Sympathetic neural regulation of skeletal muscle vascular compliance during trigeminal nerve stimulation

Our knowledge regarding sympathetic neural regulation of blood pressure and blood flow homeostasis during environmental cold stress remains incomplete because most studies have focused on steady-state measures of vasoconstriction, as inferred from vascular resistance. However, growing evidence suggests that because blood flow is pulsatile in nature, vascular mechanical properties such as compliance also play a significant role in circulatory homeostasis. Therefore, this study tested the hypothesis that trigeminal nerve stimulation (TGS) would produce sympathetically mediated reductions in skeletal muscle vascular compliance. We measured muscle sympathetic nerve activity (peroneal microneurography), heart rate (ECG), superficial femoral arterial blood flow velocity (Doppler ultrasound), and mean brachial arterial blood pressure (MAP; Finometer) during a 5-minute supine baseline rest and 3 minutes of TGS (0°C ice pack applied to the face) in 10 healthy adults (23±2 years, 1 female). Total peripheral resistance (TPR) was calculated as the quotient of MAP and cardiac output. Femoral vascular conductance (FVC) was calculated as the quotient of mean femoral blood flow and MAP. Compliance was quantified using a four-element modified Windkessel model. The mean ± standard deviation of the change (Δ) from baseline to the first (TGS-1) and third (TGS-3) minutes of TGS are reported. Mixed-effects analyses and Fisher’s LSD post-hoc t-tests were performed. TGS increased MAP during TGS-1 (Δ+9±8 mmHg, P = 0.023) and TGS-3 (Δ+11±8 mmHg, P = 0.008). Pulse pressure trended towards increasing during TGS-1 (Δ+5±7 mmHg, P = 0.053) and recovered to baseline during TGS-3 (Δ+3±6 mmHg, P = 0.111). MSNA burst frequency increased during TGS-1 (Δ+7±7 bursts/min, P = 0.011) and had a trending increase during TGS-3 (Δ+7±10 bursts/min, P = 0.082). Total MSNA (TMSNA) and burst amplitude (BA) were elevated during TGS-1 (TMSNA: Δ+1256±778 AU/min, P = 0.001; BA: Δ+37±21%, P < 0.001) and TGS-3 (TMSNA: Δ+716±636 AU/min, P = 0.015; BA: Δ+14±10%, P = 0.007). Heart rate decreased during TGS-1 (Δ7±8 bpm, P = 0.014) and returned to baseline levels during TGS-3 (Δ+3±13 bpm, P = 0.509). TPR increased during TGS-1 (Δ+5±4 mmHg/min/L, P = 0.014) and had recovered during TGS-3 (Δ+1±4 mmHg/min/L, P = 0.961). Planned contrasts revealed that FVC decreased during TGS-1 (Δ-0.158±0.204 cm/s/mmHg, P = 0.049) but not TGS-3 (Δ+0.105±0.421 cm/s/mmHg, P = 0.534). Vascular compliance decreased during TGS-1 (Δ-6.90±4.18 cm/s/mmHg ×10-4, P < 0.001) and recovered during TGS-3 (Δ-1.52±6.06 cm/s/mmHg ×10-4, P = 0.451). These data suggest that transient, sympathetically mediated reductions in skeletal muscle vascular compliance support circulatory homeostasis, particularly during the first minute of cold face-induced TGS. This study was supported by funding from a Natural Sciences and Engineering Research Council of Canada (NSERC) Master’s Canada Graduate Scholarship, an NSERC Discovery Grant, an Ontario Graduate Scholarship, and a Queen Elizabeth II Graduate Scholarship in Science and Technology. This abstract was presented at the American Physiology Summit 2026 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.