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.
Klass
Malgorzata
M
Laboratory of Applied Biology, Université Libre de Bruxelles, 28 avenue P. Héger, CP 168, 1000 Brussels, Belgium.
Baudry
Stéphane
S
Duchateau
Jacques
J
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000502:physiology*; D004558:Electric Stimulation; D006801:Humans; D009046:Motor Neurons / Q000502:physiology; D009119:Muscle Contraction / Q000502:physiology*; D053580:Muscle Strength / Q000502:physiology*; D018482:Muscle, Skeletal / Q000502:physiology*