| Keywords |
Menopause ; Exercise pressor reflex ; Blood pressure |
| Abstract |
Both obesity and menopause cause the dysfunction of autonomic nervous system. Recent human studies have reported that exercise pressor reflex (EPR)-mediated increases in blood pressure are exaggerated in obese or postmenopausal women. Whether these findings can be extended to both obese and postmenopausal women remains unclear. Mean arterial pressure (MAP), cardiac output (CO), and total vascular conductances (TVC) were measured in normal premenopausal women (NPW; n = 11; 36 ± 2 yr), normal postmenopausal women (NPOW; n = 14; 57 ± 1 yr), and overweight postmenopausal women (OPOW; n = 14; 56 ± 1 yr) at baseline, and during static handgrip at 50% maximal voluntary contraction (MVC) followed by a period of postexercise muscular ischemia (PEMI) to isolate the metabolic component of the EPR. Changes in MAP from baseline were augmented in OPOW subjects during both 50% MVC handgrip (P < 0.05), and these group differences were maintained during PEI (P < 0.05). There were no differences in heart rate (HR), stroke volume (SV), and CO during hand grip exercise and PEMI among groups. Even though there was no group difference in TVC during exercise and PEMI, the TVC tended to be abolished in OPOW group. In summary, compared with NPW subjects, OPOW group exhibit exaggerated pressor responses to handgrip exercise that are maintained during PEMI, indicating that activation of the metabolic component of the EPR is augmented in OPOW group. The exaggerated pressor response mediated by the muscle metaboreflex activation in OPOW group mainly occurs via preperial vasoconstriction with little change in CO. |