Heat shock protein 90 modulates cutaneous vasodilation during an exercise-heat stress, but not during passive whole-body heating in young women
McGarr GW, Fujii N, Schmidt MD, Muia CM, Kenny GP
Physiological reports · 8 citations
How it was studied
- Design
- Controlled clinical trial (classified by our AI screen)
- Studied in
- People
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- University or hospital
- University of Ottawa
- Government
- Natural Sciences and Engineering Research Council of Canada
- Grants
- Natural Sciences and Engineering Research Council of Canada (RGPIN 2020); Natural Sciences and Engineering Research Council of Canada (rgpin-2020-03891); Natural Sciences and Engineering Research Council of Canada (03891)
Based on 2 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2020-08-01 · Physiol Rep · vol. 8 · issue 16 · p. e14552
- Publisher
- Wiley
- Cited
- 10 citations · more than 61% of similar papers · 0.5× the field average
- References
- 37 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Thermoregulation and physiological responses · Exercise and Physiological Responses · Infrared Thermography in Medicine
- Keywords
- Geldanamycin, Medicine, Vasodilation, Thermoregulation, Nitric oxide synthase, Heat shock protein, Internal medicine, Endocrinology, Hsp90, Chemistry, Nitric oxide, Biochemistry
- MeSH
- microcirculation, skin, humans, lactams, macrocyclic, benzoquinones, ng-nitroarginine methyl ester, enzyme inhibitors, exercise, vasodilation, adult, female, hsp90 heat-shock proteins, nitric oxide synthase, hot temperature
5 authors
From CA, JP
- Gregory W. McGarrUniversity of Ottawa
- Naoto FujiiUniversity of Tsukuba; University of Ottawa
- Madison D. SchmidtUniversity of Ottawa
- Caroline M. MuiaUniversity of Ottawa
- Glen Patrick Kenny · correspondingUniversity of Ottawa
Abstract
Heat shock protein 90 (HSP90) modulates exercise-induced cutaneous vasodilation in young men via nitric oxide synthase (NOS), but only when core temperature is elevated ~1.0°C. While less is known about modulation of this heat loss response in women during exercise, sex differences may exist. Further, the mechanisms regulating cutaneous vasodilation can differ between exercise- and passive-heat stress. Therefore, in 11 young women (23 ± 3 years), we evaluated whether HSP90 contributes to NOS-dependent cutaneous vasodilation during exercise (Protocol 1) and passive heating (Protocol 2) and directly compared responses between end-exercise and a matched core temperature elevation during passive heating. Cutaneous vascular conductance (CVC%max ) was measured at four forearm skin sites continuously treated with (a) lactated Ringers solution (control), (b) 178 μM Geldanamycin (HSP90 inhibitor), (c) 10 mM L-NAME (NOS inhibitor), or (d) combined 178 μM Geldanamycin and 10 mM L-NAME. Participants completed both protocols during the early follicular (low hormone) phase of the menstrual cycle (0-7 days). Protocol 1: participants rested in the heat (35°C) for 70 min and then performed 50 min of moderate-intensity cycling (~55% VO2peak ) followed by 30 min of recovery. Protocol 2: participants were passively heated to increase rectal temperature by 1.0°C, comparable to end-exercise. HSP90 inhibition attenuated CVC%max relative to control at end-exercise (p %max relative to control for both protocols (all p < .05), they did not differ from each other. We show that HSP90 modulates cutaneous vasodilation NOS-dependently during exercise in young women, with no effect during passive heating, despite a similar NOS contribution.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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