Cardiac muscle, a type of striated muscle, is involuntary. The cells of cardiac muscle are relatively small (10 µm × 100 µm) and are interconnected through strong electrical and mechanical links. These cells form an electrical syncytium, which allows for the rapid spread of action potentials throughout the heart, facilitating synchronized contraction. This synchronization is crucial for the effective pumping action of the heart.

In contrast to skeletal muscle, the contraction of cardiac muscle relies on the interaction between actin and myosin filaments, which is triggered by an influx of extracellular calcium (Ca++). The release of Ca++ from the sarcoplasmic reticulum (SR) is also stimulated by the influx of Ca++ during an action potential, promoting actin-myosin interaction and subsequent contraction.

During relaxation, cardiac muscle cells reaccumulate Ca++ within the SR and extrude Ca++ from the cell through the 3Na+-Ca++ antiporter and the sarcolemmal Ca++ pump. The SR's Ca++ pump is associated with various proteins that form a regulosome, including endogenous micropeptide inhibitors and activators.

The force of contraction in cardiac muscle is augmented by stretch (Frank-Starling Law of the Heart) and sympathetic stimulation. In contrast, skeletal muscle increases force by recruiting more muscle fibers or by achieving tetany.

The heart can undergo hypertrophy in response to factors such as exercise, chronic pressure overload, or genetic mutations. Exercise-induced cardiac hypertrophy is typically beneficial and leads to improved cardiac performance, increased oxygen consumption, and normal relaxation. Conversely, chronic pressure overload can result in cardiac hypertrophy associated with a decreased β-adrenergic response, which may progress to dilated cardiac hypertrophy characterized by reduced contractile ability. Genetic mutations can also lead to cardiac hypertrophy, including familial hypertrophic cardiomyopathy, where a mutation in a single intracellular protein can disrupt contractile function and promote a hypertrophic response. Additionally, a microRNA has been identified that contributes to exercise-induced cardiac hypertrophy and inhibits maladaptive remodeling after ischemia/reperfusion injury.

References:
- Anderson DM, Anderson KM, Chang CL, et al. A micropeptide encoded by a putative long noncoding RNA regulates muscle performance. Cell. 2015;160:595-606.
- Endoh M. Cardiac Ca2+ signaling and Ca2+ sensitizers. Circ J. 2008;72:1915-1925.
- Haghighi K, Bidwell P, Kranias EG. Phospholamban interactome in cardiac contractility and survival: a new vision of an old friend. J Mol Cell Cardiol. 2014;77:160-167.
- Hidalgo C, Granzier H. Tuning the molecular giant titin through phosphorylation: role in health and disease. Trends Cardiovasc Med. 2013;23:165-171.
- Kobirumaki-Shimozawa F, Inoue T, Shintani SA, et al. Cardiac thin filament regulation and the Frank–Starling mechanism. J Physiol Sci. 2014;64:221-232.
- Marks AR. Calcium cycling proteins and heart failure: mechanisms and therapeutics. J Clin Invest. 2013;123(1):46-52.
- Tao L, Bei Y, Zhang H, Xiao J, Li X. Exercise for the heart: signaling pathways. Oncotarget. 2015;6:20773-20784.
- Williams GS, Boyman L, Lederer WJ. Mitochondrial calcium and the regulation of metabolism in the heart. J Mol Cell Cardiol. 2015;78:35-45.
Cardiac muscle is an involuntary, striated muscle. Cardiac muscle cells are relatively small (10 µm × 100 µm) and form an electrical syncytium with tight electrical and mechanical connections between adjacent cardiac muscle cells. Action potentials are initiated in the sinoatrial node and spread quickly throughout the heart to allow synchronous contraction, a feature important for the pumping action of the heart.
2.
Contraction of cardiac muscle involves the Ca++dependent interaction of actin and myosin filaments, as in skeletal muscle. However, unlike skeletal muscle, cardiac muscle requires an influx of extracellular Ca++ . Specifically, the influx of Ca++ during an action potential triggers release of Ca++ from the SR, which then promotes actin-myosin interaction and contraction.
3.
Relaxation of cardiac muscle involves reaccumulation of Ca++ by the SR and extrusion of Ca++ from the cell via the 3Na+-Ca++ antiporter and the sarcolemmal Ca++ pump. The Ca++ pump of the SR is associated with numerous proteins (forming a regulosome), including some endogenous micropeptide inhibitors and activators.
4.
The force of contraction of cardiac muscle is increased by stretch (Frank-Starling Law of the Heart) and by sympathetic stimulation. Skeletal muscle, in contrast, increases force by recruiting more muscle fibers or by tetany.
5.
Hypertrophy of the heart can occur in response to exercise, chronic pressure overload, or genetic mutations. The cardiac hypertrophy resulting from exercise is typically beneficial, with improved cardiac performance, increased oxygen consumption, and normal relaxation. Chronic pressure overload, on the other hand, can result in cardiac hypertrophy that is initially associated with a decreased β-adrenergic response but may progress to dilated cardiac hypertrophy, characterized by decreased contractile ability. Genetic mutations resulting in cardiac hypertrophy include familial hypertrophic
Anderson DM, Anderson KM, Chang CL, et al. A micropeptide encoded by a putative long noncoding RNA regulates muscle performance. Cell. 2015;160:595-606.
Endoh M. Cardiac Ca2+ signaling and Ca2+ sensitizers. Circ J. 2008;72:1915-1925.
Haghighi K, Bidwell P, Kranias EG. Phospholamban interactome in cardiac contractility and survival: a new vision of an old friend. J Mol Cell Cardiol. 2014;77:160-167.
Hidalgo C, Granzier H. Tuning the molecular giant titin through phosphorylation: role in health and disease. Trends Cardiovasc Med. 2013;23:165-171.
cardiomyopathy, in which a mutation in a single intracellular protein may alter contractile function and promote a hypertrophic response. Researchers have identified a microRNA that appears to contribute to the exercise-induced hypertrophy of the heart and to inhibit maladaptide remodeling after ischemia/reperfusion injury.
Kobirumaki-Shimozawa F, Inoue T, Shintani SA, et al. Cardiac thin filament regulation and the Frank–Starling mechanism. J Physiol Sci. 2014;64:221-232.
Marks AR. Calcium cycling proteins and heart failure: mechanisms and therapeutics. J Clin Invest. 2013;123(1):46-52.
Tao L, Bei Y, Zhang H, Xiao J, Li X. Exercise for the heart: signaling pathways. Oncotarget. 2015;6:20773-20784.
Williams GS, Boyman L, Lederer WJ. Mitochondrial calcium and the regulation of metabolism in the heart. J Mol Cell Cardiol. 2015;78:35-45.