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Ischemic preconditioning reduces hemodynamic response during metaboreflex activation.

Gabriele Mulliri1, Gianmarco Sainas1, Sara Magnani1

  • 1Department of Medical Sciences, Sports Physiology Laboratory, University of Cagliari, Cagliari, Italy.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|March 4, 2016
PubMed
Summary

Ischemic preconditioning (IP) reduces blood pressure responses during exercise by impairing venous return, potentially due to increased nitric oxide. This finding offers insight into exercise performance and fatigue mechanisms.

Keywords:
blood pressurecardiac preloadfatiguemyocardial contractilitystroke volume

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Area of Science:

  • Exercise Physiology
  • Cardiovascular Regulation
  • Metaboreflex

Background:

  • Ischemic preconditioning (IP) improves exercise performance and delays fatigue.
  • The exact mechanisms of IP are not fully understood.
  • IP may reduce fatigue by modulating nerve endings involved in the metaboreflex and hemodynamics.

Purpose of the Study:

  • To investigate the hypothesis that IP reduces the blood pressure response during the exercise metaboreflex.
  • To elucidate the hemodynamic mechanisms underlying IP's effects on exercise performance.

Main Methods:

  • Fourteen healthy males underwent randomized postexercise muscle ischemia (PEMI) and IP-PEMI tests.
  • The metaboreflex was elicited via dynamic handgrip exercise.
  • Hemodynamics were assessed using echocardiography and impedance cardiography.

Main Results:

  • IP significantly reduced the mean arterial pressure response during the metaboreflex compared to PEMI alone.
  • This reduction was linked to impaired venous return and stroke volume augmentation following IP.
  • Hemodynamic changes suggest IP hinders the capacity to increase venous return and cardiac preload.

Conclusions:

  • IP impacts hemodynamics during the metaboreflex primarily by impairing venous return and cardiac preload reserve.
  • This effect is hypothesized to result from increased nitric oxide production, reducing venous capacity vessel constriction.