Electromyostimulation (EMS) incorporates the use of electrical current to activate skeletal muscle and facilitate contraction. It is commonly used in clinical settings to mimic voluntary contractions and enhance the rehabilitation of human skeletal muscles. Although the beneficial effects of EMS are widely accepted, discrepancies concerning the specific responses to EMS versus voluntary actions exist. The unique effects of EMS have been attributed to several mechanisms, most notably a reversal of the recruitment pattern typically associated with voluntary muscle activation. This perspective outlines the authors' contention that electrical stimulation recruits motor units in a nonselective, spatially fixed, and temporally synchronous pattern. Furthermore, it synthesizes the evidence that supports the contention that this recruitment pattern contributes to increased muscle fatigue when compared with voluntary actions. The authors believe the majority of evidence suggests that EMS-induced motor unit recruitment is nonselective and that muscle fibers are recruited without obvious sequencing related to fiber types.

Neuromuscular electrical stimulation (NMES) is commonly used in clinical settings to activate skeletal muscle in an effort to mimic voluntary contractions and enhance the rehabilitation of human skeletal muscles. It is also used as a tool in research to assess muscle performance and/or neuromuscular activation levels. However, there are fundamental differences between voluntary- and artificial-activation of motor units that need to be appreciated before NMES protocol design can be most effective. The unique effects of NMES have been attributed to several mechanisms, most notably, a reversal of the voluntary recruitment pattern that is known to occur during voluntary muscle contractions. This review outlines the assertion that electrical stimulation recruits motor units in a nonselective, spatially fixed, and temporally synchronous pattern. Additionally, it synthesizes the evidence that supports the contention that this recruitment pattern contributes to increased muscle fatigue when compared with voluntary actions and provides some commentary on the parameters of electrical stimulation as well as emerging technologies being developed to facilitate NMES implementation. A greater understanding of how electrical stimulation recruits motor units, as well as the benefits and limitations of its use, is highly relevant when using this tool for testing and training in rehabilitation, exercise, and/or research.

Neuromuscular electrical stimulation (NMES) involves the use of electrical current to facilitate contraction of skeletal muscle. However, little is known concerning the effects of varying stimulation parameters on muscle function in humans. The purpose of this study was to determine the extent to which varying pulse duration and frequency altered torque production and fatigability of human skeletal muscle in vivo. Ten subjects underwent NMES-elicited contractions of varying pulse frequencies and durations as well as fatigue tests using stimulation trains of equal total charge, yet differing parametric settings at a constant voltage. Total charge was a strong predictor of torque production, and pulse trains with equal total charge elicited identical torque output. Despite similar torque output, higherfrequency trains caused greater fatigue. These data demonstrate the ability to predictably control torque output by simultaneously controlling pulse frequency and duration and suggest the need to minimize stimulation frequency to control fatigue.

Disuse atrophy is a common clinical phenomenon that significantly impacts muscle function and activities of daily living. The purpose of this study was to implement genome-wide expression profiling to identify transcriptional pathways associated with muscle remodeling in a clinical model of disuse. Skeletal muscle biopsies were acquired from the medial gastrocnemius in patients with an ankle fracture and from healthy volunteers subjected to 4-11 days of cast immobilization. We identified 277 misregulated transcripts in immobilized muscles of patients, of which the majority were downregulated. The most broadly affected pathways were involved in energy metabolism, mitochondrial function, and cell cycle regulation. We also found decreased expression in genes encoding proteolytic proteins, calpain-3 and calpastatin, and members of the myostatin and IGF-I pathway. Only 26 genes showed increased expression in immobilized muscles, including apolipoprotein (APOD) and leptin receptor (LEPR). Upregulation of APOD (5.0-fold, P < 0.001) and LEPR (5.7-fold, P < 0.05) was confirmed by quantitative RT-PCR and immunohistochemistry. In addition, atrogin-1/MAFbx was found to be 2.4-fold upregulated (P < 0.005) by quantitative RT-PCR. Interestingly, 96% of the transcripts differentially regulated in immobilized limbs also showed the same trend of change in the contralateral legs of patients but not the contralateral legs of healthy volunteers. Information obtained in this study complements findings in animal models of disuse and provides important feedback for future clinical studies targeting the restoration of muscle function following limb disuse in humans.