School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia.
Muscle Nerve. 2011 Jan;43(1):37-48. doi: 10.1002/mus.21778. Epub 2010 Sep 30.
Absence of α-actinin-3, encoded by the ACTN3 "speed gene," is associated with poorer sprinting performance in athletes and a slowing of relaxation in fast-twitch muscles of Actn3 knockout (KO) mice. Our first aim was to investigate, at the individual-fiber level, possible mechanisms for this slowed relaxation. Our second aim was to characterize the contractile properties of whole extensor digitorum longus (EDL) muscles from KO mice by age and gender. We examined caffeine-induced Ca(2+) release in mechanically skinned EDL fibers from KO mice, and measured isolated whole EDL contractile properties. The sarcoplasmic reticulum of KO muscle fibers loaded Ca(2+) more slowly than that of wild-types (WTs). Whole KO EDL muscles had longer twitch and tetanus relaxation times than WTs, and reduced mass and cross-sectional area. These effects occurred in both male and female mice, but they diminished with age. These changes in KO muscles and fibers help to explain the effects of α-actinin-3 deficiency observed in athletes.
缺乏由 ACTN3“速度基因”编码的α-辅肌动蛋白-3与运动员短跑成绩较差以及 Actn3 敲除 (KO) 小鼠快肌松弛速度减慢有关。我们的首要目标是在单个纤维水平上研究这种松弛减慢的可能机制。我们的第二个目标是通过年龄和性别来描述 KO 小鼠伸趾长肌 (EDL) 整体的收缩特性。我们检测了 KO 小鼠机械剥皮 EDL 纤维中咖啡因诱导的 Ca(2+)释放,并测量了分离的整个 EDL 收缩特性。与野生型 (WTs) 相比,KO 肌纤维的肌浆网加载 Ca(2+)的速度较慢。KO EDL 整体肌肉的 twitch 和 tetanus 松弛时间比 WTs 长,质量和横截面积减小。这些影响在雄性和雌性小鼠中都存在,但随着年龄的增长而减弱。KO 肌肉和纤维中的这些变化有助于解释运动员中观察到的α-辅肌动蛋白-3缺乏的影响。