Fasting improves tolerance to acute hypoxia in rats

Biochem Biophys Res Commun. 2021 Sep 10:569:161-166. doi: 10.1016/j.bbrc.2021.06.099. Epub 2021 Jul 9.

Abstract

Acute high-altitude illness seriously threatens the health and lives of people who rapidly ascend to high altitudes, but there is currently no particularly effective method for the prevention or treatment of acute high-altitude illness. In the present study, we found that fasting preconditioning effectively improved the survival rate of rats exposed to a simulated altitude of 7620 m for 24 h, and a novel animal model of rapid adaptation to acute hypoxia was established. Compared with control treatment, fasting preconditioning activated AMPK, induced autophagy, decreased ROS levels, and inhibited NF-κB signaling in the cardiac tissues of rats. Our results suggested that fasting effectively improved the acute hypoxia tolerance of rats, which was gradually enhanced with prolongation of fasting. In addition, the acute hypoxia tolerance of young rats was significantly higher than that of adult rats. These experimental results lay the foundation for achieving rapid adaptation to acute hypoxia in humans.

Keywords: AMPK; Acute high-altitude hypoxia; Autophagy; Fasting; NF-κB.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Adaptation, Physiological / physiology*
  • Age Factors
  • Aging / physiology*
  • Animals
  • Autophagy
  • Blotting, Western
  • Fasting / physiology*
  • Hypoxia / physiopathology*
  • Kaplan-Meier Estimate
  • Male
  • Membrane Proteins / metabolism
  • Microscopy, Electron, Transmission
  • Mitochondrial Proteins / metabolism
  • Myocardium / cytology
  • Myocardium / metabolism
  • Myocardium / ultrastructure
  • NF-kappa B / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / metabolism
  • Signal Transduction

Substances

  • BNIP3 protein, rat
  • Membrane Proteins
  • Mitochondrial Proteins
  • NF-kappa B
  • Reactive Oxygen Species
  • AMP-Activated Protein Kinases