Myotendinous alterations and effects of resistive loading in old age

The loss of muscle mass associated with ageing only partly explains the observed decline in muscle strength. This paper provides evidence of the contribution of muscular, tendinous and neural alterations to muscle weakness in old age and discusses the complex interplay between the changes of the contractile tissue with those of the tendinous tissue in relation to the mechanical behavior of the muscle as a whole. Despite the considerable structural and functional alterations, the elderly musculoskeletal system displays remarkable adaptability to training in old age and many of these adverse effects may be substantially mitigated, if not reversed, by resistive loading. The interplay between these muscular and tendinous adaptations has an impact both on the length-force and force-velocity relationships of the muscle and is likely to affect the range of motion, rate of force development, maximum force development and speed of movement of the older individual

Adaptability of elderly human muscles and tendons to increased loading

Senile sarcopenia, the loss of muscle mass associated with aging, is one of the main causes of muscle weakness and reduced locomotor ability in old age. Although this condition is mainly driven by neuropathic processes, nutritional, hormonal and immunological factors, as well as a reduction in physical activity, contribute to this phenomenon. Sarcopenia alone, however, does not fully account for the observed muscle weakness, as the loss of force is greater than that accounted for by the decrease in muscle size. As a consequence, a reduction in the force per unit area, both at single fibre and at whole muscle level, is observed. We recently suggested that at whole muscle level, this reduction in intrinsic force is the result of the combined effect of changes in (1) muscle architecture, (2) tendon mechanical properties, (3) neural drive (reduced agonist and increased antagonist muscle activity) and (4) single fibre-specific tension. Whereas several studies support the role of the last two factors in the loss of intrinsic muscle force with aging, alterations in muscle architecture and in tendon mechanical properties have also been shown to contribute to the above phenomenon. Indeed, sarcopenia of the human plantarflexors, represented by a 25% reduction in muscle volume, was found to be associated with a 10% reduction in fibre fascicle length and 13% reduction in pennation angle. These architectural alterations were accompanied by a 10% decrease in tendon stiffness, attributable to alterations in tendon material properties, as suggested by a 14% decrease in Young's modulus. Most of these changes may be reversed by 14 weeks of resistive training; both fibre fascicle length and tendon stiffness were found to be increased by 10 and 64%, respectively. Surprisingly, however, training had no effect on the estimated relative length–tension properties of the muscle, indicating that the effects of greater tendon stiffness and increased fascicle length cancelled out each other. It seems that natural strategies may be in place to ensure that the relative operating range of muscle remains unaltered by changes in physical activity, in old age

Voluntary activation during maximal contraction with advancing age: a brief review

It is well established that the loss of muscle mass (i.e. sarcopenia) is the primary factor contributing to the reduction in muscle force with ageing. Based on the observation that force declines at a faster rate than muscle mass, neural alterations are also thought to contribute to muscle weakness by reducing central drive to the agonist muscles and by increasing coactivation of the antagonist muscles. Researchers have attempted to quantify the contribution of impaired voluntary drive to the decline in muscle force using superimposed electrical stimulation during maximal voluntary contractions (MVCs) and by recording surface electromyographic (EMG) activity. Although reduced voluntary activation of agonist muscles and increased coactivation of antagonist muscles during a MVC have been reported with advancing age, such changes are not supported by all studies. These discrepancies may be explained by differences in sensitivity between the methods used to assess voluntary activation, as well as differences between the characteristics of the study population, the muscle group that is tested, and the type of contraction that is performed. The objective of this review is to summarize current knowledge regarding the activation of agonist and antagonist muscles during MVC in elderly and to try to clarify the disparities in literature concerning the influence of a possible deficit in voluntary activation on the maximal force capacity of muscles in elderly adults.Journal ArticleResearch Support, Non-U.S. Gov'tReviewinfo:eu-repo/semantics/publishe