Cardiac autonomic function and vasomotor symptoms: too much break and not enough accelerator?

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During the menopause transition, 60% to 80% of women experience vasomotor symptoms (VMS) or hot flashes; VMS can last anywhere from 6 months to 2 years, but in some women, can last for many years after the cessation of the menstrual cycle.1-8 In approximately one-third of women, significant VMS can impact physical functioning and quality of life.9,10 Follicle-stimulating hormone (FSH) and estradiol levels can be highly variable during the transition, culminating in the cessation of ovarian hormone production. While VMS accompany menopause, the degree and severity of VMS does not often correlate with estradiol levels. Whereas the pathophysiologic mechanisms of VMS are complex and unknown,11-13 central nervous system dysfunction with hypothalamic dysregulation as a result of fluctuations in the hormonal milieu has been hypothesized.14 The peripheral autonomic nervous system (ANS), composed of the sympathetic and parasympathetic (vagal) divisions, controls heart rate, blood pressure, vasodilation and constriction, venous capacitance, and sweating among many other functions.15 Given the critical role of ANS in vasomotor control, ANS dysfunction has also been implicated in the pathophysiology of VMS. Sympathetic predominance and/or vagal withdrawal have been implicated in hot flashes, and whether a disruption in ANS balance due to loss of ovarian hormone production contributes to VMS frequency and intensity has been studied with mixed results.16-20
In this issue of Menopause, Gibson et al21 conducted a study to examine the relationship between resting cardiac autonomic function, and the frequency and severity of VMS during menopause transition. Women were recruited from the Menopausal Treatment Using Relaxation Exercises (MaTURE) trial,22 who were perimenopausal or postmenopausal (n = 121, ages 40-59 years), with at least four hot flashes per day, and randomized to paced respiration or music-listening control intervention for 12 weeks. Cardiac impedance derived pre-ejection period (PEP), as a measure of cardiac sympathetic activity, and respiratory sinus arrhythmia (RSA), a marker of parasympathetic activity, were measured at baseline and at 12 weeks, along with VMS frequency and severity.
The main findings from the study indicate that cardiac sympathetic activity is not significantly associated with hot flash frequency or severity at baseline or over 12 weeks. In contrast, there was a trend of higher frequency of moderate-to-severe hot flashes in those with parasympathetic predominance (as measured by RSA) at baseline. Increase in RSA was positively associated with frequency of moderate-to-severe VMS over 12 weeks. Authors suggested that increased parasympathetic tone may reflect increased sensitivity to perceiving VMS. Paced respiration intervention did not result in sympathetic or parasympathetic predominance change over 12 weeks compared with music listening control.
Gibson et al should be congratulated for a well-conducted randomized study on the complex topic of autonomic function and VMS, with a slow-paced respiration intervention. Nearly 90% of subjects were retained at 12 weeks, and intervention was practiced at least 15 minutes per day per their design. Teasing apart autonomic components to assess contributions of each branch to VMS is not easy, because many things influence autonomic activity such as sound, noise, temperature, food intake, stress, and sleep.23 Similarly, VMS are impacted by emotions, stress, food, alcohol, and temperature. In this study, instead of measuring time or frequency domain heart rate variability as a global, integrative measure of autonomic function,24 PEP was used as a more specific measure of cardiac sympathetic activity, which is under beta-adrenergic influence.25 RSA was used as a measure of parasympathetic function (amplitude of high frequency oscillations of R-R interval); the ANS plays an important role in synchronizing heart rate with respiration, and fluctuations of the R-R interval by respiration represents efficiency of cardio-pulmonary interaction.

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