Menstrual cycle alters sympathetic neural responses to orthostatic stress in young, eumenorrheic women

Abstract

Sympathetic baroreflex sensitivity (BRS) and muscle sympathetic nerve activity (MSNA) responses during early follicular (EF) and midluteal (ML) phases of the menstrual cycle are controversial. We hypothesize an augmented sympathetic BRS and MSNA response to orthostatic stress during the ML phase of the menstrual cycle. MSNA, mean arterial pressure (MAP), and heart rate (HR) were recorded during progressive lower body negative pressure (LBNP) (-5, -10, -15, -20, -30, and -40 mmHg; 3 min/stage) in 13 healthy, eumenorrheic women (age 21 +/- 1 yr). Sympathetic BRS was assessed by examining relations between spontaneous fluctuations of diastolic arterial pressure and MSNA at rest and during progressive LBNP. Plasma estradiol (42 +/- 6 vs. 112 +/- 12 pg/ml; P < 0.01) and progesterone (2 +/- 0 vs. 10 +/- 2 ng/ml; P < 0.04) were elevated during the ML phase. Resting MSNA (8 +/- 1 vs. 11 +/- 1 bursts/min), MAP (79 +/- 2 vs. 78 +/- 2 mmHg), and HR (58 +/- 2 vs. 60 +/- 2 beats/min) were not different during EF and ML phases. MSNA and HR increased during progressive LBNP (P < 0.001), and the increases in MSNA burst frequency (bursts/min) and HR were similar during both phases. In contrast, increases in total MSNA (arbitrary units) during progressive LBNP were augmented during the ML phase (P < 0.04), but this response does not appear to be linked to differences in sympathetic BRS. Progressive LBNP did not change MAP during either phase. Our results demonstrate an augmentation of the MSNA response to progressive LBNP during the ML phase of the menstrual cycle. These findings suggest that hormonal fluctuations of eumenorrheic women may influence sympathoexcitation during an orthostatic challenge, but not through sympathetic baroreflex-mediated pathways.

Fig. 1.

Representative neurograms obtained from one subject during baseline, −20 mmHg lower body negative pressure (LBNP), and −40 mmHg LBNP of the early follicular and midluteal phases of the menstrual cycle. Although the menstrual cycle did not alter burst frequency between phases, the total activity based on muscle sympathetic nerve activity (MSNA) area increased during the midluteal phase.

Fig. 2.

Changes in heart rate (HR) and systolic (SAP), diastolic (DAP), and mean (MAP) arterial pressures during progressive LBNP. Subjects were examined during the early follicular (EF) and midluteal (ML) phases of the menstrual cycle. Progressive LBNP elicited increases in HR, but did not change SAP, DAP, or MAP. Hemodynamic responses were similar between menstrual phases (n = 10 subjects).

Fig. 3.

Changes in MSNA during progressive LBNP. Subjects were examined during the EF and ML phases of the menstrual cycle. Progressive LBNP elicited similar increases of MSNA burst frequency during the EF and ML phases. In contrast, progressive LBNP elicited a greater increase in total MSNA activity [arbitrary units (AU)] during the ML phases of the menstrual cycle. Reported as means ± SE (n = 7).

Fig. 4.

Linear relations between MSNA and DAP during EF and ML phases of the menstrual cycle. Progressive LBNP elicited significant reductions in the MSNA-DAP slopes during both the EF and ML phases of the menstrual cycle, indicating increased sympathetic baroreflex sensitivities during orthostatic stress. The increases in sympathetic baroreflex sensitivity were not different between the EF and ML phases. Reported as means ± SE (n = 7).

Fig. 5.

Representative linear regression slopes from one subject during baseline, −15 mmHg, and −30 mmHg LBNP. Slopes became more negative with increasing levels of LBNP, indicating sympathetic baroreflex sensitivity increased with increasing levels of orthostatic stress. Data presented are from the EF phase, since results were similar between the EF and ML phases.