Capsaicin-based analgesic balm attenuates the skeletal muscle metaboreflex in humans.

While it is well established that the exercise pressor reflex (EPR) is one of the principal mediators of the cardiovascular response to exercise, the receptors activating the group III and IV fibres that are important to EPR function remains unclear. Recent animal studies have reported that either capsaicin balm or infusion of capsazepine attenuates the pressor response to muscle contraction, indicating the transient receptor potential vanilloid1 (TRPv1) receptor (localized on the group IV afferent neuron) as an important mediator of the EPR via its metabolic component (named muscle metaboreflex). Whether these findings can be extended to human remains to be determined. To begin to address this question, blood pressure (BP, Finometer), muscle sympathetic nerve activity (MSNA, peroneal microneurography) and femoral blood flow (FBF, Doppler Ultrasound) were measured in five male subjects (24±2 yrs) at rest, during static handgrip exercise at 40% maximal voluntary contraction, and during post-exercise muscle ischemia (PEMI) to isolate the metabolic component of EPR. Trials were performed before (T0) and at 30 (T30) and 60 min (T60) after application of a commercially available analgesic balm, containing capsaicin as the active ingredient (0.1%, CAPZASIN-HP), on the volar forearm of the subject's non-dominant arm in a similar manner to that described in the manufacturer's directions. Statistical comparisons of all physiological variables were made utilizing paired t-tests and data are presented as means ± SE. Static exercise evoked increases in mean BP (+32±4 mmHg, P<0.05), MSNA (+26±5 bursts/min, P<0.05; +19±5 bursts/100 heart beats, P<0.05). The BP and MSNA responses to forearm static contraction were not affected by the application of capsaicin balm. During PEMI at T0, BP (+31±4 mmHg, P<0.05), MSNA (+27±5 bursts/min, P<0.05; +36±5 bursts/100hb, P<0.05) remained elevated compared with rest. Additionally, femoral vascular conductance (the ratio of FBF to BP) was slightly but significantly attenuated from rest during PEMI (-0.72±0.2 mL/min/mmHg, P=0.05), indicating reflex vasoconstriction. After application of capsaicin balm, the BP (+25±4 mmHg at T30; +25±2 mmHg at T60, P<0.05 vs. T0) and MSNA (+17±4 bursts/min and +21±5 bursts/100hb at T30; +15±2 bursts/min and +21±4 bursts/100 hb at T60; P<0.05 vs. T0) responses to PEMI were all significantly less than those observed at T0. Capsaicin balm also attenuated vasoconstrictory responses to PEMI (+0.27±0.18 mL/min/mmHg at T30; - 0.24±0.18 mL/min/mmHg at T60, P<0.05 vs. T0). In conclusion, capsaicin-based analgesic balm effectively attenuated BP, sympathetic and vasconstrictory responses evoked by metabolically sensitive skeletal muscle afferents in humans. These data are consistent with the concept that TRPv1 receptors contribute to the EPR in humans, via its metabolic component. [ABSTRACT FROM AUTHOR]