Muscle biopsy samples were obtained from healthy subjects in order to evaluate quantitative differences in single fibres of substrate (glycogen and triglyceride) and ion concentrations (Na+ and K+) as well as enzyme activity levels (succinate-dehydrogenase, SDH; phosphofructokinase, PFK; 3-hydroxyacyl-CoA-dehydrogenase, HAD; myosin ATPase) between human skeletal muscle fibre types. After freeze drying of the muscle specimen fragments of single fibres were dissected out and stained for myofibrillar-ATPase with preincubations at pH's of 10.3, 4.6, 4.35. Type I ("red") and II A,B, and C ("white") fibres could then be identified. Glycogen content was the same in different fibres, whereas triglyceride content was highest in Type I fibres (2-3 X Type II). No significant differences were observed for Na+ and K+ between fibre types. The activity for the enzymes studied were quite different in the fibre types (SDH and HAD, Type I is approximately 1.5 X Type II; PFK Type I is approximately 0.5 X Type II, Myosin ATPase Type I is approxiamtely 0.4 X Type II). The subgroups of Type II fibres were distinguished by differences in both SDH and PFK activities (SDH, Type II C is greater than A is greater than B; PFK, Type II B is greater than A is approximately C). It is concluded that contractile and metabolic characteristics of human skeletal fibres are very similar to many other species. One difference, however, appears to be than no Type II fibres have an oxidative potential higher than Type I fibres.

The influence of age-associated motor unit loss on contractile strength was investigated in a representative sample of healthy, active young and older men and women. In 24 younger subjects (22-38 yr) and 20 older subjects (60-81 yr) spike-triggered averaging was employed to extract a sample of surface-recorded single motor unit action potentials (S-MUAPs) from the biceps brachii and brachialis muscles. The amplitude of the maximum compound muscle action potential of the biceps brachii and brachialis muscles was divided by the mean S-MUAP amplitude to estimate the numbers of motor units present. The maximum isometric twitch contraction (MTC) and maximum voluntary contraction (MVC) of the elbow flexors were also recorded in 18 of the younger subjects and in all older subjects. The estimated numbers of motor units were significantly reduced (47%, P < 0.001) in older subjects with a mean value of 189 +/- 77 compared with a mean of 357 +/- 97 in younger subjects. The sizes of the S-MUAPs, however, were significantly larger in older subjects (23%, P < 0.01). Significant but less marked age-associated reductions in the MTC (33%, P < 0.05) and MVC (33%, P < 0.001) were also found and were similar for both men and women. These results suggest that motor unit losses, even in healthy active individuals, are a primary factor in the age-associated reductions in contractile strength.

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A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate-intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial V̇o2max, reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (succinate dehydrogenase, citrate synthase, cytochrome- c oxidase-4, mtDNA), SIRT1 activity, AMPK, pAMPK, and peroxisome proliferator-activated receptor gamma coactivator 1-α, UCP3, and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters, including nuclear respiratory factor 1, mitochondrial transcription factor A, fission-1, mitofusin-1, and polynucleotide phosphorylase levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.