Diving and exercise: The interaction of trigeminal receptors and muscle metaboreceptors on muscle sympathetic nerve activity in humans

Abstract

Swimming involves muscular activity and submersion, creating a conflict of autonomic reflexes elicited by the trigeminal receptors and skeletal muscle afferents. We sought to determine the autonomic cardiovascular responses to separate and concurrent stimulation of the trigeminal cutaneous receptors and metabolically sensitive skeletal muscle afferents (muscle metaboreflex). In eight healthy men (30 ± 2 yr) muscle sympathetic nerve activity (MSNA; microneurography), mean arterial pressure (MAP; Finometer), femoral artery blood flow (duplex Doppler ultrasonography), and femoral vascular conductance (femoral artery blood flow/MAP) were assessed during the following three experimental conditions: 1) facial cooling (trigeminal nerve stimulation), 2) postexercise ischemia (PEI; muscle metaboreflex activation) following isometric handgrip, and 3) trigeminal nerve stimulation with concurrent PEI. Trigeminal nerve stimulation produced significant increases in MSNA total activity (Δ347 ± 167%) and MAP (Δ21 ± 5%) and a reduction in femoral artery vascular conductance (Δ-17 ± 9%). PEI also evoked significant increases in MSNA total activity (Δ234 ± 83%) and MAP (Δ36 ± 4%) and a slight nonsignificant reduction in femoral artery vascular conductance (Δ-9 ± 12%). Trigeminal nerve stimulation with concurrent PEI evoked changes in MSNA total activity (Δ341 ± 96%), MAP (Δ39 ± 4%), and femoral artery vascular conductance (Δ-20 ± 9%) that were similar to those evoked by either separate trigeminal nerve stimulation or separate PEI. Thus, excitatory inputs from the trigeminal nerve and metabolically sensitive skeletal muscle afferents do not summate algebraically in eliciting a MSNA and cardiovascular response but rather exhibit synaptic occlusion, suggesting a high degree of convergent inputs on output neurons.

Sustained increases in blood pressure elicited by prolonged face cooling in humans

“…It is well established that face cooling elicits a pressor response in humans for up to 180 s (1,3,7,11,14,15,18,19,21,22). Data from the present study extend these findings and show that face cooling-induced increases in blood pressure can be sustained for at least 15 min (Fig.…”

“…It is well known that face cooling elicits robust increases in sympathetic nerve activity (11,15,21) and, thus, vascular resistance in the peripheral (11,16), visceral (6,19), and cerebral (3) vasculatures. Ultimately, these responses elevate blood pressure (1,3,7,11,14,15,18,19,21,22), as cardiac output remains largely unaffected by face Values are expressed as means Ϯ SD. RMSSD, root mean square of successive differences of the R-R interval; PU, perfusion units.…”

“…Cooling of the forehead and cheeks evokes a similar, yet less pronounced, response in humans (1,3,7,11,14,15,18,19,21,22), which occurs secondary to stimulation of the cold afferents of the trigeminal nerve (10,17). Face cooling in humans simultaneously stimulates the parasympathetic and sympathetic nervous systems, evoking bradycardia and peripheral vasoconstriction (1,3,7,11,14,15,18,19,21,22). In humans, reductions in heart rate are not sufficient to reduce cardiac output (3).…”

“…In humans, reductions in heart rate are not sufficient to reduce cardiac output (3). Therefore, blood pressure increases as a result of systemic peripheral vasoconstriction (1,3,7,11,14,15,18,19,21,22).…”

“…The hemodynamic responses to face cooling in humans have only been studied up to 180 s in duration (1,3,7,11,14,15,18,19,21,22). Thus, it is unknown whether the relative hypertensive responses elicited by face cooling, in addition to the temporal dynamics of parasympathetic and sympathetic activation, are sustained beyond 180 s. The diving reflex in diving mammals and birds persists for the duration of the dive (4).…”