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Acute intermittent hypercapnic hypoxia augments left ventricular contractility.

Scott F Thrall1, Alex M Williams2,3, Philip J Millar4

  • 1Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Kelowna, BC, Canada.

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Summary

Acute intermittent hypercapnic hypoxia (IHH) enhances cardiac contractility and left ventricular systolic function in healthy individuals. This improved heart function contributes to the blood pressure increase alongside established vascular effects.

Keywords:
acute intermittent hypoxiablood pressurecardiac contractilitylower‐body negative pressuresympathetic long‐term facilitation

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Area of Science:

  • Cardiovascular Physiology
  • Human Physiology
  • Respiratory Physiology

Background:

  • Acute intermittent hypercapnic hypoxia (IHH) is known to cause sustained increases in sympathetic activity and blood pressure.
  • The contribution of myocardial contractility to this pressor response following acute IHH remains unclear.

Purpose of the Study:

  • To investigate whether acute IHH augments left ventricular systolic function.
  • To determine if enhanced cardiac contractility contributes to the pressor response induced by IHH.

Main Methods:

  • Twenty-four healthy participants underwent repeated bouts of hypercapnic hypoxia and normocapnic normoxia.
  • Cardiac, hemodynamic, respiratory, and sympathetic measurements were taken at rest and during progressive lower body negative pressure (LBNP) before and after IHH.
  • Analysis included stroke work, ejection fraction, longitudinal strain, and end-systolic elastance.

Main Results:

  • Following IHH, stroke work, longitudinal strain, and preload-recruitable stroke work (PRSWsb) were significantly enhanced at rest.
  • During LBNP, IHH further improved ejection fraction, stroke work, longitudinal strain, end-systolic elastance, and PRSWsb.
  • Ventricular stiffness and diastolic relaxation were unaltered, but the passive/active diastolic filling ratio decreased.

Conclusions:

  • Acute IHH demonstrably increases left ventricular systolic function in humans.
  • Enhanced cardiac contractility is a significant contributor to the pressor response following IHH, complementing the known vasopressor effects.
  • These findings suggest that acute IHH impacts cardiac performance beyond just sympathetic nervous system activation.