Effects of maternal breathing rate, psychiatric status, and cortisol on fetal heart rate.

The tremendous plasticity, and activity-dependency of the developing nervous system during fetal life, make this period a prime target for investigations of influences on the course of psychobiological development. Recent research across diverse disciplines has focused on identifying early life origins of adult disease (Godfrey & Barker, 2001), and has demonstrated that factors in pregnant women’s health, such as elevations in life stress, may explain some of the individual differences in children’s future risk for physical as well as psychological disorders (Barker, 2000; Davis et al., 2004; O’Connor, Heron, Golding, Beveridge, & Glover, 2002; Van den Bergh & Marcoen, 2004; Van den Bergh et al., 2005; O’Connor et al., 2005; Pawlby, Hay, Sharp, Waters, & O’Keane, 2009). In our ongoing work, we have reasoned that if the psychological functioning of pregnant women affects offsprings’ long–term development, we should be able to identify markers of that influence when it occurs, that is, during the prenatal period. In prior reports, we showed that prenatal maternal depression, as well as high trait anxiety, predict an increase in fetal heart rate (HR) during women’s laboratory–based, acute stress experience (Stroop test) compared to fetuses of euthymic women who show no significant change in HR (Monk et al., 2000; Monk et al., 2004). Others found that maternal depression during pregnancy is associated with greater fetal movement and slower return to baseline HR following vibroaccoustic stimulation applied to the women’s abdomen (Allister, Lester, Carr, & Liu, 2001; Dieter, Emory, Johnson, & Raynor, 2008). Because increases in fetal HR are often coincident with fetal movements (DiPietro et al., 2004), these findings are consistent in suggesting that greater fetal reactivity to external stimuli maybe a characteristic of fetal neurodevelopment when women experience significant prenatal mood dysregulation. Several studies have attempted to identify characteristics of pregnant women’s physiology that are potentially mood–based, and related to alterations in fetal neurobehavior, which would support the concept of women’s psychosocial functioning being ‘transduced to the fetus’ and shaping fetal development. The maternal HPA–axis has been a focus of this research {Wadhwa, 2005 #2514;Weinstock, 2005 #2656, as it is a major effector of psychosocial stress, and anxiety and depression are associated with elevations in resting cortisol CITES, even during pregnancy (EVANS). Using a laboratory stressor paradigm similar to ours, Fink et al. found that fetuses of women who had a cortisol increase following an arithmetic task, versus those who did not, had higher resting HR and less short–term HR variability 20 minutes after the stressor task ended. There was a trend finding for participants who had a cortisol increase to report higher levels of life stress {Fink, 2010 #4937}. In other work, higher resting maternal cortisol during the 3rd trimester of pregnancy was associated with greater amplitude and amount (time spent) of fetal movement during a 50 minute observation period (DiPietro, Kivlighan, Costigan, & Laudenslager, 2009). Sandman et al., found that higher levels of placenta–derived corticotropin releasing hormone (pCRH) (which, in contrast to CRH in the hypothalamus, shows increased synthesis in response to glucocorticoid exposure), is linked to increased fetal HR reactivity (‘arousal’) studied in a vibroaccoustic habituation paradigm (Sandman, Wadhwa, Chicz-DeMet, Porto, & Garite, 1999). Taken together, these studies raise the following question: are differences in fetal HR associated with maternal psychiatric status also related to differences in maternal cortisol levels? So far, we have found minimal indication that women’s psychobiological experience was being ‘transduced’ to the fetus and determining the fetal HR response to women’s exposure to a laboratory stressor. Our results showed no psychiatric diagnostic group differences in women’s cardiorespiratory activity that paralleled the group differences observed in fetal HR reactivity (Monk et al., 2000; Monk et al., 2004), and, across all subjects, only a small inverse association between changes in women’s systolic blood pressure and fetal HR (Monk et al., 2004). Instead, based on our results, we have posited that women’s significant cardiorespiratory reactivity during the stressor task functions as a stimulus that triggers a HR increase in fetuses of depressed or anxious women who already have been shaped over the course of gestation to be more reactive (Monk et al., 2004). To support this interpretation, we sought in this study to manipulate an acute change in maternal cardiorespiratory activity, and investigate it as a stimulus that could differentiate reactive from non–reactive fetuses, while simultaneously considering whether maternal cortisol level is associated with fetal HR. That is, a correlation between maternal cortisol and fetal HR in the laboratory likely reflects maternal–fetal experiences outside the laboratory, and thus finding an association would support the hypothesis that women’s psychosocial functioning shapes fetal development via maternal HPA–axis functioning. Specifically, the purpose of the present study was to replicate our prior results showing a greater fetal HR increase during maternal laboratory stress associated with women’s diagnosis of clinical depression (Monk et al., 2004), and to determine whether higher levels of women’s cortisol is associated with higher fetal HR. We also used a paced breathing task, in which participants increase and decrease their respiration rate according to a standardized protocol (Wilhelm, Grossman, & Coyle, 2004), to manipulate a specific aspect of women’s physiological activity (rapid changes in breathing) to determine its effects on fetal HR, and as a stimulus that reveals differences in fetal HR reactivity.