但在出生较小的大鼠中进行早期运动训练并没有重编程效应，可以防止成年骨骼肌中线粒体生物发生标志物的减少。
