HighlightsLoss of muscle mass with age is due to atrophy and loss of individual muscle fibres.Anabolic resistance is fundamental in age-related fibre atrophy.Fibre loss is associated with denervation and remodelling of motor units.The plasticity of both factors should be considered in future research.

No abstract

Muscle motor unit numbers decrease markedly in old age, while remaining motor units are enlarged and can have reduced neuromuscular junction transmission stability. However, it is possible that regular intense physical activity throughout life can attenuate this remodeling. The aim of this study was to compare the number, size, and neuromuscular junction transmission stability of tibialis anterior (TA) motor units in healthy young and older men with those of exceptionally active master runners. The distribution of motor unit potential (MUP) size was determined from intramuscular electromyographic signals recorded in healthy male Young (mean ± SD, 26 ± 5 years), Old (71 ± 4 years) and Master Athletes (69 ± 3 years). Relative differences between groups in numbers of motor units was assessed using two methods, one comparing MUP size and muscle cross‐sectional area (CSA) determined with MRI, the other comparing surface recorded MUPs with maximal compound muscle action potentials and commonly known as a “motor unit number estimate (MUNE)”. Near fiber (NF) jiggle was measured to assess neuromuscular junction transmission stability. TA CSA did not differ between groups. MUNE values for the Old and Master Athletes were 45% and 40%, respectively, of the Young. Intramuscular MUPs of Old and Master Athletes were 43% and 56% larger than Young. NF jiggle was slightly higher in the Master Athletes, with no difference between Young and Old. These results show substantial and similar motor unit loss and remodeling in Master Athletes and Old individuals compared with Young, which suggests that lifelong training does not attenuate the age‐related loss of motor units.

The contributions of fiber atrophy, fiber loss, in situ specific force, and voluntary activation to weakness in sarcopenia remain unclear. To investigate, 40 older (20 women; age 72 ± 4 years) and 31 younger adults (15 women, age 22 ± 3 years) completed measurements. The knee extensor maximal voluntary torque (MVC) was measured as well as voluntary activation, patella tendon moment arm length, muscle volume, and fascicle architecture to estimate in situ specific force. Fiber cross-sectional area (FCSA), fiber numbers, and connective tissue contents were also estimated from vastus lateralis biopsies. The MVC, quadriceps volume, and specific force were 39%, 28%, and 17% lower, respectively, in old compared with young, but voluntary activation was not different. The difference in muscle size was due in almost equal proportions to lower type II FCSA and fewer fibers. Five years later (n = 23) the MVC, muscle volume and voluntary activation in old decreased an additional 12%, 6%, and 4%, respectively, but there was no further change in specific force. In situ specific force declines relatively early in older age and reduced voluntary activation occurs later, but the overall weakness in sarcopenia is mainly related to loss of both type I and II fibers and type II fiber atrophy.