Myocardial metabolism and the neural control of coronary vessels
- Concept
- For completeness
The heart runs mostly on fat and needs oxygen every beat. Without it, energy runs out in minutes and recovery takes longer than the blockage.
Also called: Cardiac energy metabolism, Stunning and hibernation
See it in 3D: LAD (anterior descending artery) · Right coronary artery · Coronary sinus
What it is
The resting heart takes most of its energy from fatty acids, with glucose and lactate filling the rest, and it has very little anaerobic reserve. In ischemia it shifts to glycolysis, lactate builds up and ATP is broken down to adenosine, which dilates vessels but leaves the cell. Nerves act on coronary vessels directly (α constriction, β dilation) and indirectly through changes in cardiac work, and the indirect effect usually wins.
How it works, step by step
- The heart extracts ≈ 70–80% of O₂ from coronary blood at rest, so more demand must be met by more flow.
- In ischemia oxidative phosphorylation stops; glycolysis continues briefly and lactate and H⁺ rise.
- ATP falls to ADP and AMP, and AMP is converted to adenosine, which dilates arterioles and can cause pain.
- Adenosine and other purines diffuse into the blood, so the cell loses its adenine nucleotide pool.
- After reperfusion, ATP stays low for a long time, and calcium overload and free radicals depress contraction (stunning).
- Sympathetic drive raises O₂ use, and the local metabolic dilation it causes outweighs direct α-mediated constriction.
Regulation
- +Metabolic factors (adenosine, low O₂, K⁺, H⁺, CO₂, NO): Main controller: dilate coronary arterioles in proportion to cardiac work.
- −Sympathetic α-receptors (epicardial vessels): Direct constriction; may contribute to vasospasm.
- +Sympathetic β₂-receptors (intramuscular arterioles): Direct dilation.
- +Vagal stimulation: Slight direct dilation, outweighed by less cardiac work (flow falls overall).
Clinical notes
- Myocardial infarction: irreversible injury starts after ≈ 20–40 min of complete ischemia, earliest in the subendocardium.
- Vasospastic angina: transient spasm of an epicardial coronary artery, typically at rest.
- Beta blockers lower O₂ demand (rate, contractility); nitrates lower preload and dilate epicardial coronaries; some anti-anginal agents shift fuel use toward glucose.
Test yourself
Think of the answer, then tap the question to see it.
What is the main fuel of the resting heart?
Fatty acids (≈ 70% of its energy), oxidized in mitochondria; glucose and lactate supply most of the rest.
Why does myocardial ATP stay low for a long time after a brief ischemic episode?
ATP is broken down to adenosine, which leaves the cell; new adenine nucleotides must be made again, which is slow.
Why does sympathetic stimulation increase coronary flow despite α-receptor constriction?
It increases heart rate and contractility, so metabolic vasodilators rise; their dilation outweighs the direct α-constriction.
How does hibernating myocardium differ from stunned myocardium?
Hibernating muscle has chronically reduced flow and reduced contraction that improve when flow is restored; stunned muscle has normal flow restored after ischemia but contraction recovers slowly.
Connections
See it in 3D3
The structures of Durgical's 3D anatomy where it happens.
In Biochemistry4
In Pharmacology2
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: Myocardial Infarction (StatPearls (NCBI Bookshelf), 2024); Stable Angina (StatPearls (NCBI Bookshelf), 2024); Anatomy, Thorax, Heart Left Anterior Descending (LAD) Artery (StatPearls (NCBI Bookshelf), 2026).
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Representative model, for educational purposes only.