Bypassing the systemic cardiorespiratory threshold: neuromuscular electrical stimulation elicits a SPARC response through accelerated glycolytic flux.

BACKGROUND

Secreted protein acidic and rich in cysteine (SPARC) is a myokine with potential tumor-suppressive properties. SPARC secretion typically requires vigorous-intensity exercise. Neuromuscular electrical stimulation (NMES) non-selectively recruits glycolytic Type II muscle fibers, potentially inducing intense localized metabolic stress despite a low systemic cardiorespiratory demand.

PURPOSE: This study aimed to investigate the acute effects of a single bout of NMES at an intensity corresponding to the first ventilatory threshold (VT1) on circulating SPARC levels in healthy young subjects.

METHODS

Thirteen healthy men (21.0 ± 0.7 years) participated in a randomized crossover study: Control (rest) and 30 min NMES at the maximum tolerable intensity with a heart rate (HR) ceiling 120% of VT1. Serum SPARC, lactate, and glucose levels were measured before and after each session.

RESULTS

NMES significantly increased serum SPARC (616.0 ± 200.9 to 739.2 ± 279.8 ng/mL, p = 0.0078, d = 0.61) and blood lactate (1.4 ± 0.4 to 4.8 ± 1.5 mmol/L, p < 0.0001, d = 8.42) levels while reducing glucose levels (p = 0.0377, d = - 0.92). The correlation between Δ SPARC and Δ Lactate (r = 0.37, p = 0.21) showed a positive trend consistent with the effect size observed in a previous high-intensity exercise study.

CONCLUSION

NMES at VT1 intensity increases circulating SPARC levels by bypassing the systemic cardiorespiratory threshold via accelerated glycolytic flux and subsequent lactate accumulation. This study provides a physiological framework for NMES as a potential strategy to induce SPARC responses in populations where strenuous volitional exertion is limited.

TRIAL REGISTRATION: UMIN-CTR (UMIN000060258).