Central command activation during exercise is an essential mechanism to sustain diving bradycardia

Previous studies have shown that the bradycardic response to diving is maintained or enhanced during exercise. However, the integrative mechanism by which diving-induced bradycardia supersedes exercise-induced tachycardia remains unclear. This study aimed to elucidate the contributions of central and peripheral afferent mechanisms to the diving response in humans under controlled laboratory conditions. Thirty-two healthy participants [17 males, 15 females; mean age: 22 ± 3 yr; body mass index (BMI): 24 ± 4 kg/m²] were exposed to simulated diving via trigeminal nerve stimulation (TGS) under three experimental conditions: <i>1</i>) voluntary light (LEx) and moderate (MEx) leg cycling exercise, <i>2</i>) passive exercise and the cold pressor test (CPT), and <i>3</i>) a combination of voluntary exercise and CPT. Continuous beat-to-beat heart rate (HR) and arterial blood pressure were measured, with surface electromyography confirming the absence of voluntary muscle contractions during passive cycling. TGS elicited significant bradycardia at rest, and this response was increased during voluntary LEx, and preserved during voluntary MEx when compared with rest. In contrast, compared with rest, the HR response to TGS during passive exercise was significantly attenuated, whereas CPT completely abolished the bradycardic response to TGS. However, during LEx combined with CPT, TGS elicited a significant bradycardic response when compared with CPT alone. Overall, these findings suggest that <i>1</i>) central command activation is an essential mechanism for sustaining the diving bradycardia; <i>2</i>) isolated peripheral afferent reflexes exert inhibitory feedback to regulate diving-induced bradycardia; and <i>3</i>) central and peripheral afferent feedback are important mechanisms by which volitional skeletal muscle contractions modulate the cardiovascular adjustments to "diving."<b>NEW & NOTEWORTHY</b> Diving triggers conflicting heart rate control pathways: the diving response induces bradycardia, whereas muscular contraction engages neural signals that can cause tachycardia. Although bradycardia persists during exercise, the mechanisms by which diving-induced bradycardia overrides exercise-induced tachycardia are unclear. Our findings show that central command activation is essential for sustaining diving bradycardia, whereas peripheral afferent reflexes provide inhibitory feedback. These results advance our understanding of cardiovascular adaptations to diving, with implications for marine biology and exercise physiology.