Effect of Voltage-Dependent Potassium Channel Antagonism on Thermal Hyperemia in Skeletal Muscle of Humans

We recently identified a critical role for voltage-dependent potassium (KV) channels in pharmacological vasodilation in human skeletal muscle. However, the extent to which these findings translate to physiological vasodilation remains unknown. Acute heat exposure increases skeletal muscle blood flow, but the contribution of KV channels to this hyperemic response is unclear. PURPOSE: Therefore, the purpose of this study was to test the hypothesis that KV channel antagonism would attenuate thermal hyperemia in skeletal muscle of humans. METHODS: We utilized microdialysis to directly measure local blood flow at two sites in the vastus lateralis muscle of 6 healthy adults (4 women, 26 ± 5 yrs) via the ethanol washout technique. One probe was perfused with 0.9% saline, while the other probe was perfused with the KV channel antagonist 4-aminopyridine (26.6 mM). Pulsed short-wave diathermy was used to induce deep heating of the vastus lateralis for 90 min. Local temperature was measured within ~2-3 cm of each microdialysis probe via a thermocouple. RESULTS: Pulsed short-wave diathermy increased skeletal muscle temperature from baseline (34.1 ± 0.6 °C) through 90 min of heating (38.5 ± 0.6 °C; P < 0.01). However, the accompanying increase in blood flow at 90 min of heat exposure (Δ 18.3 ± 6.4 ml min-1 100g-1) was attenuated when perfused with 4-aminopyridine (Δ 5.6 ± 8.5 ml min-1 100g-1; P = 0.01). CONCLUSION: These preliminary data suggest that KV channels may contribute to thermal hyperemia in skeletal muscle of humans.