Capsaicin-based Analgesic Balm Decreases Pressor Responses
Capsaicin-based Analgesic Balm Decreases Pressor Responses
Capsaicin-based analgesic balm decreases pressor responses evoked by muscle afferents. Physically active individuals use countless analgesic balm (AB) products with various active ingredients daily. Despite this, few studies have investigated the mechanism of action and efficacy of AB.
Purpose: We examined the effects of capsaicin (CAP) application on pressor responses evoked by muscle contraction (MC), which are mediated by group III and IV muscle afferents.
Methods: Heart rate (HR), blood pressure, and end-tidal CO2 were monitored in cats (N = 12) decerebrated under halothane. Decerebration eliminated anesthesia use and effects from the higher brain. Electrical stimulation of L7 and S1 ventral roots evoked static hindlimb MC (30 s). After control runs, a commercial CAP (4.95% Oleoresin Capsicum) AB was applied to the skin over the contracting muscles of one hindlimb. MC were evoked every 10 min, alternating between hindlimbs. Data were analyzed with RM ANOVA and Tukey post hoc test.
Results: Changes in peak mean arterial pressure (MAP) induced by static ipsilateral MC were significantly attenuated at 20 min and tended to approach baseline levels at 40 min after CAP application. The mean (±SEM) of the peak MAP for the ipsilateral side just before application (T = 0), at 20 min (T+20), and 40 min (T+40) were 28.3 mm Hg ± 6.4, 13.8 mm Hg ±2.9, and 22.6 mm Hg ± 5.2, respectively. There were no significant changes in HR.
Conclusions: Cardiovascular effects due to activation of group III and IV afferent fibers were significantly attenuated by the application of CAP. The time course of the effects appeared to support the need for repeated CAP application for pain relief. Central nervous system circuitry responsible for this effect awaits elucidation.
Pain is an inevitable part of an active lifestyle. Although there are many pain relieving methods, those in sports medicine and physically active individuals often utilize cheap and convenient over-the-counter analgesic balms for the relief of minor aches and pains. In fact, topical analgesic balm (AB) usage has grown to a $150 million industry with over 34% of all American adults using them annually. Despite their popularity, comparatively few studies have addressed the efficacy and mechanism of action of AB. Our previous study focused on a commonly used combination of capsaicin (CAP) and methyl salicylate. The present study addressed the single active ingredient CAP, which is often the sole active ingredient of many AB.
CAP is well studied in terms of its pharmacological properties. The vanilloid receptor subtype 1 (VR1), a nonselective cation channel and thermal sensor, is thoroughly characterized as the target of CAP. Initial administration of CAP produces itching, pricking, and burning pain due to excitation of nociceptors. These initial effects are followed by a period of hyperalgesia. Repeated CAP application causes prolonged hypalgesia or nociceptor desensitization. This last effect appears within a week and can last 3 wk after application ceases. These effects are dependent on the concentration and duration of application.
Not all mechanisms that account for the analgesic effects of CAP are clearly understood. CAP's analgesic properties are thought to have a variety of mechanisms of action, including local effects on nerve fibers, depletion of neurotransmitters, counterirritation, engagement of the "gate control" mechanism, and suggested placebo effects. Although not a popular explanation of AB effects, topically administered CAP may block nerve fibers directly or deplete neurotransmitter substances. Dray offers a more accepted explanation: CAP is believed to cause counterirritant effects. Counterirritants inflame or irritate the skin, increase cutaneous blood flow, stimulate or depress pain receptors, and stimulate thermoreceptors. By activating nociceptors with a peripheral noxious stimulus, counterirritants inhibit the response of central neurons that transmit pain. Another speculation is that rubbing or massaging AB onto the skin during application may engage the "gate control" mechanism by activating Aβ fibers. Finally, some suggest that a placebo effect is the most likely source of the analgesic effects acting through the power of suggestion. The power of suggestion psychologically stimulates the nervous system. Price and colleagues used heat induced experimental pain and a placebo analgesic cream to analyze factors that contribute to the magnitude of placebo analgesia. Although placebo effects are closely associated with expectancy, they found that no relationship exists between placebo effects and the desire for relief. This suggests that any analgesic effect experienced from an AB is not primarily due to psychological factors.
Capsaicin-based analgesic balm decreases pressor responses evoked by muscle afferents. Physically active individuals use countless analgesic balm (AB) products with various active ingredients daily. Despite this, few studies have investigated the mechanism of action and efficacy of AB.
Purpose: We examined the effects of capsaicin (CAP) application on pressor responses evoked by muscle contraction (MC), which are mediated by group III and IV muscle afferents.
Methods: Heart rate (HR), blood pressure, and end-tidal CO2 were monitored in cats (N = 12) decerebrated under halothane. Decerebration eliminated anesthesia use and effects from the higher brain. Electrical stimulation of L7 and S1 ventral roots evoked static hindlimb MC (30 s). After control runs, a commercial CAP (4.95% Oleoresin Capsicum) AB was applied to the skin over the contracting muscles of one hindlimb. MC were evoked every 10 min, alternating between hindlimbs. Data were analyzed with RM ANOVA and Tukey post hoc test.
Results: Changes in peak mean arterial pressure (MAP) induced by static ipsilateral MC were significantly attenuated at 20 min and tended to approach baseline levels at 40 min after CAP application. The mean (±SEM) of the peak MAP for the ipsilateral side just before application (T = 0), at 20 min (T+20), and 40 min (T+40) were 28.3 mm Hg ± 6.4, 13.8 mm Hg ±2.9, and 22.6 mm Hg ± 5.2, respectively. There were no significant changes in HR.
Conclusions: Cardiovascular effects due to activation of group III and IV afferent fibers were significantly attenuated by the application of CAP. The time course of the effects appeared to support the need for repeated CAP application for pain relief. Central nervous system circuitry responsible for this effect awaits elucidation.
Pain is an inevitable part of an active lifestyle. Although there are many pain relieving methods, those in sports medicine and physically active individuals often utilize cheap and convenient over-the-counter analgesic balms for the relief of minor aches and pains. In fact, topical analgesic balm (AB) usage has grown to a $150 million industry with over 34% of all American adults using them annually. Despite their popularity, comparatively few studies have addressed the efficacy and mechanism of action of AB. Our previous study focused on a commonly used combination of capsaicin (CAP) and methyl salicylate. The present study addressed the single active ingredient CAP, which is often the sole active ingredient of many AB.
CAP is well studied in terms of its pharmacological properties. The vanilloid receptor subtype 1 (VR1), a nonselective cation channel and thermal sensor, is thoroughly characterized as the target of CAP. Initial administration of CAP produces itching, pricking, and burning pain due to excitation of nociceptors. These initial effects are followed by a period of hyperalgesia. Repeated CAP application causes prolonged hypalgesia or nociceptor desensitization. This last effect appears within a week and can last 3 wk after application ceases. These effects are dependent on the concentration and duration of application.
Not all mechanisms that account for the analgesic effects of CAP are clearly understood. CAP's analgesic properties are thought to have a variety of mechanisms of action, including local effects on nerve fibers, depletion of neurotransmitters, counterirritation, engagement of the "gate control" mechanism, and suggested placebo effects. Although not a popular explanation of AB effects, topically administered CAP may block nerve fibers directly or deplete neurotransmitter substances. Dray offers a more accepted explanation: CAP is believed to cause counterirritant effects. Counterirritants inflame or irritate the skin, increase cutaneous blood flow, stimulate or depress pain receptors, and stimulate thermoreceptors. By activating nociceptors with a peripheral noxious stimulus, counterirritants inhibit the response of central neurons that transmit pain. Another speculation is that rubbing or massaging AB onto the skin during application may engage the "gate control" mechanism by activating Aβ fibers. Finally, some suggest that a placebo effect is the most likely source of the analgesic effects acting through the power of suggestion. The power of suggestion psychologically stimulates the nervous system. Price and colleagues used heat induced experimental pain and a placebo analgesic cream to analyze factors that contribute to the magnitude of placebo analgesia. Although placebo effects are closely associated with expectancy, they found that no relationship exists between placebo effects and the desire for relief. This suggests that any analgesic effect experienced from an AB is not primarily due to psychological factors.
