Oxidative capacity of human muscle fiber types: effects of age and training status

Abstract

Morphometry and oxidative capacity of slow-twitch (type I) and fast-twitch (type IIa and IIb) muscle fibers obtained from vastus lateralis needle biopsies were compared between younger (21-30 yr) and older (51-62 yr) normal fit (maximal O2 uptake = 47.0 vs. 32.3 ml.kg-1.min-1) and endurance-trained (66.3 vs. 52.7 ml.kg-1.min-1) men (n = 6/group). The older groups had smaller type IIa (31%) and IIb (40%) fiber areas and fewer capillaries surrounding these fibers than did younger groups. The reduced type II fiber areas and capillary contacts associated with aging were also observed in the older trained men. However, the capillary supply per unit type II fiber area was not affected by age but was enhanced by training. Additionally, on the basis of quantitative histochemical analysis, succinate dehydrogenase activities of type IIa fibers in the older trained men [4.07 +/- 0.68 (SD) mmol.min-1.l-1] were similar to those observed in younger trained men (4.00 +/- 0.48 mmol.min-1.l-1) and twofold higher than in older normal fit men (2.01 +/- 0.65 mmol.min-1.l-1; age x fitness interaction, P < 0.05). Type I muscle fibers were unaffected by age but were larger and had more capillary contacts and higher succinate dehydrogenase activities in the trained groups. The findings of this study suggest that aging results in a decrease in type II fiber size and oxidative capacity in healthy men and that this latter effect can be prevented by endurance training. Conclusions regarding the effects of age and training status on muscle capillarization depend largely on how these data are expressed.

Effects of Age and Sex on Postprandial Glucose Metabolism

“…Visceral fat was measured by a single-slice computerized tomographic scan at the level of L2/L3 (30). Peak oxygen uptake (VO 2max ) was measured using a standard treadmill stress test (31). Knee extensor strength was measured by having each subject lift a progressively higher weight using a bilateral leg press machine (Cybex, Medway, MA) until the one-repetition maximum was reached.…”

Reduced muscle oxidative capacity is independent of O2 availability in elderly people

“…If true, this increased O 2 diffusion during exercise in the elderly would then result in a preserved intracellular O 2 pressure (iPO 2 ), which drives mitochondrial respiration (Wilson et al 1977;Richardson et al 1999;Richardson et al 1995). In line with this possibility, O 2 diffusing capacity appears to be well preserved in the elderly as the capillary to fiber area ratios is maintained (Chilibeck et al 1997;Proctor et al 1995) and may actually be increased when capillary to fiber area is normalized for mitochondrial volume (Mathieu-Costello et al 2005). In addition, the reduction in muscle blood flow does not necessarily translate into a reduced O 2 supply to the mitochondria as, in this scenario, the erythrocyte transit time through the capillary is prolonged, which allows higher O 2 extraction by the tissues (Richardson 1998).…”

Skeletal Muscle Dysfunction in Patients with Chronic Obstructive Pulmonary Disease

“…For instance, one study, in which proper control subjects had similar physical activity levels to those of COPD patients, revealed reductions of quadriceps muscle endurance in the COPD patients that cannot be explained by a mere lack of physical activity since reductions in the proportion of type I fi bers in quadriceps muscles of COPD patients are relatively greater than in the control group (Couillard et al 2002). Indeed, while sedentary lifestyle is associated with reduction of quadriceps muscle type I fi ber proportion, from 60%-65% in healthy active control subjects to about 40% in inactive subjects (Proctor et al 1995;Houmard et al 1998), the proportion of type I fi bers in quadriceps muscles of COPD patients reaches as low as 19% (Gosker et al 2002;Allaire et al 2004;Richardson et al 2004). It is also worth noting that prolonged periods of exercise training exerts a relatively small infl uence on the proportion of type I fi bers in quadriceps muscles of COPD patients, and only partially reverses reductions in oxidative enzyme activities (citrate synthase and 3-hydroxyacyl-CoA dehydrogenase) in the muscle (Maltais et al 1996;Whittom et al 1998).…”