학술논문
Cyclooxygenase inhibition does not blunt thermal hyperemia in skeletal muscle of humans.
Document Type
Academic Journal
Author
Richey RE; Department of Physiology and Anatomy, Human Vascular Physiology Laboratory, University of North Texas Health Science Center, Fort Worth, Texas, United States.; Ruiz YI; Department of Physiology and Anatomy, Human Vascular Physiology Laboratory, University of North Texas Health Science Center, Fort Worth, Texas, United States.; Cope HL; Department of Physiology and Anatomy, Human Vascular Physiology Laboratory, University of North Texas Health Science Center, Fort Worth, Texas, United States.; Moore AM; Department of Physiology and Anatomy, Human Vascular Physiology Laboratory, University of North Texas Health Science Center, Fort Worth, Texas, United States.; Walsh MA; Department of Physiology and Anatomy, Human Vascular Physiology Laboratory, University of North Texas Health Science Center, Fort Worth, Texas, United States.; Garfield TC; Department of Internal Medicine and Geriatrics, University of North Texas Health Science Center, Fort Worth, Texas, United States.; Olivencia-Yurvati AH; Department of Physiology and Anatomy, Human Vascular Physiology Laboratory, University of North Texas Health Science Center, Fort Worth, Texas, United States.; Department of Surgery, University of North Texas Health Science Center, Fort Worth, Texas, United States.; Romero SA; Department of Physiology and Anatomy, Human Vascular Physiology Laboratory, University of North Texas Health Science Center, Fort Worth, Texas, United States.
Source
Publisher: American Physiological Society Country of Publication: United States NLM ID: 8502536 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1522-1601 (Electronic) Linking ISSN: 01617567 NLM ISO Abbreviation: J Appl Physiol (1985) Subsets: MEDLINE
Subject
Language
English
Abstract
Acute heat exposure increases skeletal muscle blood flow in humans. However, the mechanisms mediating this hyperemic response remain unknown. The cyclooxygenase pathway is active in skeletal muscle, is heat sensitive, and contributes to cutaneous thermal hyperemia in young healthy humans. Therefore, the purpose of this study was to test the hypothesis that cyclooxygenase inhibition would attenuate blood flow in the vastus lateralis muscle during localized heating. Twelve participants (6 women) were studied on two separate occasions: 1 ) time control (i.e., no ibuprofen); and 2 ) ingestion of 800 mg ibuprofen, a nonselective cyclooxygenase inhibitor. Experiments were randomized, counter-balanced, and separated by at least 10 days. Pulsed short-wave diathermy was used to induce unilateral deep heating of the vastus lateralis for 90 min, whereas the contralateral leg served as a thermoneutral control. Microdialysis was utilized to bypass the cutaneous circulation and directly measure local blood flow in the vastus lateralis muscle of each leg via the ethanol washout technique. Heat exposure increased muscle temperature and local blood flow (both P < 0.01 vs. baseline). However, the thermal hyperemic response did not differ between control and ibuprofen conditions ( P ≥ 0.2). Muscle temperature slightly decreased for the thermoneutral leg ( P < 0.01 vs. baseline), yet local blood flow remained relatively unchanged across time for control and ibuprofen conditions (both P ≥ 0.7). Taken together, our data suggest that inhibition of cyclooxygenase-derived vasodilator prostanoids does not blunt thermal hyperemia in skeletal muscle of young healthy humans. NEW & NOTEWORTHY Acute heat exposure increases skeletal muscle blood flow in humans. However, the mechanisms mediating this hyperemic response remain unknown. Using a pharmacological approach combined with microdialysis, we found that thermal hyperemia in the vastus lateralis muscle was well maintained despite the successful inhibition of cyclooxygenase. Our results suggest that cyclooxygenase-derived vasodilator prostanoids do not contribute to thermal hyperemia in skeletal muscle of young healthy humans.