Trigeminal reflex regulation of sympathetic neural communication strategies in human muscle sympathetic nerve activity

This study tested the hypothesis that during localized facial cooling the human trigeminal reflex regulates sympathetic neuronal communication strategies. In 15 healthy individuals, we measured action potential (AP) discharge in muscle sympathetic nerve activity (MSNA; peroneal microneurography and continuous wavelet transform) during baseline (BSL) and 3 min of trigeminal nerve stimulation (TGS; cold pack on face). Face temperature and discomfort were measured. TGS increased total integrated MSNA via differential regulation of sympathetic AP discharge vs. AP recruitment. TGS increased sympathetic AP discharge frequency (BSL: 216 ± 150, TGS-1: 511 ± 335, TGS-2: 476 ± 323, TGS-3: 340 ± 160 APs/min, all <i>P</i> < 0.01). By contrast, TGS recruited previously silent larger sympathetic APs during TGS-1 and TGS-2, but not TGS-3 (BSL: 13 ± 3, TGS-1: 18 ± 4, TGS-2: 17 ± 4 clusters, both <i>P</i> < 0.01, TGS-3: 15 ± 4 clusters, <i>P</i> = 0.17). Compared with BSL, the sympathetic AP latency-size relationship was reset downward to faster latencies during TGS-1 (Δ -63 ± 6 ms, <i>P</i> < 0.01) and TGS-2 (Δ -31 ± 13 ms, <i>P</i> = 0.02) but not TGS-3 (Δ -8 ± 1 ms, <i>P</i> = 0.32). Across BSL and TGS, sympathetic AP recruitment (<i>r</i> = 0.58; <i>P</i> < 0.01) and latency (<i>r</i> = -0.52; <i>P</i> < 0.01) were related to perceptual discomfort but not face temperature. Thus, during localized facial cooling, trigeminal reflex activation and perceptual discomfort increase the discharge of previously active sympathetic neurons, recruit previously silent larger neurons, and reduce neuronal discharge latency.<b>NEW & NOTEWORTHY</b> Trigeminal reflex activation with localized facial cooling augmented human muscle sympathetic nerve activity by increasing the discharge of previously active action potentials (AP) and recruiting a subpopulation of larger previously silent APs. Also, trigeminal reflex activation reduced the latency of all active APs. Sympathetic AP recruitment and latency changes were associated with perceptual discomfort but not face temperature. These data advance our understanding regarding the trigeminal and perceptual mechanisms governing human sympathetic neural communication strategies.