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      Sex differences in blood pressure regulation during ischemic isometric exercise: the role of the β-adrenergic receptors

      1 , 1 , 2 , 1
      Journal of Applied Physiology
      American Physiological Society

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          Abstract

          We sought to investigate whether the β-adrenergic receptors play a pivotal role in sex-related differences in arterial blood pressure (BP) regulation during isometric exercise. Sixteen volunteers (8 women) performed 2 min of ischemic isometric handgrip exercise (IHE) and 2 min of postexercise circulatory occlusion (PECO). Heart rate (HR) and beat-to-beat arterial BP were continuously measured. Beat-to-beat estimates of stroke volume (ModelFlow) were obtained and matched with HR to calculate cardiac output (Q̇) and total peripheral resistance (TPR). Two trials were randomly conducted between placebo and nonselective β-adrenergic blockade (40 mg propranolol). Under the placebo condition, the magnitude of the BP response in IHE was lower in women compared with men. During PECO, the BP remained elevated and the sex differences persisted. The β-blockade attenuated the BP response during IHE in men (∆57 ± 4 vs. ∆45 ± 7 mmHg, P = 0.025) due to a reduction in Q̇ (∆3.7 ± 0.5 vs. ∆1.8 ± 0.2 L/min, P = 0.012) while TPR was not affected. In women, however, the BP response during IHE was unchanged (∆27 ± 3 vs. ∆28 ± 3 mmHg, P = 0.889), despite attenuated Q̇ (∆2.7 ± 0.4 vs. ∆1.3 ± 0.2 L/min, P = 0.012). These responses were mediated by a robust increase in TPR under β-blockade (∆−0.2 ± 0.4 vs. ∆2.2 ± 0.7 mmHg·L −1·min, P = 0.012). These findings demonstrate that the sex differences in arterial BP regulation during ischemic IHE are mediated by β-adrenergic receptors.

          NEW & NOTEWORTHY We found that the blood pressure response during isometric exercise in women is mediated by increases in cardiac output, whereas in men it is mediated by increases in both cardiac output and total peripheral resistance. In addition, women showed a robust increase in total peripheral resistance under β-blockade during isometric exercise and muscle metaboreflex activation. These findings demonstrate that sex differences in blood pressure regulation during isometric exercise are mediated by β-adrenergic receptors.

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          Most cited references38

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          Observations in man upon a blood pressure raising reflex arising from the voluntary muscles.

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            Sex differences in sympathetic neural-hemodynamic balance: implications for human blood pressure regulation.

            Among young normotensive men, a reciprocal balance between cardiac output and sympathetic nerve activity is important in the regulation of arterial pressure. In young women, the balance among cardiac output, peripheral resistance, and sympathetic nerve activity is unknown. Consequently, the aim of this study was to examine the relationship of cardiac output and total peripheral resistance to muscle sympathetic nerve activity in young women. Multiunit peroneal recordings of muscle sympathetic nerve activity were obtained in 17 women (mean+/-SEM: age 24+/-3 years) and 21 men (mean+/-SEM: age 25+/-5 years). Mean resting muscle sympathetic nerve activity was lower in women compared with men (19+/-3 versus 25+/-1 bursts minute(-1); P 0.05) or cardiac output (r=0.23; P>0.05) in women. Our results demonstrate that men and women rely on different integrated physiological mechanisms to maintain a normal arterial pressure despite widely varying sympathetic nerve activity among individuals. These findings may have important implications for understanding how hypertension and other disorders of blood pressure regulation occur in men and women.
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              Sex and ageing differences in resting arterial pressure regulation: the role of the β-adrenergic receptors.

              In men, muscle sympathetic nerve activity (MSNA) is positively related to total peripheral resistance (TPR) and inversely related to cardiac output (CO). However, this relationship was not observed in young women. We aimed to investigate whether simultaneous β-adrenergic stimulation offsets this balance in young women. Furthermore, we aimed to examine whether the ability of the β-adrenergic receptors to offset the transduction of MSNA into vasoconstrictor tone was lost in postmenopausal women. We measured MSNA (peroneal microneurography), arterial pressure (brachial line), CO (Modelflow), TPR and changes in forearm vascular conductance (FVC) to increasing doses of noradrenaline (NA; 2, 4 and 8 ng (100 ml)(-1) min(-1)) before and after systemic β-blockade with propranolol in 17 young men, 17 young women and 15 postmenopausal (PM) women. The percentage and absolute change in FVC to the last two doses of NA were greater during β-blockade in young women (P 0.05). Before β-blockade there was no relationship of MSNA to TPR or mean arterial pressure (MAP) in young women. Following β-blockade, MSNA became positively related to TPR (r = 0.59, P < 0.05) and MAP (r = 0.58, P < 0.05). In the PM women and young men, MSNA was positively associated with TPR. β-Blockade had no effect on this relationship. Our data suggest that the β-adrenergic receptors offset α-adrenergic vasoconstriction in young women but not young men or PM women. These findings may explain in part the tendency for blood pressure to rise after menopause in women.
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                Author and article information

                Journal
                Journal of Applied Physiology
                Journal of Applied Physiology
                American Physiological Society
                8750-7587
                1522-1601
                August 01 2019
                August 01 2019
                : 127
                : 2
                : 408-414
                Affiliations
                [1 ]NeuroV̇ASQ̇–Integrative Physiology Laboratory, Faculty of Physical Education, University of Brasília, Brasilia, Distrito Federal, Brazil
                [2 ]Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada
                Article
                10.1152/japplphysiol.00270.2019
                6732446
                31219771
                c20f1401-871d-4ae3-be0c-5eb45cb06f89
                © 2019
                History

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