Aging Skeletal Muscle: Response to Exercise
Aging Skeletal Muscle: Response to Exercise
复制标题
骨骼肌老化：对运动的反应
DOI：
10.1249/00003677-199401000-00006
复制
发表时间：
1994
影响因子：
5.7
通讯作者：
G. Cartee
中科院分区：
文献类型：
--
作者：
G. Cartee
老年大鼠许多承重肌肉的质量下降，继发于纤维萎缩，尤其是 IIb 型纤维萎缩，在成年大鼠的大部分生命周期中，肌纤维损失相对较少。在人类中，肌肉萎缩是进行性纤维损失和纤维萎缩共同作用的结果。在这两个物种中，组织化学确定的纤维类型的比例在整个生命周期的成年部分相对稳定。人类和大鼠老年体力丧失的主要原因是肌肉质量减少。阻力训练主要通过增加纤维 CSA 来增加老年人和大鼠的肌肉质量和力量。老年大鼠的肌肉毛细血管活动没有变化，但老年狗的肌肉毛细血管活动减少。显然，真正久坐的老年人的毛细血管作用会下降。耐力训练可以增强毛细血管作用，即使运动量少得多，年老的老鼠和人类也可以达到与活跃的年轻老鼠相当的毛细血管水平。雄性大鼠和人类收缩活动期间的血流量减少，但老年雌性大鼠或狗的血流量却没有减少。久坐的老年大鼠和人类的许多肌肉的氧化能力都会下降。通过耐力训练，这两个物种的老年人的肌肉氧化能力水平与接受相同训练的年轻人非常相似。无论年龄大小，大鼠在运动一次后，肌肉胰岛素刺激的葡萄糖转运都会增强。耐力训练会提高年轻和中年大鼠的肌肉 GLUT-4 水平，但不会提高老年大鼠的肌肉 GLUT-4 水平，这可能是因为老年大鼠在跑步机上训练的速度较慢。中年（47-62岁）男性和女性可以通过相对短暂（12-14周）的耐力训练大幅增加肌肉GLUT-4；尚未对老年人（> 70-80 岁）进行研究。在老年大鼠和人类中，耐力训练可降低 LDH 活性，而不会改变 PFK 或磷酸化酶。在老年大鼠中，收缩活动期间的肌肉糖原消耗、CP消耗和乳酸积累被夸大，这显然是由于肌肉氧化能力和血流量降低而继发的。老年人的静息肌糖原浓度降低，部分原因可能是久坐的生活方式。尽管几个月的耐力训练可以提高老年人的肌糖原浓度，但并不能使其恢复到年轻水平。耐力训练可以极大地提高老年时的耐力，至少部分是通过最初在青年时期描述的相同机制，即增加肌肉氧化能力，从而有助于减少糖原消耗。（摘要截断为 400 字）
The mass of many weight-bearing muscles declines in old rats, secondary to the atrophy of fibers, particularly of type IIb, with relatively little loss of muscle fibers during most of the adult life span. In humans, muscle atrophy is the result of a combination of progressive fiber loss and fiber atrophy. In both species, the proportion of histochemically determined fiber types is relatively stable across the adult portion of the life span. The loss of strength in old age is predominantly accounted for by reduced muscle mass in humans and rats. Resistance training leads to increased muscle mass and strength in old humans and rats, primarily by increasing fiber CSA. Muscle capillarity is unchanged in old rats but decreases in old dogs. Apparently, capillarity declines in truly sedentary older people. Endurance training enhances capillarity, and old rats and humans can attain levels of capillarity comparable to their active young counterparts, even when performing considerably less exercise. Blood flow during contractile activity is reduced in male rats and humans but not in old female rats or dogs. Oxidative capacity declines in many muscles of sedentary old rats and humans. With endurance training, old individuals from both species attain levels of muscle oxidative capacity quite similar to those in identically training young individuals. Muscle insulin-stimulated glucose transport is enhanced in rats after a bout of exercise, regardless of age. Endurance training elevates muscle GLUT-4 levels in young and middle-aged, but not old, rats, perhaps because the old rats trained at slower treadmill speeds. Middle-aged (47-62 yr) men and women can substantially increase muscle GLUT-4 with relatively brief (12-14 wk) endurance training; older humans (> 70-80 yr) have not been studied. Endurance training leads to reduced LDH activity without altering PFK or phosphorylase in old rats and humans. Muscle glycogen depletion, CP depletion, and lactate accumulation during contractile activity are exaggerated in old rats, apparently secondary to reduced muscle oxidative capacity and blood flow. Resting muscle glycogen concentration is diminished in older humans, probably in part because of a more sedentary lifestyle. Although several months of endurance training raises muscle glycogen concentration in older people, it does not restore it to youthful levels. Endurance training can greatly improve endurance in old age, at least in part by the same mechanism originally described in youth, i.e., an increase in muscle oxidative capacity, which contributes to reduced glycogen depletion.(ABSTRACT TRUNCATED AT 400 WORDS)