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Experimental Physiology 91.3 pp 483-498
DOI: 10.1113/expphysiol.2005.032896
© The Physiological Society 2006
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Review Article

Myotendinous plasticity to ageing and resistance exercise in humans

N. D. Reeves1, M. V. Narici1 and C. N. Maganaris1

1 Institute for Biophysical and Clinical Research into Human Movement, Manchester Metropolitan University, MMU Cheshire, Alsager Campus, Hassall Road, Alsager, Cheshire ST7 2HL, UK

The age-related loss of muscle mass known as senile sarcopenia is one of the main determinants of frailty in old age. Molecular, cellular, nutritional and hormonal mechanisms are at the basis of sarcopenia and are responsible for a progressive deterioration in skeletal muscle size and function. Both at single-fibre and at whole-muscle level, the loss of force exceeds that predicted by the decrease in muscle size. For single fibres, the loss of intrinsic force is mostly due to a loss in myofibrillar protein content. For whole muscle, in addition to changes in neural drive, alterations in muscle architecture and in tendon mechanical properties, exemplified by a reduction in tendon stiffness, have recently been shown to contribute to this phenomenon. Resistance training can, however, cause substantial gains in muscle mass and strength and provides a protective effect against several of the cellular and molecular changes associated with muscle wasting and weakness. In old age, not only muscles but also tendons are highly responsive to training, since an increase in tendon stiffness has been observed after a period of increased loading. Many of the myotendinous factors characterizing ageing can be at least partly reversed by resistance training.

(Received 28 November 2005; accepted after revision 1 February 2006; first published online 9 February 2006)
Corresponding author N. D. Reeves: Institute for Biophysical and Clinical Research into Human Movement, Manchester Metropolitan University, MMU Cheshire, Alsager Campus, Hassall Road, Alsager, Cheshire ST7 2HL, UK. Email: n.reeves{at}mmu.ac.uk




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