Physiology of Onset of Labour
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Direct answer
Onset of labour is the coordinated shift from uterine quiescence to active contractions, driven mainly by prostaglandins, changes in the oestrogen to progesterone balance and rising myometrial responsiveness. A fetal hypothalamic-pituitary-adrenal signal, acting partly through placental corticotrophin-releasing hormone, is thought to increase prostaglandin production and prepare the cervix for ripening. True labour is defined by regular contractions that progressively change the cervix.
What you must remember
- Quiescence: progesterone keeps the uterus in a quiet state for most of pregnancy.
- Functional progesterone withdrawal: circulating progesterone stays high, but its effect on the myometrium is thought to fall, possibly through changing receptor isoforms.
- Fetal signal: rising fetal cortisol is thought to raise placental corticotrophin-releasing hormone; the sheep model of a cortisol-driven oestrogen shift is not proven in humans.
- Prostaglandins: PGE2 and PGF2-alpha from decidua and membranes ripen the cervix and stimulate contractions.
- Cervical ripening: collagen breakdown, hydration and leucocyte infiltration soften and efface the cervix.
- Myometrial activation: oxytocin receptors increase and gap junctions such as connexin 43 form, so contractions become coordinated.
- Braxton Hicks: irregular, non-progressive contractions that do not dilate the cervix.
- Oxytocin role: mainly sustains and augments labour, while prostaglandins are central to initiation and ripening.
The sequence from fetal signal to contractions
Labour onset is best learnt as a chain in which each step makes the next more likely. The steps overlap in time, so the sequence is a conceptual model rather than a strict timetable.
- Fetal signal: The fetal hypothalamic-pituitary-adrenal axis matures, and rising cortisol stimulates placental corticotrophin-releasing hormone. Fetal maturity signals are considered a key trigger in many models, although the sheep model of a cortisol-driven oestrogen rise is not established in humans.
- Placental endocrine shift: Corticotrophin-releasing hormone rises in the placenta, promoting prostaglandin synthesis in the decidua and membranes.
- Functional progesterone withdrawal: A higher oestrogen to progesterone ratio, along with altered progesterone receptor isoforms, is thought to reduce the quiescent effect on the myometrium.
- Prostaglandin and cytokine surge: Prostaglandins and inflammatory mediators are produced in the decidua, membranes and cervix, driving the changes that precede labour. Inflammatory cytokines also rise, which is one reason infection can trigger preterm labour.
- Cervical ripening: Collagen remodelling, hyaluronan change and leucocyte infiltration soften and efface the cervix before dilatation begins.
- Myometrial activation: Oxytocin receptors increase and gap junctions form, so contractions become coordinated, regular and effective.
Viva angles on labour onset
Physiology questions reward distinguishing initiation from maintenance and true labour from false labour.
- Trap: Crediting oxytocin with starting labour Correct: oxytocin mainly sustains and augments contractions, while prostaglandins are central to initiation and ripening.
- Trap: Assuming progesterone levels fall sharply at term Correct: circulating levels do not fall sharply, and the change is in its functional effect on the myometrium.
- Trap: Equating Braxton Hicks contractions with true labour Correct: true labour brings regular contractions with progressive cervical change, while Braxton Hicks do not.
- Trap: Attributing cervical ripening to uterine contractions Correct: ripening precedes effective contractions and depends on prostaglandins and inflammatory change.
Frequently asked questions
Why is progesterone withdrawal considered in the onset of labour?
Progesterone maintains uterine quiescence, and at term its effect on the myometrium is thought to fall even though circulating levels remain high. Changes in progesterone receptor isoforms are proposed as the mechanism, which is why the process is called functional withdrawal.
What role do prostaglandins play in the onset of labour?
Prostaglandins PGE2 and PGF2-alpha, released by the decidua and fetal membranes, drive cervical ripening and stimulate uterine contractions. Their effect is the basis of prostaglandin agents used for labour induction.
How do Braxton Hicks contractions differ from true labour?
Braxton Hicks contractions are irregular, usually painless or mild, and do not cause cervical dilatation or effacement. True labour contractions are regular, increase in strength and frequency, and produce progressive change in the cervix.
What starts the fetal signal for labour?
The fetal signal is thought to come from maturation of the fetal hypothalamic-pituitary-adrenal axis, which raises cortisol and stimulates placental corticotrophin-releasing hormone. This is thought to promote prostaglandin synthesis and a higher oestrogen to progesterone effect, though human evidence is incomplete.