A structure-function analysis of the left ventricle.
Edward P SnellingRoger S SeymourJ Edward F GreenLeith C R MeyerAndrea FullerAnna HawDuncan MitchellAnthony P FarrellMary-Ann CostelloAdian IzwanMargaret BadenhorstShane K MaloneyPublished in: Journal of applied physiology (Bethesda, Md. : 1985) (2016)
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 O2·s-1·cm-3 of tissue at rest to ∼600 nmol O2·s-1·cm-3 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 O2·s-1·cm-3 of mitochondria at rest and ∼3,600 nmol O2·s-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.
Keyphrases
- left ventricular
- high intensity
- mitral valve
- physical activity
- hypertrophic cardiomyopathy
- heart failure
- acute myocardial infarction
- blood pressure
- resistance training
- cardiac resynchronization therapy
- pulmonary hypertension
- cell death
- aortic stenosis
- left atrial
- coronary artery disease
- randomized controlled trial
- congenital heart disease
- metabolic syndrome
- intensive care unit
- systematic review
- minimally invasive
- adipose tissue
- hypertensive patients
- endoplasmic reticulum
- weight loss