Aging skeletal muscle: response to exercise.

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)