Respiratory plasticity: differential actions of continuous and episodic hypoxia and hypercapnia

Respir Physiol. 2001 Dec;129(1-2):25-35. doi: 10.1016/s0034-5687(01)00280-8.


The objectives of this paper are: (1) to review advances in our understanding of the mechanisms of respiratory plasticity elicited by episodic versus continuous hypoxia in short to intermediate time domains (min to h); and (2) to present new data suggesting that different patterns of hypercapnia also elicit distinct forms of respiratory plasticity. Episodic, but not continuous hypoxia elicits long-term facilitation (LTF) of respiratory motor output. Phrenic LTF is a serotonin-dependent central neural mechanism that requires: (a) activation of spinal serotonin receptors; and (b) spinal protein synthesis. Continuous and episodic hypercapnia also elicit different mechanisms of plasticity. Continuous, severe hypercapnia (25 min of approximately 10% inspired CO(2)) elicits long-term depression (LTD) of phrenic motor output (-33+/-8% at 60 min post-hypercapnia) in anesthetized rats. In contrast, 3,5 min hypercapnic episodes do not elicit LTD (9+/-17% at 60 min). We hypothesize that the response of respiratory motoneurons to serotonergic and noradrenergic modulation may contribute to pattern sensitivity to hypoxia and hypercapnia.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Chemoreceptor Cells / physiopathology
  • Humans
  • Hypercapnia / physiopathology*
  • Hypoxia / physiopathology*
  • Motor Neurons / physiology
  • Neuronal Plasticity*
  • Respiratory System / innervation*