K_V channels contribute to thermal hyperaemia in skeletal muscle of humans

Localized application of heat is used therapeutically to reduce skeletal muscle pain and improve mobility and recovery in various populations. The efficacy of this thermal therapy is considered to be partly a result of increased blood flow in the skeletal muscle directly exposed to heat (i.e. thermal hyperaemia). However, the mechanisms mediating thermal hyperaemia in skeletal muscle of humans remain poorly understood. Voltage-dependent potassium (K_V) channels play a pivotal role linking upstream vasodilatory signals to electro-mechanical mechanisms that mediate vascular smooth muscle relaxation. Therefore, the present study aimed to test the hypothesis that K_V channel antagonism would attenuate thermal hyperaemia in skeletal muscle of humans. We used microdialysis to directly measure local blood flow via the ethanol washout technique at two sites in the vastus lateralis muscle of 10 healthy adults (seven women). One probe was perfused with 0.9% saline, whereas the other was perfused with the K_V channel antagonist 4-aminopyridine (26.6 mm). Pulsed short-wave diathermy was used to induce deep heating of the vastus lateralis for 90 min. Muscle temperature was measured midway between the microdialysis probes via a thermocouple. Baseline blood flow did not differ between probes (P = 0.684). Pulsed short-wave diathermy increased skeletal muscle temperature through 90 min of heating (P < 0.001). However, the accompanying increase in blood flow at 90 min was attenuated when perfused with 4-aminopyridine (P = 0.0222). These data suggest that K_V channels substantially contribute to thermal hyperaemia in skeletal muscle of humans. KEY POINTS: The efficacy of thermal therapy is considered to be partly a result of increased blood flow in the skeletal muscle directly exposed to heat (i.e. thermal hyperaemia). However, the mechanisms mediating thermal hyperaemia in skeletal muscle remain poorly understood. Voltage-dependent potassium (K_V) channels play a pivotal role as downstream effectors that mediate vascular smooth muscle relaxation. Therefore, we tested the hypothesis that K_V channel antagonism would attenuate thermal hyperaemia in skeletal muscle of humans. Using microdialysis, we found that K_V channel antagonism with 4-aminopyridine attenuated thermal hyperaemia at 90 min of localized heating, when this vasodilatory response was the greatest. We identified a critical role for K_V channels in human skeletal muscle thermal hyperaemia, establishing these channels as important downstream effectors of this vasodilatory response.