Institute for Physical Activity and Nutrition, School of Exercise and Nutrition Sciences, Deakin University, Geelong, VIC, 3125, Australia.
Department of Physiology, The University of Melbourne, VIC, 3010, Australia.
J Physiol. 2018 Jan 15;596(2):163-180. doi: 10.1113/JP275339. Epub 2017 Dec 18.
Cardiac hypertrophy following endurance-training is thought to be due to hypertrophy of existing cardiomyocytes. The benefits of endurance exercise on cardiac hypertrophy are generally thought to be short-lived and regress to sedentary levels within a few weeks of stopping endurance training. We have now established that cardiomyocyte hyperplasia also plays a considerable role in cardiac growth in response to just 4 weeks of endurance exercise in juvenile (5-9 weeks of age) rats. The effect of endurance exercise on cardiomyocyte hyperplasia diminishes with age and is lost by adulthood. We have also established that the effect of juvenile exercise on heart mass is sustained into adulthood.
The aim of this study was to investigate if endurance training during juvenile life 'reprogrammes' the heart and leads to sustained improvements in the structure, function, and morphology of the adult heart. Male Wistar Kyoto rats were exercise trained 5 days week for 4 weeks in either juvenile (5-9 weeks of age), adolescent (11-15 weeks of age) or adult life (20-24 weeks of age). Juvenile exercise training, when compared to 24-week-old sedentary rats, led to sustained increases in left ventricle (LV) mass (+18%; P < 0.05), wall thickness (+11%; P < 0.05), the longitudinal area of binucleated cardiomyocytes (P < 0.05), cardiomyocyte number (+36%; P < 0.05), and doubled the proportion of mononucleated cardiomyocytes (P < 0.05), with a less pronounced effect of exercise during adolescent life. Adult exercise training also increased LV mass (+11%; P < 0.05), wall thickness (+6%; P < 0.05) and the longitudinal area of binucleated cardiomyocytes (P < 0.05), despite no change in cardiomyocyte number or the proportion of mono- and binucleated cardiomyocytes. Resting cardiac function, LV chamber dimensions and fibrosis levels were not altered by juvenile or adult exercise training. At 9 weeks of age, juvenile exercise significantly reduced the expression of microRNA-208b, which is a known regulator of cardiac growth, but this was not sustained to 24 weeks of age. In conclusion, juvenile exercise leads to physiological cardiac hypertrophy that is sustained into adulthood long after exercise training has ceased. Furthermore, this cardiac reprogramming is largely due to a 36% increase in cardiomyocyte number, which results in an additional 20 million cardiomyocytes in adulthood.
耐力训练后引起的心肌肥厚被认为是由于现有心肌细胞的肥大所致。耐力运动对心肌肥厚的益处通常是短暂的，在停止耐力训练后数周内会恢复到久坐不动的水平。我们现在已经确定，仅仅在幼年（5-9 周龄）大鼠进行 4 周的耐力运动，心肌细胞增生也在心脏生长中发挥了相当大的作用。随着年龄的增长，耐力运动对心肌细胞增生的影响会减弱，到成年时会消失。我们还发现，幼年运动对心脏质量的影响会持续到成年期。
本研究旨在探讨青少年时期的耐力训练是否“重新编程”了心脏，并导致成年心脏的结构、功能和形态持续改善。雄性 Wistar Kyoto 大鼠在青少年（11-15 周龄）、成年（20-24 周龄）时期分别进行 5 天/周、4 周的耐力训练。与 24 周龄的安静大鼠相比，幼年运动训练导致左心室（LV）质量持续增加（+18%；P<0.05）、壁厚度增加（+11%；P<0.05）、双核心肌细胞的纵向面积增加（P<0.05）、心肌细胞数量增加（+36%；P<0.05）、单核心肌细胞的比例增加一倍（P<0.05），而青少年时期的运动训练则效果不明显。成年运动训练也增加了 LV 质量（+11%；P<0.05）、壁厚度（+6%；P<0.05）和双核心肌细胞的纵向面积（P<0.05），尽管心肌细胞数量或单核和双核心肌细胞的比例没有变化。青少年或成年运动训练均不改变静息心功能、LV 腔室尺寸和纤维化水平。在 9 周龄时，幼年运动显著降低了 microRNA-208b 的表达，microRNA-208b 是一种已知的心脏生长调节剂，但这种作用在 24 周龄时并未持续。总之，青少年运动导致的生理性心肌肥厚可持续到成年期，即使在运动训练停止后很久也是如此。此外，这种心脏重编程主要归因于心肌细胞数量增加 36%，导致成年后额外增加 2000 万个心肌细胞。
