Abstract
Acute heat exposure increases skeletal muscle blood flow in humans. However, the vasodilator mechanisms mediating this hyperemic response remain unknown. The cyclooxygenase pathway is active in skeletal muscle, is heat sensitive, and contributes to cutaneous vasodilation during heat exposure in young healthy humans. Therefore, the purpose of this investigation was to test the hypothesis that inhibition of cyclooxygenase via high dose ingestion of ibuprofen would attenuate blood flow in the vastus lateralis muscle during localized heating. Four participants (26 ± 2 yrs) were studied on two separate occasions: 1) time control; 2) ingestion of 800 mg ibuprofen, a non-selective cyclooxygenase inhibitor. Experiments were randomized, counter-balanced, and separated by at least 10 days. 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. Pulsed short-wave diathermy was used to induce deep heating of the vastus lateralis for 90 min, whereas the contralateral leg served as a thermoneutral control. Local muscle temperature was measured within ~1-2 cm of each microdialysis probe via a thermocouple. Temperature of the vastus lateralis measured through 90 min of heating did not differ between conditions (control, 39.2 ± 1.0 °C; ibuprofen, 39.7 ± 1.0 °C; P = 0.6 for interaction). Interestingly, local blood flow increased during heat exposure, but did not differ between control (baseline, 15 ± 11 mL· min-1 · 100g-1; 30 min, 23 ± 12 mL· min-1 · 100g-1; 60 min, 25 ± 12 mL· min-1 · 100g-1; 90 min, 38 ± 12 mL· min-1 · 100g-1) and ibuprofen (baseline, 14 ± 11 mL· min-1 · 100g-1; 30 min, 29 ± 12 mL· min-1 · 100g-1; 60 min, 32 ± 12 mL· min-1 · 100g-1; 90 min, 53 ± 12 mL· min-1 · 100g-1; P = 0.2 for interaction) conditions. Muscle temperature and local blood flow did not differ between conditions or across time for the thermoneutral leg (both P > 0.3). Taken together, cyclooxygenase-derived vasodilator prostanoids do not appear to contribute to thermal hyperemia in skeletal muscle of young healthy humans. This work was supported by grants from the National Institutes of Health (T32 AG020494; R01AG059314) and the American Heart Association (TPA958179). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.