Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women

1997 ◽  
Vol 83 (2) ◽  
pp. 477-484 ◽  
Author(s):  
E. M. Brooks ◽  
A. L. Morgan ◽  
J. M. Pierzga ◽  
S. L. Wladkowski ◽  
J. T. O’Gorman ◽  
...  

Brooks, E. M., A. L. Morgan, J. M. Pierzga, S. L. Wladkowski, J. T. O’Gorman, J. A. Derr, and W. L. Kenney. Chronic hormone replacement therapy alters thermoregulatory and vasomotor function in postmenopausal women. J. Appl. Physiol. 83(2): 477–484, 1997.—This investigation examined effects of chronic (≥2 yr) hormone replacement therapy (HRT), both estrogen replacement therapy (ERT) and estrogen plus progesterone therapy (E+P), on core temperature and skin blood flow responses of postmenopausal women. Twenty-five postmenopausal women [9 not on HRT (NO), 8 on ERT, 8 on E+P] exercised on a cycle ergometer for 1 h at an ambient temperature of 36°C. Cutaneous vascular conductance (CVC) was monitored by laser-Doppler flowmetry, and forearm vascular conductance (FVC) was measured by using venous occlusion plethysmography. Iontophoresis of bretylium tosylate was performed before exercise to block local vasoconstrictor (VC) activity at one skin site on the forearm. Rectal temperature (Tre) was ∼0.5°C lower for the ERT group ( P < 0.01) compared with E+P and NO groups at rest and throughout exercise. FVC: mean body temperature (Tb) and CVC: Tb curves were shifted ∼0.5°C leftward for the ERT group ( P < 0.0001). Baseline CVC was significantly higher in the ERT group ( P < 0.05), but there was no interaction between bretylium treatment and groups once exercise was initiated. These results suggest that 1) chronic ERT likely acts centrally to decrease Tre, 2) ERT lowers the Tre at which heat-loss effector mechanisms are initiated, primarily by actions on active cutaneous vasodilation, and 3) addition of exogenous progestins in HRT effectively blocks these effects.

1998 ◽  
Vol 85 (2) ◽  
pp. 505-510 ◽  
Author(s):  
E. M. Brooks-Asplund ◽  
W. L. Kenney

Postmenopausal women on estrogen replacement therapy (ERT) regulate body core temperature at a lower baseline level at rest in a thermoneutral environment. We conducted a series of studies to test whether, in a thermoneutral environment, chronic (≥2 yr) oral ERT significantly alters baseline skin blood flow (SkBF) and cutaneous vascular conductance (CVC) and whether ERT alters maximal CVC (CVCmax) and SkBF in postmenopausal women. In the first set of studies, forearm blood flow (FBF) was measured by venous-occlusion plethysmography in 24 postmenopausal women: 8 not taking exogenous hormone therapy (No HRT group), 8 on ERT, and 8 receiving combination of estrogen and progesterone therapy, at rest and during prolonged (1 h) local heating of the forearm at 42°C. Mean arterial pressure (MAP) was measured by brachial auscultation before each set of FBF measurements to calculate forearm vascular conductance (FVC = FBF/MAP). SkBF was measured by laser-Doppler flowmetry (LDF), and CVC was calculated as LDF/MAP and standardized as %CVCmax. Baseline FVC, %CVCmax, and maximal FVC were not significantly different among the three groups of women. In the second set of experiments, LDF in ERT and No HRT groups was measured at rest in both thermoneutral and warm environments. %CVCmax was again not significantly different between ERT and No HRT groups at thermoneutral ambient temperatures and increased similarly in the warm environment. Therefore, chronic exogenous ERT does not appear to influence either baseline or maximal SkBF.


1997 ◽  
Vol 29 (Supplement) ◽  
pp. 190
Author(s):  
E. M. Brooks ◽  
A. L. Morgan ◽  
J. M. Pierzga ◽  
S. L. Wladkowski ◽  
J. T. O'Gorman ◽  
...  

2005 ◽  
Vol 153 (4) ◽  
pp. 527-533 ◽  
Author(s):  
J A Kanaley ◽  
I Giannopoulou ◽  
S Collier ◽  
R Ploutz-Snyder ◽  
R Carhart

Objective: This study examined the effect of hormone-replacement therapy (HRT) use on the incremental GH response to aerobic exercise in postmenopausal women and established whether racial differences in the GH response were seen at rest and in response to exercise. Methods: 13 white (n = 6, HRT; n = 7, no HRT) and seven black women (no HRT) were studied on two occasions, a control day and an exercise day (30 min at 70% VO2max on a cycle ergometer). Blood was sampled every 10 min for a 4-h period and analyzed for GH using an ultrasensitive chemiluminescent assay. Results: The mean 4-h GH concentration was higher on both study days in the HRT women than the non-HRT users. The integrated GH concentrations were greater in the HRT women both at rest and in response to exercise (rest, 352 ± 53 min μg l−1; exercise, 711 ± 57 min μg l−1; P < 0.01) than in the non-HRT women (rest, 157 ± 87 min μg l−1; exercise, 248 ± 94 min μg l−1). The incremental GH response was greater in the HRT users than in the non-HRT women (358 ± 130 versus 90.8 ± 94 min μg l−1, respectively; P < 0.05). GH-production rate during the 4-h period was greater in the HRT women than in the non-HRT women (P < 0.01), due to an increase in the GH mass secreted/pulse (P < 0.05), with no change in GH pulse number or GH half-life. No racial differences in the mean 4-h GH concentrations or integrated GH concentrations were found at rest or in response to exercise. Conclusion: HRT use resulted in a greater incremental exercise response compared with non-HRT users, due to changes in the secretory pulse characteristics in the HRT users. This study also demonstrated that no racial differences exist at rest and in response to exercise in the morning hours.


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