Influence of menopause status and age on integrated central and peripheral hemodynamic responses to subsystolic cuffing during submaximal exercise

Abstract

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.

Keywords: aging women; cardiac output; exercise pressor reflex; group III-Aδ and IV-C neural afferents; regional circulatory occlusion.

Fig. 1.

Temporally aligned raw data tracings of mean arterial pressure (MAP) beginning at control (CTL) exercise and continuing throughout exercise during 2-min periods of subsystolic regional circulatory occlusion (RCO) separated by 2-min periods of RCO deflation. Moving from left to right, gray shaded regions represent 2-min periods of subsystolic RCO at 20, 40, 60, 80, or 100 mmHg, respectively. A: tracing of an adult woman in premenopause. B: tracing of a woman in postmenopause.

Fig. 2.

MAP responses at baseline rest, during control exercise, or periods of exercise during 2-min periods of subsystolic RCO. Data are means ± SD. A: absolute measurements of MAP. B: %change in MAP from the CTL exercise period to each subsystolic RCO period. ^‡Within-group difference compared with CTL exercise, P < 0.05; †Different from zero in premenopause, P < 0.05; #Different from zero in both pre- and postmenopause, P < 0.05; *Different from zero in postmenopause, P < 0.05. All significance determined after Tukey's honest significant difference (HSD) post hoc testing.

Fig. 3.

Systemic vascular resistance index (SVR_I) responses at baseline rest, during control exercise, or periods of exercise during 2-min periods of subsystolic RCO. Data are means ± SD. A: absolute measurements of SVR_I. B: %change in SVR_I from the CTL exercise period to each subsystolic RCO period. ^‡Within-group difference compared with CTL exercise, P < 0.05; *Different from zero in postmenopause, P < 0.05. All significance determined after Tukey's HSD post hoc testing.

Fig. 4.

Cardiac function responses at baseline rest, during CTL exercise, or periods of exercise during 2-min periods of subsystolic RCO. Data are means ± SD. A: absolute measurements of cardiac index (Q_I). B: %change in Q_I from the CTL exercise period to each subsystolic RCO period. C: absolute measurements of stroke volume index (SV_I). D: %change in SV_I from the CTL exercise period to each subsystolic RCO period. E: absolute measurements of heart rate (HR). F: %change in HR from the CTL exercise period to each subsystolic RCO period. ^‡Within-group difference compared with CTL exercise, P < 0.05; †Different from zero in premenopause, P < 0.05; #Different from zero in both pre- and postmenopause, P < 0.05; *Different from zero in postmenopause, P < 0.05. All significance determined after Tukey's HSD post hoc testing.

Fig. 5.

Arterial carbon dioxide tension [modeled using Pa_CO2 = 5.5 + (0.90 × Pet_CO2) − (0.0021 × V_T) from Jones et al. (23) where Pa_CO2 is arterial carbon dioxide tension, Pet_CO2 is end-tidal partial pressure of carbon dioxide, and V_T is tidal volume], the ventilatory equivalent for end-tidal CO₂ tension ratio [minute ventilation (V̇e)/Pet_CO2], or tidal volume-to-inspiratory time ratio (V_T/T_i) responses during exercise with subsystolic RCO or during the acute 20-s period following RCO deflation during exercise. Data are means ± SD. A: absolute Pa_CO2. B: absolute V̇e/Pet_CO2. C: absolute V_T/T_i.

Fig. 6.

Rating of perceived exertion (RPE, 6–20 Borg's scale) responses at baseline rest, during CTL exercise, or periods of exercise during 2-min periods of subsystolic RCO. Data are means ± SD. A: absolute measurements of RPE. B: %change in RPE from the CTL exercise period to each subsystolic RCO period. ^‡Within-group difference compared with CTL exercise, P < 0.05; †Different from zero in premenopause, P < 0.05; #Different from zero in both pre- and postmenopause, P < 0.05. All significance determined after Tukey's HSD post hoc testing.