Key result
Transient regional circulatory occlusion at 80 mmHg during exercise increased mean arterial pressure significantly more in postmenopausal compared to premenopausal women (17% vs 4%, P=0.02).
Why the study?
Does transient subsystolic regional circulatory occlusion during exercise augment systemic vascular resistance and mean arterial pressure in postmenopausal compared to premenopausal women?
RCT (n=28)
randomized
Does transient subsystolic regional circulatory occlusion during exercise augment systemic vascular resistance and mean arterial pressure in postmenopausal compared to premenopausal women?
Postmenopausal women exhibit augmented systemic vascular resistance and mean arterial pressure responses to subsystolic regional circulatory occlusion during exercise compared to premenopausal women, independent of age.
Should not yet change exercise recommendations; hypothesis-generating for menopause-specific vascular reactivity and requires prospective validation.
Although pathophysiological links between postmenopause and healthy aging remain unclear, both factors are associated with increased blood pressure and sympathetic nerve activity (SNA) in women. Activation of polymodal musculoskeletal neural afferents originating within adventia of venules modulates SNA and blood pressure control during exercise in healthy adults. We hypothesized transient subsystolic regional circulatory occlusion (RCO) during exercise sensitizes these afferents leading to augmented systemic vascular resistance (SVR)-mediated increased mean arterial pressure (MAP) in postmenopause vs. premenopause. Normotensive women in premenopause or postmenopause (n = 14 and 14; ages: 30 ± 9 and 55 ± 7 yr, respectively; P < 0.01) performed: 1) peak exercise testing and 2) fixed-load cycling at 30% peak workload (48 ± 11 and 38 ± 6 W, respectively; P < 0.01), whereby the initial 3 min were control exercise without RCO (CTL), thereafter including 2 min of bilateral-thigh RCO to 20, 40, 60, 80, or 100 mmHg (randomized), with 2 min deflation between RCO. Both MAP (17 ± 4 vs. 4 ± 4%, P = 0.02) and SVR (16 ± 8 vs. -3 ± 8%, P = 0.04) increased at 80 mmHg from CTL in postmenopause vs. premenopause, respectively. However, cardiac index was similar in postmenopause vs. premenopause at 80 mmHg from CTL (1 ± 6 vs. 7 ± 6%, respectively; P = 0.15). There was no continuous effect of aging in MAP (P = 0.12), SVR (P = 0.07), or cardiac index (P = 0.18) models. These data suggest transient locomotor subsystolic RCO sensitizes musculoskeletal afferents, which provoke increased SVR to generate augmented MAP during exercise in postmenopause. These observations provide a novel approach for understanding the age-independent variability in exercise blood pressure control across the normotensive adult pre- to postmenopause spectrum.
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Iterson et al. (2016) conducted an RCT in Normotensive premenopause and postmenopause (n=28). Transient subsystolic regional circulatory occlusion (RCO) vs. Control exercise without RCO (CTL) and premenopausal women was evaluated on Increase in mean arterial pressure (MAP) at 80 mmHg from control (p=0.02). Transient regional circulatory occlusion at 80 mmHg during exercise increased mean arterial pressure significantly more in postmenopausal compared to premenopausal women (17% vs 4%, P=0.02).
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