Abstract
A recent meta-analysis revealed that cardiac vagal activity (mostly indicated by vagally-mediated heart rate variability; HRV) decreases significantly from the follicular to luteal menstrual cycle phase in naturally-cycling participants. However, the question remains as to whether cyclical changes in estradiol (E2), progesterone (P4), or both are responsible for HRV fluctuations. We present the first studies to use repeated measures of E2, P4, and HRV across the cycle to model both the unique and interactive effects of person-centered E2 and P4 on HRV in multilevel models. In study one, 40 naturally-cycling participants were assessed weekly across four weeks, and were blind to the cycle focus of the study. In study two, 50 naturally-cycling participants were examined in three precisely defined cycle phases via ovulation testing. Both studies revealed that only P4 was correlated with HRV, such that higher-than-usual P4 significantly predicted lower-than-usual HRV within a given participant. In line with this, cycle phase comparisons revealed lower HRV in the mid-luteal phase (characterized by elevated P4) than in other phases. No significant main or interactive effects of E2 on HRV were found. Future female health studies should investigate individual differences in these effects and potential consequences of cyclical HRV changes on daily functioning.
Highlights
Cardiac vagal activity describes the restorative parasympathetic innervation of the heart, which is exercised by the vagus nerve
A significant random slope was observed for P4, indicating significant individual differences in the degree to which changes in P4 were associated with changes in HFlog
Only P4 was significantly associated with lower HFlog
Summary
Cardiac vagal activity describes the restorative parasympathetic innervation of the heart, which is exercised by the vagus nerve (tenth cranial nerve). The most commonly used indicator for cardiac vagal activity is the vagally-mediated components of heart rate variability (HRV). RSA describes the degree to which the heart rate changes between inhaling and exhaling air from the lungs, which shows no sensitivity to sympathetic nervous system activity but is mediated by the vagal nerve. This has led to the use of tonic RSA levels as a proxy for vagally-mediated HRV [14]
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