Low-intensity neuromuscular electrical stimulation elicits detectable metaboreflex-mediated sympathetic responses in humans.

Neuromuscular electrical stimulation (NMES) augments sympathetic and pressor responses compared with voluntary contraction (VOL), even at low contraction intensities; however, the mechanisms underlying these responses remain incompletely understood. Under low-intensity, short-duration VOL, metaboreflex activation is typically minimal because metabolic stress is limited. Therefore, examining NMES under these conditions may provide insight into whether the unique activation pattern associated with electrically evoked contractions alters the conditions required for detectable metaboreflex-mediated sympathetic responses. Accordingly, we examined muscle sympathetic nerve activity (MSNA) and cardiovascular responses during low-intensity NMES with post-exercise circulatory occlusion (PECO). Ten young adults completed two randomized tasks: VOL and NMES. Participants performed 30 s of isometric elbow flexion at ~10% maximal voluntary torque, followed immediately by 2 min of PECO to isolate metaboreflex-mediated responses. MSNA was recorded using microneurography, and beat-by-beat blood pressure (BP), heart rate (HR), stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were continuously measured. Compared with VOL, NMES elicited greater increases in systolic and diastolic arterial pressures during both contraction and PECO (main effect of condition, both P < 0.01). MSNA burst frequency and incidence also increased during NMES and remained elevated during PECO, whereas the corresponding responses during VOL were minimal (interaction, both P < 0.001). In contrast, HR, SV, CO and TPR responses did not differ between conditions. These findings demonstrate that low-intensity, short-duration NMES can elicit detectable metaboreflex-mediated sympathetic and pressor responses under conditions in which such responses are typically minimal during voluntary exercise.