Athena Vale
The human heart is a powerful organ, beating about 100,000 times a day. With so much activity, why doesn't it tire like other muscles in the body? The heart is made of cardiac muscle, which has distinct features that allow it to contract in a coordinated fashion and resist fatigue. This unique property of the cardiac muscle is due to its composition of special cells called cardiomyocytes, which have a high density of mitochondria—the energy powerhouse of the cell. This high density of mitochondria results in a skyrocketed energy output, making the cardiac muscle highly resistant to fatigue.
| Characteristics | Values |
|---|---|
| Cardiac muscle fatigue | Rare |
| Reason | High density of mitochondria |
| Metabolically flexible | |
| Well vascularized | |
| High oxygen extraction | |
| High aerobic respiration | |
| Active relaxation process | |
| Distinct structure | |
| Cardiac muscle fatigue causes | Sarcoplasmic reticulum failure |
| Reduction in Ca-transport activity |
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What You'll Learn
Cardiac muscle is resistant to fatigue
The cardiac muscle, or myocardium, is the thick middle layer of the heart. It is one of three types of muscle in the body, the other two being skeletal and smooth muscle. The myocardium is surrounded by a thin outer layer called the epicardium (or visceral pericardium) and an inner endocardium.
Cardiac muscle has distinct features that allow it to contract in a coordinated fashion and resist fatigue. The individual cardiac muscle cell (cardiomyocyte) is a tubular structure composed of chains of myofibrils, which are rod-like units within the cell. The myofibrils consist of repeating sections of sarcomeres, which are the fundamental contractile units of the muscle cells. Sarcomeres are composed of long proteins that organize into thick and thin filaments, called myofilaments. Thin myofilaments contain the protein actin, and thick myofilaments contain the protein myosin. The myofilaments slide past each other as the muscle contracts and relaxes.
The cardiac muscle does not relax and prepare for the next heartbeat simply by ceasing contraction; it occurs in an active process called Lusitropy. During lusitropy, Sarco/endoplasmic reticulum Ca-ATPase (SERCA) pumps on the membrane of the sarcoplasmic reticulum use ATP hydrolysis to transfer calcium back into the sarcoplasmic reticulum (SR) from the cytosol. The regulatory protein phospholamban can control the rate at which the SERCA pumps calcium into the SR.
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Cardiomyocytes have a high density of mitochondria
The heart is a powerful organ that beats about 100,000 times every day. Each heartbeat involves the force needed to pump blood around the body, which is comparable to the energy needed to squeeze a tennis ball. Unlike other muscle cells in the body, cardiomyocytes are highly resistant to fatigue. This is because they have a high density of mitochondria, which are the energy houses of the cell. Cardiomyocytes have up to 10 times the density of mitochondria compared to other muscle cells, which gives them a much higher energy output.
Mitochondria are central to the maturation of cardiomyocytes. They respond to metabolic changes and transition from small, fragmented mitochondria to large organelles capable of producing enough ATP to support the contractile function of the heart. This maturation process is likely not just a response to overall cardiomyocyte maturation but may instead be a mediator of the molecular processes triggering maturation.
Cardiomyocytes are the individual cells that make up the cardiac muscle, also known as the myocardium. The primary function of cardiomyocytes is to contract, generating the pressure needed to pump blood through the circulatory system. The outside of the cardiomyocyte is surrounded by a plasma membrane called the sarcolemma, which acts as a barrier between extracellular and intracellular contents. Invaginations of the sarcolemma into the cytoplasm of the cardiomyocyte are called T-tubules, and they contain numerous proteins that allow for the exchange of ions with extracellular fluid surrounding the cell.
Cardiac muscle fatigue can be induced by excessive stimulation, hypersensitive excitation-contraction coupling, or diminished performance capacity. This fatigue is correlated with sarcoplasmic reticulum failure, which is associated with impaired sarcoplasmic reticulum Ca-transport activity.
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Cardiomyocytes are well-vascularised and good at extracting oxygen
The cardiac muscle, or myocardium, is the thick middle layer of the heart. It is surrounded by a thin outer layer called the epicardium (or visceral pericardium) and an inner endocardium. Cardiomyocytes are the individual cells that make up the cardiac muscle. They are tubular structures composed of chains of myofibrils, which are rod-like units within the cell.
Cardiomyocytes are well-vascularised and excel at extracting oxygen. This is crucial as the primary function of cardiomyocytes is to contract, generating the pressure required to pump blood through the circulatory system. To accomplish this, the cardiac muscle has distinct features that allow it to contract in a coordinated fashion and resist fatigue. The heart beats about 100,000 times a day, exerting the force to squeeze a tennis ball each time. Unlike skeletal muscles, the heart rarely tires due to its composition of cardiomyocytes, which are highly resistant to fatigue.
Cardiomyocytes are surrounded by a plasma membrane called the sarcolemma, which acts as a barrier between extracellular and intracellular contents. Invaginations of the sarcolemma, called T-tubules, contain proteins that facilitate ion exchange with the extracellular fluid surrounding the cell. The T-tubules run adjacent to enlarged areas of the sarcoplasmic reticulum, which stores and releases calcium ions to facilitate muscle contraction and relaxation. This process is known as Lusitropy and is essential for the heart's continuous pumping action.
The availability of oxygen is critical for cardiomyocyte survival and energy demands. During normal heart function, over 95% of ATP regeneration in cardiomyocytes comes from oxidative phosphorylation in the mitochondria. However, when oxygen supply is low, as in ischemia, β-oxidation of fatty acids slows, and anaerobic glycolysis increases. This reduced oxygen availability can lead to ischemia/reperfusion injury, causing significant heart damage.
In summary, cardiomyocytes are well-vascularised and efficient at extracting oxygen to meet their high-energy demands. Their dense mitochondrial network and specialised structure enable them to resist fatigue and maintain the heart's continuous pumping action, making them uniquely suited for their vital role in the cardiovascular system.
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The heart is metabolically flexible
The heart is an incredibly powerful organ, beating about 100,000 times every day. Each heartbeat requires a force similar to that needed to squeeze a tennis ball. This force is generated by the contraction of the cardiac muscle, which is made up of special cells called cardiomyocytes. These cells are highly resistant to fatigue.
Cardiomyocytes are similar to other muscle cells in that they are primarily powered by mitochondria, the energy house of the cell. However, cardiomyocytes have up to 10 times the density of mitochondria, giving them a much higher energy output. This high energy output is necessary to meet the heart's very high energy demand. The heart must continuously produce large amounts of ATP to sustain its contractile function. If not replaced, the heart's ATP stores would be depleted in just 2 to 10 seconds, resulting in contractile failure.
The heart achieves this continuous production of ATP by metabolizing a variety of fuels, including fatty acids, glucose, lactate, ketones, pyruvate, and amino acids. This process, known as mitochondrial oxidative phosphorylation, requires a large amount of oxygen. The heart consumes more oxygen per unit weight than any other organ in the body. The heart's ability to readily shift between different energy substrates to maintain ATP production is known as metabolic flexibility.
Metabolic flexibility is driven by cellular and organelle processes, particularly in the mitochondria. It is regulated by peroxisome proliferator-activated receptors (PPARs) and estrogen-related receptors (ERRs), which control the transcription of genes involved in fuel metabolism in the heart. Metabolic flexibility is also influenced by substrate availability and uptake, which can be disrupted by conditions such as obesity and diabetes.
In summary, the heart is metabolically flexible due to its ability to efficiently utilize various energy substrates to meet its high energy demands. This flexibility is regulated by complex cellular processes and influenced by external factors such as fuel availability and metabolic disorders.
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Sarcoplasmic reticulum failure and cardiac muscle fatigue
The cardiac muscle, or myocardium, is an incredibly powerful organ, beating about 100,000 times a day. Unlike skeletal muscles, the heart rarely tires due to its composition of special cells called cardiomyocytes, which are highly resistant to fatigue. Cardiomyocytes are the individual cells that make up the cardiac muscle, and their primary function is to contract, generating the pressure needed to pump blood through the circulatory system.
The cardiomyocyte is a tubular structure composed of chains of myofibrils, which consist of repeating sections of sarcomeres, the fundamental contractile units of the muscle cells. The sarcomeres are composed of long proteins that organize into thick and thin filaments, called myofilaments, which slide past each other as the muscle contracts and relaxes. This process is activated by the release of calcium from the sarcoplasmic reticulum (SR) when delivering an action potential to the muscle, in a process called excitation-contraction coupling.
The SR is the major organelle in muscle responsible for the regulation of intracellular free calcium ([Ca2+]f) concentration, which is essential for muscle contraction. However, studies have shown that SR function, both Ca2+ release and uptake, is impaired following fatiguing contractile activity. This impairment in SR Ca2+-transport activity is associated with the development of muscle fatigue due to exhaustive exercise or relative functional overload.
Furthermore, the role of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) is crucial in normal muscle function, fatigue, and disease. SERCA pumps on the membrane of the SR use ATP hydrolysis to transfer calcium back into the SR from the cytosol during the active process of Lusitropy, which allows the cardiac muscle to relax and prepare for the next heartbeat. Impairment of SERCA function can contribute to sarcoplasmic reticulum failure and subsequent cardiac muscle fatigue.
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Frequently asked questions
No, cardiac muscles are resistant to fatigue.
The cardiac muscle is made of special cells called cardiomyocytes, which have a high density of mitochondria (the energy house of the cell). This gives them a much higher energy output and makes them incredibly good at extracting oxygen for aerobic respiration.
The relaxation of the cardiac muscle occurs through an active process called Lusitropy. During Lusitropy, the Sarco/endoplasmic reticulum Ca-ATPase (SERCA) pumps on the membrane of the sarcoplasmic reticulum use ATP hydrolysis to transfer calcium back into the sarcoplasmic reticulum from the cytosol.
