Background <p>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.</p> Purpose <p>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.</p> Methods <p>Thirteen healthy men (21.0 ± 0.7 years) participated in a randomized crossover study: Control (rest) and 30&#xa0;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.</p> Results <p>NMES significantly increased serum SPARC (616.0 ± 200.9 to 739.2 ± 279.8 ng/mL, <i>p</i> = 0.0078, <i>d</i> = 0.61) and blood lactate (1.4 ± 0.4 to 4.8 ± 1.5 mmol/L, <i>p</i> &lt; 0.0001, <i>d</i> = 8.42) levels while reducing glucose levels (<i>p</i> = 0.0377, <i>d</i> = − 0.92). The correlation between Δ SPARC and Δ Lactate (<i>r</i> = 0.37, <i>p</i> = 0.21) showed a positive trend consistent with the effect size observed in a previous high-intensity exercise study.</p> Conclusion <p>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.</p> Trial registration <p>UMIN-CTR (UMIN000060258).</p>