A lower stroke volume, heart rate, and arteriovenous oxygen difference at maximal exercise all contribute to the age-related decline in VO2max. Effects of age and training on VO2max, maximal cardiac output, and stroke volume cannot be fully explained by differences in body composition. In sedentary subjects, however, the sex difference in maximal cardiac output and stroke volume can be accounted for by the greater percentage of body fat in women than in men.

To examine the effects of aging on human skeletal muscle, 10 men and 10 women, 64 +/- 1 yr old (Mean +/- SE), and 10 men and 10 women, 24 +/- 1 yr old, were studied. All subjects were sedentary nonsmokers who were carefully screened for latent cardiovascular, metabolic, or musculoskeletal disease. Needle biopsy samples were obtained from the lateral gastrocnemius muscle and examined using histochemical and biochemical techniques. The percentage of Type I, Type IIa, and Type IIb fibers did not differ with age. However, Type I fibers occupied a larger percent of total muscle area in the older men and women (60.6 +/- 2.6 vs 53.6 +/- 2.0%; p less than .05), because Type IIa and Type IIb fibers were 13-31% smaller (p less than .001) in these subjects. Muscle capillarization and mitochondrial enzyme (i.e., succinate dehydrogenase, citrate synthase, and beta-hydroxyacyl-CoA dehydrogenase) activities were also approximately 25% lower (p less than .001-.05) in the old subjects. Although it is difficult to determine whether these differences are due to aging itself or are simply due to inactivity, these structural and biochemical changes probably contribute to the decreases in muscle mass, strength, and endurance often observed in healthy but sedentary older men and women.

Previous studies of endurance exercise training in older men and women generally have found only minimal skeletal muscle adaptations to training. To evaluate the possibility that this may have been due to an inadequate training stimulus, we studied 23 healthy older (64 +/- 3 yr) men and women before and after they had trained by walking/jogging at 80% of maximal heart rate for 45 min/day 4 days/wk for 9-12 mo. This training program resulted in a 23% increase in maximal O2 consumption. Needle biopsy samples of the lateral gastrocnemius muscle were obtained before and after training and analyzed for selected histochemical and enzymatic characteristics. The percentage of type I muscle fibers did not change with training. The percentage of type IIb fibers, however, decreased from 19.1 +/- 9.1 to 15.1 +/- 8.1% (P less than 0.001), whereas the percentage of type IIa fibers increased from 22.1 +/- 7.7 to 29.6 +/- 9.1% (P less than 0.05). Training also induced increases in the cross-sectional area of both type I (12%; P less than 0.001) and type IIa fibers (10%; P less than 0.05). Capillary density increased from 257 +/- 43 capillaries/mm2 before training to 310 +/- 48 capillaries/mm2 after training (P less than 0.001) because of increases in the capillary-to-fiber ratio and in the number of capillaries in contact with each fiber. Lactate dehydrogenase activity decreased by 21% (P less than 0.001), whereas the activities of the mitochondrial enzymes succinate dehydrogenase, citrate synthase, and beta-hydroxyacyl-CoA dehydrogenase increased by 24-55% in response to training (P less than 0.001-0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The adaptive response of maximal aerobic power (VO2max) to endurance exercise training was compared in 53 men and 57 women, aged 60-71 yr. The subjects were healthy and had been sedentary for at least 2 yr. Pretraining VO2max was measured during graded treadmill walking on two occasions. These values were reproducible (24.4 +/- 4.7 vs. 24.4 +/- 4.6 (SD) ml.min-l.kg-1; r = 0.96). Subjects trained primarily by walking and running for 9-12 mo, averaging 3.9 +/- 0.6 days/wk and 45 +/- 5 min/day at 80 +/- 5% of maximal heart rate (HRmax). Average improvement in VO2max (ml.min-1.kg-1) was 24 +/- 12% (range 0-58%). Relative improvement was not significantly different in men and women (26 +/- 12 vs. 23 +/- 12%, ml.min-1.kg-1; 21 +/- 10 vs 19 +/- 10%, l/min). When subjects were divided into three groups by age (60-62, 63-66, 67-71 yr), there were no significant differences among the groups in the relative increase in VO2max (21% vs. 19% vs. 18%, 1/min). Correlation analysis also yielded a nonsignificant relationship between improvement and age (r = -0.13). To examine the effect of initial fitness level on the adaptive response to exercise, pretraining VO2max was correlated with the absolute improvement in VO2max. This relationship was not significant in either men (r = 0.04) or women (r = -0.23). In conclusion, in healthy people aged 60-71 yr, VO2max adapts to endurance exercise training to the same relative extent as in young people, and this adaptation is independent of gender, age, and initial level of fitness.

Endurance exercise training induces a significant increase in the respiratory capacity of skeletal muscle. This is reflected by a training-induced increase in mitochondrial enzyme activity. One consequence of this adaptation is that there is a decreased reliance on carbohydrate utilization with a concomitant increase in fat utilization, resulting in an improvement in endurance capacity. Recently it has been reported that 7-14 days of cycle ergometer exercise training does not induce an increase in mitochondrial enzyme levels in skeletal muscle but, nevertheless, results in smaller decreases in phosphocreatine and glycogen and smaller increases in Pi and lactate in muscle in response to the same exercise after compared with before training. However, previous studies in rats have shown that an adaptive increase in mitochondrial enzymes is already evident after only 2 days of exercise training. In view of this discrepency, the present study was performed to reevaluate the effect of short-term training (7-10 days) on mitochondrial enzymes in skeletal muscle of humans. Twelve subjects [6 men and 6 women, 27 +/- 5 (SE) yr old] underwent 7 (n = 5) or 10 days (n = 7) of cycle ergometer exercise for 2h/day at 60-70% of peak O2 consumption. Peak O2 consumption was increased by 9% (from 2.97 +/- 0.16 to 3.24 +/- 0.17 l/min) in response to training. Blood lactate levels were lower at the same absolute work rates after than before training. The activities of citrate synthase, beta-hydroxyacyl-CoA dehydrogenase, mitochondrial thiolase, and carnitine acetyltransferase were increased by approximately 30% in response to training. The results of the present study provide evidence that in humans, as in rats, the adaptive increase in mitochondrial enzymes in skeletal muscle occurs fairly rapidly in response to exercise training. They provide no support for the claim that this adaptive response is delayed for > 2 wk after the onset of training.