title: Effect of passive heat stress on arterial stiffness.
abstract: Arterial compliance, the inverse of arterial stiffness, is a prognostic indicator of arterial health. Central and peripheral arterial compliance decrease with acute cold stress and may increase postexercise when exercise-induced elevations in core temperature are likely still to be present. Increased blood flow through the conduit arteries associated with elevated core temperature increases shear stress, which in turn releases nitric oxide and other endothelium-derived factors. These changes, in conjunction with supportive in vitro data, suggest that elevated core temperature may indirectly increase central and peripheral arterial compliance (i.e. decrease arterial stiffness). The purpose of this study was to test the hypothesis that increased core temperature decreases central and peripheral arterial stiffness, as measured with pulse wave velocity (PWV). Using Doppler ultrasound, carotid-femoral (central) and carotid-radial (peripheral) arterial PWVs were measured from eight subjects (age 37 ± 11 years; mass 68.8 ± 11.1 kg; height 171 ± 3 cm) before and during passive heat-stress-induced increases in core temperature of 0.47 ± 0.05, 1.03 ± 0.12 and 1.52 ± 0.07°C (i.e. baseline, 0.5, 1.0 and 1.5°C, respectively). Changes in PWV were evaluated with one-way repeated-measures ANOVA. When analysed as group means, neither central (677 ± 161, 617 ± 72, 659 ± 74 and 766 ± 207 cm s(-1); P = 0.12) nor peripheral PWV (855 ± 192, 772 ± 95, 759 ± 49 and 858 ± 247 cm s(-1); P = 0.56) changed as core temperature increased from baseline to 0.5, 1.0 and 1.5°C, respectively. However, individual changes in central (average r = -0.89, P < 0.05) and peripheral PWV (average r = -0.93, P < 0.05) with heat stress were significantly correlated with normothermic baseline PWV. In conclusion, these data suggest that the magnitude by which heat stress reduced PWV was predicated upon normothermic PWV, with the individuals having the highest normothermic PWV being most responsive to the heat-stress-induced reductions in PWV.
authors.affiliation: Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital Dallas, 7232 Greenville Avenue, Dallas, TX 75231, USA.
authors.forename: Matthew S
authors.initials: MS
authors.lastname: Ganio
authors.forename: R Matthew
authors.initials: RM
authors.lastname: Brothers
authors.forename: Shigeki
authors.initials: S
authors.lastname: Shibata
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Hastings
authors.forename: Craig G
authors.initials: CG
authors.lastname: Crandall
mesh_terms: D000328:Adult; D001158:Arteries / Q000502:physiology*; D001783:Blood Flow Velocity / Q000502:physiology; D003187:Compliance; D005260:Female; D006358:Hot Temperature; D006801:Humans; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow; D012881:Skin Temperature; D014655:Vascular Resistance; D059289:Vascular Stiffness