Trigeminal nerve stimulation modulates the haemodynamic response at exercise onset

Research has yet to investigate the effects of trigeminal nerve stimulation on cardiovascular regulation at exercise onset. Therefore, this study tested the hypothesis that trigeminal nerve stimulation alters reflex cardiovascular regulation at exercise onset in humans. In nine healthy adults (23 ± 2 years; 5 females), we measured mean arterial pressure (MAP; Finometer), heart rate (HR; ECG), cardiac output (CO; Modelflow equation), total vascular conductance (TVC; calculated as the quotient of CO and MAP), femoral vascular conductance (FVC; Doppler ultrasound; calculated as the quotient of femoral blood flow and MAP), and cardiovagal baroreflex sensitivity (cvBRS; sequence technique) during the first 30 seconds of isometric handgrip exercise (IHG; 35% max voluntary contraction, MVC) performed under control conditions and during trigeminal nerve stimulation (TGS; 0°C ice pack applied to the forehead and cheeks). Data (mean ± SD) are reported for a 5-minute baseline (BSL), 30-second IHG, 3-minute BSL with TGS (BSL + TGS), and 30-second IHG plus TGS (IHG + TGS). A two-way repeated measures analysis of variance (ANOVA) and Holm-Šídák tests evaluated the central and peripheral haemodynamic responses to IHG, TGS, and IHG + TGS. Statistical significance was set at P ≤ 0.05. Compared to BSL, the IHG-mediated increase in MAP (BSL: 85 ± 14 mmHg, IHG: 93 ± 13 mmHg; P < 0.01), was attributed to the elevated HR (BSL: 67 ± 7 beats/min, IHG: 73 ± 8 beats/min; P = 0.02) and CO (BSL: 5.9 ± 1.8 L/min, IHG: 6.6 ± 2.0 L/min; P < 0.01) response. IHG did not affect FVC (BSL: 1.1 ± 0.5 mL/mmHg/min, IHG: 1.1 ± 0.6 mL/mmHg/min; P = 0.66) or TVC (BSL: 0.07 ± 0.02 L/min/mmHg, IHG: 0.07 ± 0.02 L/min/mmHg; P = 0.37). IHG decreased cvBRS (BSL: 26 ± 7 ms/mmHg, IHG: 16 ± 5 ms/mmHg; P = 0.04). Compared to BSL, TGS increased MAP (BSL: 85 ± 14 mmHg, BSL + TGS: 92 ± 13 mmHg; P < 0.01) via reduced FVC (BSL: 1.1 ± 0.5 mL/mmHg/min, BSL + TGS: 0.8 ± 0.5 mL/mmHg/min; P = 0.03) and TVC (BSL: 0.07 ± 0.02 L/min/mmHg, TGS: 0.06 ± 0.02; P = 0.04). TGS did not alter HR (BSL: 67 ± 7 beats/min, BSL + TGS: 66 ± 11 beats/min; P = 0.47) or CO (BSL: 5.9 ± 1.8 L/min, BSL + TGS: 6.0 ± 2.0 L/min; P = 0.72). Compared to IHG, the rise in HR was attenuated with IHG + TGS (IHG: 73 ± 8 beats/min, IHG + TGS: 62 ± 12 beats/min; P < 0.01). cvBRS was similar during IHG and IHG + TGS (IHG: IHG: 16 ± 5 ms/mmHg, IHG + TGS: 15 ± 7 ms/mmHg; P = 0.95). MAP was greater during IHG + TGS than IHG (IHG: 93 ± 13 mmHg, IHG + TGS: 107 ± 18 mmHg; P < 0.01). The elevated MAP during IHG + TGS resulted from decreased FVC (IHG: 1.1 ± 0.6 mL/mmHg/min; IHG + TGS: 0.5 ± 0.4 mL/mmHg/min; P < 0.01) and LVC (IHG: 0.07 ± 0.02 L/min/mmHg, IHG + TGS: 0.05 ± 0.03 L/min/mmHg; P < 0.01). These findings suggest that to maintain blood pressure homeostasis upon activation of the trigeminal reflex during brief IHG exercise, healthy humans demonstrate augmented vasoconstrictor responses that compensate for the attenuated reflex-mediated rises in heart rate. This work was supported by the Natural Sciences and Engineering Research Council of Canada and Ontario Graduate Scholarship (OGS). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.