The contraction of skeletal muscles depends on the regulation of the nervous system and the coordination of neuromuscular function. The smallest motor nervous system associated with muscle contraction is the motor unit (MU), which consists of an efferent motor neuron and all of the muscle fibres it innervates. Muscle tissue also undergoes adaptive alternations in response to external stimuli, such as the gradual decline in muscle mass and strength during ageing, and atrophy following muscle disuse. A number of studies have demonstrated that different types of voluntary movements, such as resistance exercise training (RET), can prevent or attenuate such alternations to a certain extent via increases in muscle protein synthesis (MPS).
However, certain situations such as post-operative bed rest render RET interventions an unachievable option. Neuromuscular electrical stimulation (NMES) can be applied as a surrogate; acting to evoke involuntary contraction of the target muscles via electrical current applied to the muscle belly. Although NMES stimulation has been widely tested in the intensive care environment, results have shown variable efficacy- perhaps due to the multi-organ failure and associated catabolic systemic environment encountered by the majority of these patients.
It has recently shown that in post-operative abdominal surgery patients, 5-days of NMES, performed at frequency of 30 Hz in a 1 second "on", 1 second "off" contraction pattern, can mitigate losses in muscle mass and function. However, this study 'borrowed' a protocol from previous intensive care literature, and as such may not be optimal with regards to frequency or contraction pattern. Given that this protocol was highly tolerated by patients in a previous study (i.e., based on 30 min of daily NMES, patients in this study said they would tolerate it for 45 to 240 (mean 90) min), it is plausible that higher frequency NMES (\~100 Hz), enabling greater force production may be both viable and result in further mitigation of muscle mass and function losses. It has also been demonstrated that the time muscle is under loaded tension during RET may be an important modulator of MPS and subsequent gains in muscle mass. Therefore, increasing the contraction relative to relaxation time during NMES (e.g., 3 seconds on, 1 second off) may be another feasible and perhaps more beneficial strategy to reduce muscle mass losses in populations where an increase in frequency may not be possible or tolerable.
Knowing that muscle maintenance is based on a dynamic equilibrium between MPS and muscle protein breakdown, the impact of different NMES protocols on MPS, associated cell signalling, and nutrient delivery pathways needs to be explored so that an optimal intervention can be tested in clinical settings associated with disuse atrophy. To date, no previous studies have compared differing frequencies of NMES on the muscle metabolic responses in older adults, nor the effect of differing NMES-induced contraction patterns.
