Evidence for potentiation in sympathetic neurovascular transduction following exercise in normotensive adults.

Abstract

Following a single bout of dynamic exercise, vascular conductance increases while sympathetic nerve traffic appears unchanged. Discordance between vascular and sympathetic responses may reflect modulation in vasoconstrictor responsiveness. The primary objective was to evaluate sympathetic neurovascular transduction following cycling exercise. The secondary objective was to explore mechanisms contributing to altered sympathetic neurovascular transduction by manipulating limb vascular conductance using local heating of the foot. We hypothesized that sympathetic neurovascular transduction would decrease following cycling exercise but would be unchanged by lower limb heating. Sixteen adults (22 ± 3 years; 43 ± 8 mL/kg/min; 8 female) underwent measurements of heart rate (electrocardiography), mean arterial pressure (MAP; photoplethysmography), muscle sympathetic nerve activity (MSNA; microneurography), and femoral vascular conductance (FVC; Duplex ultrasound) across 3 interventions: cycling exercise (60-min, 60%VO_2peak, n=16), time-control (60-min, n=16), and lower limb heating (foot submersion into 40°C water, n=9). MSNA-FVC transduction was quantified using signal averaging. Compared to control, exercise did not alter MSNA (P=0.72), but increased FVC (P<0.01) and MSNA-FVC transduction (-8.6 ± 4.5 vs. -15.1±5.7 mL/min/100mmHg; P<0.01). Compared to exercise, heating did not alter MSNA (P=0.71) and tended evoke larger increases in resting FVC (P=0.09). However, increases in MSNA-FVC transduction following exercise tended to persist when compared to heating (-8.7 ± 8.0 vs. -15.1 ± 5.9 mL/min/100mmHg; P=0.06). Contrary to our hypothesis, these findings provide evidence for potentiated sympathetic neurovascular transduction following acute cycling exercise in healthy adults. The observed increase in neurovascular transduction appears independent of resting vasomotor tone.