Heat acclimation-induced elevated glycogen, glycolysis, and low thyroxine improve heart ischemic tolerance

Mirit Eynan, Tanya Knubuvetz, Uri Meiri, Gil Navon, Gary Gerstenblith, Zohar Bromberg, Yonathan Hasin, Michal Horowitz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Based on our observations of energy sparing in heat-acclimated (AC) rat hearts, we investigated whether changes in preischemic glycogen level, glycolytic rate, and plasma thyroxine level mediate cardioprotection induced in these hearts during ischemia-reperfusion insults. Control (C) (24°C), AC (34°C, 30 days), acclimated-euthyroid (34°C + 3 ng/ml L-thyroxine), and control hypothyroid (24°C + 0.02% 6-n-propyl-2-thiouracil) groups were studied. Preischemic glycogen was higher in AC than in C hearts [39.0 ± 8.5 vs. 19.2 ± 4.2 (SE) μmol glucose/g wet wt; P < 0.0006], and the lactate produced vs. glycogen level during total ischemia (13C-NMR spectroscopy) was markedly slower (AC: -0.82x, r = 0.98 vs. C: -4.7x, r = 0.9). Time to onset of ischemic contracture was lengthened, and the fraction of hearts experiencing ischemic contracture was lowered. Pulse pressure recovery was improved in AC compared with C animals before, but not after, absolute sodium iodoacetate-induced glycolysis inhibition. Acclimated-euthyroid hearts exhibited decreased ischemic tolerance, whereas induced hypothyroidism in C improved cardiotolerance. Thus higher preischemic glycogen and slowed glycolysis are associated with hypothyroidism and are likely important mediators of the improved ischemic tolerance exhibited by AC hearts.

Original languageEnglish
Pages (from-to)2095-2104
Number of pages10
JournalJournal of Applied Physiology
Issue number6
StatePublished - Dec 2002


  • Glycolytic flux
  • Hypothyroidism
  • Ischemia
  • Rat
  • [C]glucose nuclear magnetic resonance spectroscopy


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