Cited by 195Cardiac Ischemia and ReperfusionCardiovascular and exercise physiologyHeat shock proteins research

Short-term exercise improves myocardial tolerance to in vivo ischemia-reperfusion in the rat

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Demirel, Haydar A., Powers, Scott K., Zergeroglu, Murat A., Shanely, R. Andrew, Hamilton, Karyn, Coombes, Jeff, Naito, Hisashi·2001·Journal of Applied Physiology

Abstract

These experiments examined the independent effects of short-term exercise and heat stress on myocardial responses during in vivo ischemia-reperfusion (I/R). Female Sprague-Dawley rats (4 mo old) were randomly assigned to one of four experimental groups: 1) control, 2) 3 consecutive days of treadmill exercise [60 min/day at 60-70% maximal O2 uptake (VO2 max)], 3) 5 consecutive days of treadmill exercise (60 min/day at 60-70% VO2 max), and 4) whole body heat stress (15 min at 42 degrees C). Twenty-four hours after heat stress or exercise, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was maintained for 30-min followed by a 30-min period of reperfusion. Compared with control, both heat-stressed animals and exercised animals (3 and 5 days) maintained higher (P < 0.05) left ventricular developed pressure (LVDP), maximum rate of left ventricular pressure development (+dP/dt), and maximum rate of left ventricular pressure decline (-dP/dt) at all measurement periods during both ischemia and reperfusion. No differences existed between heat-stressed and exercise groups in LVDP, +dP/dt, and -dP/dt at any time during ischemia or reperfusion. Both heat stress and exercise resulted in an increase (P < 0.05) in the relative levels of left ventricular heat shock protein 72 (HSP72). Furthermore, exercise (3 and 5 days) increased (P < 0.05) myocardial glutathione levels and manganese superoxide dismutase activity. These data indicate that 3-5 consecutive days of exercise improves myocardial contractile performance during in vivo I/R and that this exercise-induced myocardial protection is associated with an increase in both myocardial HSP72 and cardiac antioxidant defenses.

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Crossref · 10.1152/jappl.2001.91.5.2205

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Authors
Demirel, H. A., Powers, S. K., Zergeroglu, M. A., Shanely, R. A., Hamilton, K., Coombes, J., & Naito, H.
Affiliations
  • University of Florida (US)
  • Department of Exercise and Sport Sciences and Physiology and the Center for Exercise Science, University of Florida, Gainesville, Florida 32611
Venue
Journal of Applied Physiology
Published
2001-11-01
Volume
91
Issue
5
Pages
2205-2212
ISSN
  • 0161-7567 (ISSN-L)
  • 8750-7587
  • 1522-1601
OpenAlex
W2169002616
Cited by
195
References
38
Citations by year
2026: 3 · 2025: 1 · 2024: 3 · 2023: 5 · 2022: 4 · 2021: 9 · 2020: 2 · 2019: 3 · 2018: 8 · 2017: 14 · 2016: 5 · 2015: 19 · 2014: 8 · 2013: 12 · 2012: 14
FWCI
3.09
Type
journal article
Language
en
Open access
Locations
  • Journal of Applied Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • Figshare (submittedVersion)
  • Appalachian State University
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
Keywords
exercise training, myocardial ischemia-reperfusion injury, heat stress, cardiac contractility, HSP72, glutathione, manganese superoxide dismutase, antioxidant defense, cardioprotection, coronary artery occlusion, left ventricular pressure
MeSH terms
Animals, Antioxidants, Blood Pressure, Coronary Vessels, Physical Exertion, Female, Heart, Hot Temperature, Heat-Shock Proteins, Myocardium, Physical Conditioning, Animal, Stress, Psychological, Myocardial Reperfusion Injury, Rats, Sprague-Dawley, Ventricular Dysfunction, Left, HSP72 Heat-Shock Proteins, Rats

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