Smooth and Cardiac Muscle

Part 2 · Excitable Tissues · Chapter 9 of 47

Learning objectives

By the end of this page you should be able to:

• Describe the ventricular action potential and explain why heart muscle cannot be tetanised.
• Explain calcium-induced calcium release and how cardiac contraction is graded.
• Describe how smooth muscle is activated through calmodulin and myosin light-chain kinase.
• Explain the latch state and why smooth muscle can hold tone economically.
• Distinguish single-unit and multi-unit smooth muscle.
• Apply these ideas to exercise, cardiac rehabilitation, blood pressure and continence.

Why it matters

When a patient exercises, heart rate and stroke volume rise, and the smooth muscle of blood vessels redistributes blood towards working muscle. When the heart is damaged, lost muscle is replaced by scar. When the bladder fills, its smooth muscle relaxes to accommodate the volume.

The structural comparison of the three muscle types is set out in Muscle (Human Anatomy). This page explains how cardiac and smooth muscle work differently from skeletal muscle.

Cardiac muscle

Heart muscle is striated like skeletal muscle, with the same sarcomeres and cross-bridge cycle. Its cells are short and branched, joined end to end by intercalated discs. Gap junctions in the discs let the impulse pass straight from cell to cell, so the whole chamber contracts as one.

The ventricular action potential

Figure 1 · The ventricular action potential

The upstroke (phase 0) is driven by fast sodium channels, as in nerve. What follows is different. After a brief notch, the voltage stays near zero for about 200 milliseconds, the plateau. Calcium enters through L-type channels during this time, balanced by potassium leaving [1]. Repolarisation follows as potassium channels open more widely.

Because the action potential is so long, the muscle stays refractory until its contraction is nearly over. A second impulse cannot arrive in time to summate. The heart therefore cannot be tetanised, which guarantees that it relaxes and refills between beats.

The heart’s own pacemaker cells and the spread of excitation through the conducting system are covered in Chapter 11.

Excitation–contraction coupling in the heart

Figure 2 · Calcium-induced calcium release

In skeletal muscle, voltage sensors pull the SR release channels open mechanically. In heart muscle, the calcium that enters through L-type channels is itself the trigger. It opens the cardiac ryanodine receptors and releases a much larger amount of calcium from the SR. This is calcium-induced calcium release [1].

Relaxation depends on removing calcium. Most is pumped back into the SR; some is pushed out of the cell by the sodium–calcium exchanger [1].

How cardiac force is graded

Every heart cell contracts with every beat, so the heart cannot recruit more units as skeletal muscle does. Instead, force is adjusted in two ways.

First, by changing the amount of calcium reaching the filaments. Sympathetic stimulation increases calcium entry and SR uptake, so beats are both stronger and shorter [1]. Second, by stretch: a more filled ventricle contracts more forcefully, the Frank–Starling mechanism covered in Chapter 12.

Can heart muscle regenerate?

For a long time, heart muscle cells were thought to be fixed from birth. Bergmann and colleagues used carbon-14 from Cold War nuclear tests, built into DNA, to date human heart cells. They found that cardiomyocytes do renew, but slowly: about 1% a year at age 25, falling to 0.45% at 75 [3].

Fewer than half of the heart’s muscle cells are exchanged in a lifetime [3]. That is far too slow to replace the muscle lost in a heart attack, which is why an infarct heals as scar.

Smooth muscle

Smooth muscle lines blood vessels, airways, the gut, bladder and uterus. Its cells are spindle-shaped and have no sarcomeres. Actin filaments anchor to dense bodies scattered through the cell and on its membrane, so the cell shortens in all directions, a little like a balloon being squeezed.

Activation through myosin

Figure 3 · How smooth muscle contracts

Smooth muscle has no troponin. Calcium, entering from outside and released from the SR, binds a protein called calmodulin. Calcium–calmodulin activates myosin light-chain kinase, which adds a phosphate to the myosin head. Only phosphorylated myosin cycles rapidly [2].

A second enzyme, myosin light-chain phosphatase, removes the phosphate. If a head loses its phosphate while still attached to actin, it detaches only slowly. Hai and Murphy called these slow, non-cycling attachments latch bridges [2].

The latch state lets smooth muscle maintain force with reduced phosphorylation, fewer cross-bridge cycles and less ATP [2]. That is how arteries hold their tone, and sphincters stay closed, for hours at little energy cost.

Single-unit and multi-unit smooth muscle

Figure 4 · Single-unit and multi-unit smooth muscle

Single-unit smooth muscle behaves like a sheet. Gap junctions spread activity from cell to cell, pacemaker cells may set a rhythm, and stretch itself can trigger contraction. The gut and uterus work this way.

Multi-unit smooth muscle is controlled cell by cell through its nerve supply, giving fine control. The muscles of the iris are an example.

Smooth muscle also shows stress relaxation. When a hollow organ such as the bladder is slowly filled, the muscle gradually relaxes, so pressure rises little until the organ is quite full.

Clinical relevance for the physiotherapist

• Cardiac rehabilitation. Lost heart muscle is replaced by scar, not new muscle [3]. Exercise training improves function mainly through the remaining muscle, the circulation and skeletal muscle.
• Heart rate and drugs. Beta-blockers reduce the sympathetic effect on cardiac calcium handling, blunting heart rate and force responses to exercise [1]. Use perceived exertion as well as heart rate to set intensity.
• Calcium channel blockers. These act on L-type channels in heart and vascular smooth muscle and can lower blood pressure and heart rate.
• Blood pressure on exercise. Vascular smooth muscle in working muscle relaxes while vessels elsewhere constrict, redistributing blood.
• Airways. Bronchial smooth muscle contraction narrows airways in asthma; inhaled bronchodilators relax it.
• Continence. The bladder wall’s smooth muscle and the urethral sphincters work with the skeletal pelvic floor, which is the part physiotherapists can train directly.

Assessment and application

Common mistakes

• Saying the heart grades force by recruitment. Every cell contracts every beat.
• Forgetting the plateau when drawing the cardiac action potential.
• Giving smooth muscle troponin. It uses calmodulin and myosin light-chain kinase [2].
• Assuming heart muscle cannot renew at all. It does, but very slowly [3].
• Confusing smooth muscle tone with spasticity, which is a disorder of skeletal muscle control.

Exam preparation

Long answer

Compare the mechanisms of contraction in skeletal, cardiac and smooth muscle.

• Excitation: the action potential in each (Figure 1).
• Calcium source and sensor: SR versus calcium-induced release versus calmodulin (Figures 2 and 3) [1, 2].
• Grading of force in each type.
• Tetanus, refractoriness and tone; latch state [2].
• Comparison table and clinical notes.

Short notes

• Calcium-induced calcium release [1].
• Latch state [2].
• Single-unit versus multi-unit smooth muscle.
• Cardiomyocyte renewal [3].

Viva and practical

• “Why can’t the heart be tetanised?” — its refractory period lasts almost as long as its contraction [1].
• “How does smooth muscle hold tone cheaply?” — latch bridges maintain force with less ATP [2].
• “Does heart muscle regenerate?” — only very slowly, about 1% a year in young adults [3].
• Practical: take a radial pulse and comment on rate and rhythm.

Current evidence

Exam and traditional teaching

Heart muscle cells are described as permanent, never replaced after birth.

What the evidence adds

Carbon-14 dating shows that human cardiomyocytes do renew, at about 1% a year in young adults and less with age, with fewer than half replaced in a lifetime [3].

What the student should understand

For practical purposes heart muscle lost in an infarct is not replaced, so rehabilitation works with what remains. The finding of slow renewal is a research direction, not yet a treatment.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Quick review

Further reading

References

1. Bers DM. Cardiac excitation-contraction coupling. Nature. 2002 Jan 10;415(6868):198–205. doi:10.1038/415198a PMID 11805843 Review
2. Hai CM, Murphy RA. Regulation of shortening velocity by cross-bridge phosphorylation in smooth muscle. American Journal of Physiology. 1988 Jul;255(1 Pt 1):C86–C94. doi:10.1152/ajpcell.1988.255.1.C86 PMID 3389402 Experimental and modelling study
3. Bergmann O, Bhardwaj RD, Bernard S, et al. Evidence for cardiomyocyte renewal in humans. Science. 2009 Apr 3;324(5923):98–102. doi:10.1126/science.1164680 PMID 19342590 Human study

Related topics

• Previous: Chapter 8 — Skeletal Muscle Contraction
• Next: Chapter 10 — The Heart as a Pump: the Cardiac Cycle
• Muscle (Human Anatomy)
• Cardiac rehabilitation

Reviewed by the Physiotherapist India Team. · Human Physiology contents