A structure-function analysis of the left ventricle

E.P. Snelling, R.S. Seymour, J.E.F. Green, L.C.R. Meyer, A. Fuller, A. Haw, Duncan Mitchell, A.P. Farrell, M.A. Costello, A. Izwan, M. Badenhorst, Shane Maloney

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    6 Citations (Scopus)


    © 2016 the American Physiological Society.This study presents a structure-function analysis of the mammalian left ventricle and examines the performance of the cardiac capillary network, mitochondria, and myofibrils at rest and during simulated heavy exercise. Left ventricular external mechanical work rate was calculated from cardiac output and systemic mean arterial blood pressure in resting sheep (Ovis aries; n = 4) and goats (Capra hircus; n = 4) under mild sedation, followed by perfusion-fixation of the left ventricle and quantification of the cardiac capillary-tissue geometry and cardiomyocyte ultrastructure. The investigation was then extended to heavy exercise by increasing cardiac work according to published hemodynamics of sheep and goats performing sustained treadmill exercise. Left ventricular work rate averaged 0.017 W/cm3 of tissue at rest and was estimated to increase to ~0.060 W/cm3 during heavy exercise. According to an oxygen transport model we applied to the left ventricular tissue, we predicted that oxygen consumption increases from 195 nmol O2s-1 cm-3 of tissue at rest to ~600 nmol O2s-1 cm3 during heavy exercise, which is within 90% of the oxygen demand rate and consistent with work remaining predominantly aerobic. Mitochondria represent 21-22% of cardiomyocyte volume and consume oxygen at a rate of 1,150 nmol O2s-1 cm-3 of mitochondria at rest and ~3,600 nmol O2s-1 cm-3 during heavy exercise, which is within 80% of maximum in vitro rates and consistent with mitochondria operating near their functional limits. Myofibrils represent 65-66% of cardiomyocyte volume, and according to a Laplacian model of the left ventricular chamber, generate peak fiber tensions in the range of 50 to 70 kPa at rest and during heavy exercise, which is less than maximum tension of isolated cardiac tissue (120-140 kPa) and is explained by an apparent reserve capacity for tension development built into the left ventricle.
    Original languageEnglish
    Pages (from-to)900-909
    Number of pages10
    JournalJournal of Applied Physiology
    Issue number4
    Publication statusPublished - 1 Oct 2016


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