Myocardial Metabolism
Myocardial Metabolism - Related Videos
07:45
Acute Myocardial Infarction in Rats
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Cited by 110 •
2011
The rat model of acute myocardial infarction (AMI) is useful to study the consequence of a MI on cardiac pathophysiological and physiological function.
05:41
Metabolic Profile Analysis of Zebrafish Embryos
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Cited by 42 •
2013
Zebrafish represent a powerful vertebrate model that has been under-utilised for metabolic studies. Here we describe a rapid way to measure the in vivo metabolic profile of developing zebrafish that allows the comparison of different mitochondrial function parameters between genetically or pharmacologically manipulated embryos, thereby increasing the applicability of this organism.
08:23
LAD-Ligation: A Murine Model of Myocardial Infarction
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Cited by 87 •
2009
This video demonstrates how to use a fast and reliable model to study pathobiological and pathophysiological processes of myocardial ischemia.
10:19
An Introduction to Cell Metabolism
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2023
In cells, critical molecules are either built by joining together individual units like amino acids or nucleotides, or broken down into smaller components. Respectively, the reactions responsible for this are referred to as anabolic and catabolic. These reactions require or produce energy typically in the form of a “high-energy” molecule called ATP. Together, these processes make up “Cell Metabolism,” and are hallmarks of healthy, living cells.JoVE’s introduction to cell metabolism briefly...
09:45
Histological Quantification of Chronic Myocardial Infarct in Rats
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Cited by 13 •
2016
The post-mortem assessment of myocardial infarction (MI) in rodents is based on quantification of the infarct on stained heart sections. We describe an accurate method to quantify the infarct size using systematic sampling of harvested rat hearts from base to apex and image analyses of trichrome-stained histological sections.
FAQs
Cardiac muscle adjusts its energy strategy as oxygen supply and workload change. With adequate oxygen, mitochondrial oxidative phosphorylation supports efficient ATP production for sustained contraction, relaxation, and cellular maintenance. When oxygen becomes limited, metabolism shifts toward less efficient anaerobic pathways, helping explain why ischemic conditions can disrupt cardiac energy balance and function.
The heart can use fatty acids, glucose, lactate, and other substrates to support ATP production. This flexibility allows energy generation to respond to changing physiological conditions rather than relying on one fuel source. Comparing which substrates are used under different conditions helps researchers examine how cardiac energetics adapt to workload, oxygen availability, and disease.
Hormonal signals help regulate how cardiomyocytes manage available energy substrates and respond to changing demands. Their effects occur alongside oxygen availability and workload, influencing the balance among fatty acid, glucose, lactate, and other fuel use. Studying these signals provides a mechanistic link between systemic metabolic regulation and cardiac cellular function.
Exercise and ischemia impose different metabolic conditions on the heart. Exercise changes cardiac workload and therefore alters energy requirements, while ischemia reduces oxygen availability and promotes a shift toward less efficient anaerobic pathways. Comparing these states helps clarify how the myocardium preserves contraction when demand rises or when oxidative energy production is constrained.
Heart failure research uses myocardial metabolism to investigate how impaired cardiac energetics may contribute to reduced performance. Examining ATP-generating pathways, substrate use, oxygen dependence, and responses to hormonal signals can reveal metabolic changes associated with the failing heart. This perspective supports investigation of mechanisms rather than focusing only on the resulting clinical dysfunction.
Metabolic changes provide information about how cardiac muscle responds to exercise, ischemia, and metabolic disease. Researchers can use this biological context to identify mechanisms linked to abnormal cardiac energetics and heart failure. Such knowledge may guide diagnostic strategies and help evaluate therapeutic approaches designed to address altered energy production or substrate use.