The phosphocreatine overshoot occurs independent of myocardial work

L. J. Kaplan, C. F. Bellows, S. Carter, H. Blum, G. J.R. Whitman

Research output: Contribution to journalArticlepeer-review


Although the exact mechanism(s) responsible for the phosphocreatine/ATP overshoot have not been completely elucidated, our data demonstrate that the overshoot does not stem from reduced myocardial work, and consequently, reduced utilization of phosphocreatine (PCr). Additionally, we highlight a basic difference in the physiologic responses of skeletal and cardial muscle to work demands. By understanding the bioenergetic derangements which accompany reperfusion injury, one may hope to better salvage post-ischemic myocardium.

Original languageEnglish (US)
Pages (from-to)245-248
Number of pages4
Issue number4
StatePublished - 1995
Externally publishedYes


  • myocardial work
  • phosphocreatine overshoot
  • post-ischemic myocardium

ASJC Scopus subject areas

  • Biochemistry


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