Histochemical and Enzymatic Comparison of the Gastrocnemius Muscle of Young and Elderly Men and Women

Abstract

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.

A morphometric study on human muscle mitochondria in aging

“…These functional features are consistent with a significant age-related decay in the activity of several mitochondrial enzymes reported both in muscles from human beings (3) as well as laboratory animals (4). With reference to human studies, also the number of mitochondria per gram of tissue decreases in subjects over 50 years of age (5,6). The functional outcome of these changes is a marked reduction in aerobic endurance which appears to be correlated to mitochondrial density and to the specific metabolic competence of each organelle in providing adequate amounts of adenosinetriphosphate (ATP) (7).…”

“…In these groups, higher percentages of more convoluted and distorted organelles (Plei histograms and distributions in Figs. [2][3][4][5] were also evident. The present findings confirm previous reports documenting a substantial lifespan preservation of muscle mitochondria ultrastructural features not only in physiological aging, but also in a severe pathological condition, such as chronic fatigue syndrome, where a decline of the mitochondrial metabolic competence is reported to be a typical alteration (12,13).…”

“…Muscle aging is a complex process affected by a marked variability due to multiple individual determinants including: muscle disuse, malnutrition and the physiological decline of cardiovascular, nervous and locomotion systems (2,23). All these causal events contribute to the macroscopic, physiological and incessant muscle atrophy occurring in aging (also referred to as sercopenia) which is not always associated with a significant decrease of the quality of muscle performances (24) because of the plastic condition of the muscle tissue reported even in aging (5,6,25). The recently introduced molecular biology techniques have clearly documented an increase of mitochonddal DNA (mtDNA) deletions in the rodent and primate skeletal muscle with aging (26,27).…”

Coupling between skeletal muscle fiber size and capillarization is maintained during healthy aging

“…Values in type I fibres were around 45% greater than those in type II, but there were no age or sex differences in the oxidative capacity of fibres (reflecting the volume density of mitochondria) signifying a remarkable preservation in aged muscle in spite of the substantial muscle fibre morphological remodelling. Previous reports of age‐related reduction in the oxidative capacity from rat muscles44 and the human gastrocnemius45 may be due to an age‐related decrease in physical activity levels, whereas our physically and socially active participants likely benefited from activity‐related maintenance of oxidative capacity 46, 47…”

“…If so regular physical activity, which will increase muscle blood flow and hence endothelial shear stress, may prevent some of the age‐related capillary rarefaction. Indeed, in master athletes, the capillary‐to‐fibre ratio was larger than in activity‐matched young controls,47 while in sedentary older people the capillary‐to‐fibre ratio was reduced 45…”