Stress is one of the commonest and underappreciated causes of reproductive frailty in women. The stress system leads to adaptive responses via mobilization of hormonal systems. Adaptability and resistance to stress are fundamental to life. The response to stressors depends on the type of stressor, the timing and duration of stress, the genetic predisposition, personality characteristics, and the way of coping with stress. The hypothalamic-pituitary-adrenal (HPA) axis has a direct inhibitory action on the hypothalamic-pituitary-ovarian (HPO) axis at multiple levels. Acute and chronic stress impairs reproduction, eventually acting on varying mechanisms. Undernutrition, over-training, and psychological stress contribute to hypothalamic amenorrhea via reduced HPO activity. In utero stress exposure is a significant predictor of subsequent adult telomere length. Some of the metabolic consequences of intrauterine growth restriction can be mitigated by ensuring early appropriate catch-up growth, while avoiding excessive weight gain if relative hypercortisolism is not installed. The effect of maternal stress on fetuses regarding fetal HPA axis responsiveness (increased or decreased) remains under investigation. Maternal stress and depression are associated with structural and functional changes of brain parts such as hippocampus. In utero stress modifies epigenetically components of the HPA axis which can be transmitted transgenerationally.
Keywords: Exercise; Fetal cortisol; Hypothalamic amenorrhea; Intrauterine growth restriction; Stress.
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