Motor unit plasticity is defined as the ability of motoneurons and their respective effector muscles to physically and functionally change as a result of activity, age, and other factors.
Motor unit plasticity has implications for improved athletic performance and resistance to immobility as a result of age.
[1] Resistance training has been shown to dramatically increase performance of motor units of the larger muscle groups.
[2] Motor unit plasticity of the larger muscle groups is extremely important for athletes, especially those participating in high impact and fast pace sports such as track and field, martial arts, and American football.
Motor unit plasticity can be measured in many ways, the most important of which being neural firing frequency, EMG amplitude, muscle force output, pre-synaptic inhibition, and synchronization.
Studies incorporating electromyography have proven that adaptation mechanisms occurring as a result of resistance training can drastically increase the maximal firing frequency of a motoneuron.
On average, at the end of a one-month period of consistent and repetitive resistance training, EMG amplitude reaches a plateau.
[5] Motor unit recruitment is frequently associated with synchronization and is defined as the order and number of neurons that are needed to perform a movement.
[5] As a general rule, the opposite effects of resistance training are seen as a result of age and inactivity of the motor unit.
Fast twitch muscle units have the ability to produce great amounts of force but they do not resist fatigue for long periods of time whereas slow twitch muscle units do not produce great amounts of force but can resist fatigue for very long periods of time.
However, despite their drastic differences in structure and function, studies have shown that these types of muscle show the same trends in plasticity as a result of training and aging.
On the contrary, inactivity of the motor unit proved to significantly decrease the amount of acetylcholine receptors on the effector muscle and have no effect on nerve terminal branching.
[10] It is assumed that this loss of acetylcholine receptors due to inactivity is a result of a decrease in muscle fiber size.