Smooth muscles are in the iris (pupil contraction), skin (hair muscles that cause goose bumps), walls of vessels and hollow internal organs: bronchi, lower part of esophagus, stomach, gallbladder, intestine, reproductive and urogenital organs, glands and their ducts. Connective tissue is made up of proteins: collagen and elastin. Average smooth muscle cell is 25-50 µm long and 2-5 µm wide. Actin and myosin are not organized in sarcomeres so no striations are visible under light microscope. Smooth muscle cells are pretty non-organized and meet each other in different angles. In vessels they are arranged circumferentially and they change vessel’s diameter by contracting. Smooth muscles are innervated by sympathetic and parasympathetic (autonomous) nerves. It takes about 500 ms for a smooth muscle to reach peak contraction.


Stimulus for smooth muscle contraction comes from muscle cells (peristalsis pacemakers in intestinal wall), intestinal wall distension (from moving food), autonomic nervous system (sympathetic nerves cause contraction, parasympathetic nerves cause relaxation), hormones (adrenalin causes smooth muscle relaxation, vasopressin causes vasoconstriction, oxytocin causes contraction of uterus during childbirth). We can’t consciously control contraction of smooth muscles.

Other substances which affect smooth muscle contraction: potassium, calcium, magnesium, serotonin, prostacyclin, nitric oxide (NO2), histamine, medications (nitroglycerin), drugs (cocaine causes vasoconstriction, morphine causes vasodilatation) and some alkaloids and poisons.

Smooth muscle cells obtain energy for contraction from aerobic breakdown of glucose and fatty acids. Energy from anaerobic metabolism is used for trans-membrane transport.

Smooth muscles are of two types: tonic muscles in vessels sustain long contraction, phasic muscles in intestine contract rapidly.

Regeneration of smooth muscle

Repairing process in smooth muscle includes hypertrophy only. It is not usual that new smooth muscle cells are formed.

Cardiac (heart) muscle

Cardiac muscle is striated and can not be directly voluntary controlled. Latin word for the whole heart muscle is myocard. While heart is contracting it pumps the blood through the circulatory system. Heart doesn’t get oxygen from the blood flowing through it but from two coronary arteries arising from aorta. If they are obliterated for 20-40 minutes (e.g. from blood clot) or if the demand for oxygen exceeds oxygen deliverance, myocardial infarct can occur; a part of the heart will be permanently damaged since cardiac muscle fibres can not regenerate and a scar will form. This is called heart attack.

Heart muscle fibres are about 10-20 µm wide and 50-100 µm long. They can use glucose, fatty acids, amino acids and lactate as a source of energy. Cardiac muscle cells are rich in mitochondria and get highly oxygenated blood so all the above mentioned substances are broken down by the aerobic way even during hard exercise. Heart grows only by enlarging of heart muscular cells (hypertrophy) and not with their multiplying.

Heart beating

Cardiac muscle contraction is myogenic – it stimulates its own contraction. A single cardiac cell contracts at a steady rate independent of the nervous system. If two cardiac cells are in contact, whichever contracts first, will stimulate the other to contract (via intercalated discs in the cell wall). Sinoatrial (SA) node in the wall of right atrium is a group of cardiac cells which act as a primary pacemaker. The stimulus for contraction of the heart originates in the SA node (not in the brain). Sympathetic nerve fibres increase heart rate and parasympathetic nerve fibres decrease heart rate. Excitation wave from SA node propagates through electrical conduction system toward other heart cells. If SA node is impaired some other cardiac muscle cell will start to act like pacemaker and this usually causes derangement of heart beat – arrhythmia.

Average heart rate in an adult at rest is 72/minute. Heart rate between 60-100/min at rest is considered as normocardia, over 100/min as tachycardia, below 60 as bradycardia. Bradycardia as low as 38/min can be normal in athletes. For a cardiac muscle time to peak contraction may be around 150 ms. A heart beats even when taken out of the body (e.g. during transport for transplantation).

Appendix: Effects of adrenalin, potassium, calcium and magnesium on muscle:

Adrenalin lowers the threshold of excitation of motor units so the skeletal muscle is excited faster, and it reaches peak contraction early and the contraction is stronger. It dilates bronchi thus enabling additional oxygen inflow. It dilates arteries in skeletal muscles and constricts arteries in smooth muscles in gut and skin thus redirecting blood flow towards skeletal muscles. It relaxes gut muscles (may lead to constipation). It dilates pupils, increases heart rate and stroke volume (volume of blood expelled from heart in one beat). It enhances breakdown of glycogen in liver thus increasing blood glucose concentration. It enhances glycolysis and breakdown of fatty acids in skeletal and heart muscle cells.

Potassium enables propagation of excitation in nerve and muscle fibres.

Both hypo- and hyperkalemia cause muscle weakness and cramps. Both hypo- and hyperkalemia cause derangement of heart beat – arrhythmia, if severe, may be lethal. Conditions listed can occur quickly in kidney or adrenal gland disease, after a period of irregular eating (small potassium intake while fasting), in alcohol abuse or after taking oral or intravenous potassium.

Calcium is essential for contraction of all muscle types. Hypercalcemia (e.g. from renal disease, cancer, lithium) can cause muscle weakness and hypertension. Excess calcium taken orally (antacids) can cause constipation to some people but this is not proved. Hypocalcemia (from parathyroid gland failure or lack of vitamin D) causes numbness and, when severe, tetanic muscle cramps and hypotension because of heart failure.

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