PURPOSE: Based on previous evidence of muscle fiber injury and decreased blood flow in the extensor carpi radialis brevis (ECRB) muscle in lateral epicondylitis (LE), we hypothesized that there would also be an abnormal (vasoconstrictive) vascular response to adrenaline in the ECRB muscle in LE. METHODS: In a case-control study, we measured skeletal muscle blood flow in 8 patients with LE and in 8 healthy controls in response to a 30-minute intravenous infusion ofadrenaline. We used local clearance of technetium-99m in the main portion of the ECRB muscle to calculate muscle blood flow. RESULTS: In support of the hypothesis, the blood flow response to the adrenaline infusion was markedly different in the 2 study groups. Whereas the continuous decrease in technetium-99m clearance rate over time was interrupted by the adrenaline-induced vasodilatory effect in the control group, we detected no such effect in the patient group. CONCLUSIONS: In the ECRB muscle in LE, there is a shift in the balance of vasodilatory and vasoconstrictory influences of adrenaline, leading to vasoconstriction during low-dose adrenaline infusion. The adverse adrenaline effect is similar to what was previously observed after minor muscle injury. Whether the vasoregulatory change, by causing relative muscle ischemia, represents the primary etiology in LE or results from muscle injury cannot be determined, but it is likely to contribute to the development and continuation of chronic muscle pain in LE. New ways of thinking about the condition may be required, and pharmacological treatment might be an option to improve the blood supply and avoid further damage to the affected ECRB muscle-tendon unit.
RCT Entities:
PURPOSE: Based on previous evidence of muscle fiber injury and decreased blood flow in the extensor carpi radialis brevis (ECRB) muscle in lateral epicondylitis (LE), we hypothesized that there would also be an abnormal (vasoconstrictive) vascular response to adrenaline in the ECRB muscle in LE. METHODS: In a case-control study, we measured skeletal muscle blood flow in 8 patients with LE and in 8 healthy controls in response to a 30-minute intravenous infusion of adrenaline. We used local clearance of technetium-99m in the main portion of the ECRB muscle to calculate muscle blood flow. RESULTS: In support of the hypothesis, the blood flow response to the adrenaline infusion was markedly different in the 2 study groups. Whereas the continuous decrease in technetium-99m clearance rate over time was interrupted by the adrenaline-induced vasodilatory effect in the control group, we detected no such effect in the patient group. CONCLUSIONS: In the ECRB muscle in LE, there is a shift in the balance of vasodilatory and vasoconstrictory influences of adrenaline, leading to vasoconstriction during low-dose adrenaline infusion. The adverse adrenaline effect is similar to what was previously observed after minor muscle injury. Whether the vasoregulatory change, by causing relative muscle ischemia, represents the primary etiology in LE or results from muscle injury cannot be determined, but it is likely to contribute to the development and continuation of chronic muscle pain in LE. New ways of thinking about the condition may be required, and pharmacological treatment might be an option to improve the blood supply and avoid further damage to the affected ECRB muscle-tendon unit.