Title: Functional differences between cardiac and skeletal muscle

 

Key words: cardiac muscle, skeletal muscle, myosin, oxidative pathways, glucose oxidation, citric acid, pentose phosphate, voluntary muscle, oxygen debt, lactic acidosis, muscle fatigue, neuroendocrine, involuntary, fatty acids, conduction system, cardiac conduction, atrial, atrium, action potentials, sarcomeres, AV node, Purkinje fibres, Purkinjee fibres, syncytial, myocardium, transmission velocity, stimulation, muscle, rhythmic, systole, diastole, stretch receptors, venous return, Frank-Starling, atrial distension, autonomic control, sympathetic stimulation, cardiac output, parasympathetic stimulation, calcium ions, cell membranes, extracellular fluid, intracellular, catecholamines, membrane, permeability, sodium, repolarisation, depolarisation, calcium ion flux, vagal, stimulation, muscle contraction, fatigue

 

Date: Oct 2006

 

Category: The body

 

Nutrimed Module:

 

Type: Article

 

Author: Morgan, G

 

Functional differences between cardiac and skeletal muscle

Structural and cellular differences reflect functional differences between cardiac and skeletal muscle. Though both are composed of striated muscle fibres, research has shown differences in the myosin and protein composition (Weeks 1976, Zak 1983) and the oxidative pathways used by these two types of cells. Physiologically, the ability of skeletal muscle to perform rapid high-intensity exercise utilising glucose oxidation via the citric acid and pentose phosphate pathways reflects the prerequisite of the voluntary musculature to respond to a potential fear and flight situation by incurring an oxygen debt, lactic acidosis and muscle fatigue.

 

Cardiac muscle by contrast is characterised by involuntary neuroendocrine control of its function through the autonomic nervous system and a reliance on the beta-oxidation of fatty acids for its energy supply. Cardiac muscle function has evolved to enable the heart to pump blood around the body in a smooth and rhythmical way in response to the body’s oxygen demands. To do this the heart has evolved a specialised conduction system which enables action potentials arising in the atrial SA node to be transmitted via the AV node and the Purkinjee fibres to the sarcomeres in a linear and synchronised manner. The ‘syncytial’ nature of cardiac muscle and the low electrical resistance of adjoining sarcomeres’ intercalated discs, allows the smooth transmission of an action potential to all parts of the myocardium.

 

These action potentials travel much more slowly than in skeletal muscle due to the fact that the transmission velocity along cardiac muscle fibres is only 1/10th that of skeletal muscle. In addition the unique prolongation of the action potential of cardiac muscle cells (200 msec compared with 5 msec of skeletal muscle) renders heart muscle largely unresponsive to further stimulation during a large part of the systole-diastole cycle. Faster transmission velocities in the conduction system (0.02-4 metres/sec against the 0.3-0.5 metres/sec of sarcomeres) allow a closer and more rhythmic control of the cycle to be achieved.

 

Being involuntary, heart function is more closely under the control of the autonomic nervous system than that of the musculoskeletal system. Striated muscle of both the skeletal and cardiac systems respond to stretch but in cardiac muscle the so-called ‘Frank-Starling mechanism’ is of particular importance as it enables the heart to respond to greater levels of venous return and atrial distension by increasing the force of its contraction and the degree of cardiac output. Autonomic control via receptors augments this underlying response. Sympathetic stimulation can increase cardiac output 2- 3 fold and parasympathetic stimulation can reduce it by 50%. This is brought about by the direct effect of neurotransmitters on cell membranes.

 

The prolonged depolarisation phase and plateau of the sarcomere action potential spike is due to the presence of ‘slow calcium-sodium’ channels in the cell membranes of cardiac sarcomeres. Via an expanded T tubule system (25 times larger than in skeletal muscle cells) and which is in contact with the extracellular fluid, large amounts of calcium ions are able to move intracellularly during this phase leading to a strong and sustained muscular contraction. Catecholamines, by increasing membrane permeability to both sodium and calcium ions, increase this effect.

 

Correspondingly acetylcholine (Ach) release following vagal stimulation leads to increased potassium permeability during the repolarisation phase and reduced cardiac muscle responsiveness. In addition stretching of sarcomeres renders them more sensitive to the raised levels of calcium ion flux found in cardiac muscle (Hibberd 1982, Kentish 1986).

 

The net result of these adaptations is that cardiac muscle cells are able to contract more slowly and more strongly when subjected to a load whilst sustaining a rhythmic pattern of muscle contraction which is not subject to fatigue. Here as elsewhere structure matches function.

 

References

1. Howland R. (2002) Lecture notes. Surrey University

2. Guyton AC. (1992) Human physiology and mechanics of disease. 5th ed. WB Saunders Company

3. Weeds AG. (1976) Light chains for slow twitch muscle myosin. Europ J Biochem 66: 157-173

4. Zak R, Galhotra SS. (1983) Contractile and regulatory proteins. In: Cardiac Metabolism, ed. Drake-Holland AJ & Noble MIM. John Wiley & Sons Ltd

5. Hibberd & Jewell. (1982) Calcium- and length-dependant force production in rat ventricular muscle. J Physiol 329: 527-540

6. Kentish et al. (1986) Comparison between the sarcomere length-force relations of intact and skinned trabeculae from rat right ventricle. Influence of calcium on these relations. Circ Res 58: 755-768