Skeletal Muscle Contraction

Part 2 · Excitable Tissues · Chapter 8 of 47

Learning objectives

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

• Describe excitation–contraction coupling step by step.
• Explain the cross-bridge cycle and the roles of calcium and ATP.
• Explain twitch, summation and tetanus, and how recruitment and rate coding grade force.
• Describe the three energy systems and how intensity and duration change their contribution.
• Summarise current understanding of the mechanisms of muscle fatigue.
• Describe the neural and morphological adaptations to strength training.

Why it matters

Strength and endurance are two of the most common goals in physiotherapy. Choosing load, repetitions, speed and rest well depends on knowing what happens inside the muscle fibre.

The structure of muscle, the sarcomere, fibre architecture and fibre types are covered in Muscle (Human Anatomy). This page does not repeat them. It concentrates on how the fibre is switched on, how its force is controlled, how it is fuelled, and how it changes with use.

Excitation–contraction coupling

The neuromuscular junction (Chapter 7) produces an action potential in the muscle fibre membrane. The problem is getting that signal to the filaments deep inside a fibre that may be 100 μm wide. The answer is the T-tubule system and the sarcoplasmic reticulum (SR).

Figure 1 · Excitation–contraction coupling

The action potential spreads down the T-tubules. There, voltage-sensing proteins called dihydropyridine receptors change shape. In skeletal muscle they are mechanically linked to calcium release channels, the ryanodine receptors, in the membrane of the neighbouring SR.

Calcium floods into the cytoplasm and binds troponin C. This moves tropomyosin away from the binding sites on actin, and myosin heads can attach. As long as calcium stays high, cross-bridges keep cycling.

Relaxation is active. Calcium pumps in the SR membrane use ATP to pull calcium back into the store. When calcium falls, tropomyosin covers the binding sites again and the fibre relaxes.

The cross-bridge cycle

Figure 2 · The cross-bridge cycle

Each myosin head attaches to actin, pivots in the power stroke, releases, and re-cocks. A new molecule of ATP is needed to release the head from actin. Without ATP, heads stay attached, which is why muscles stiffen after death in rigor mortis.

Many heads cycle out of step with one another, so some are always attached. The filaments slide past each other and the sarcomere shortens. How force depends on sarcomere length and shortening speed is covered in Muscle (Human Anatomy).

Twitch, summation and tetanus

A single action potential produces a brief contraction, a twitch. Because the twitch lasts much longer than the action potential, a second impulse can arrive before the fibre has relaxed. The two contractions then add together.

Figure 3 · Twitch, summation and tetanus

As stimulation frequency rises, twitches fuse into a smooth, sustained contraction called tetanus, with several times the force of a single twitch. Normal voluntary contractions are mostly unfused or partly fused tetani, smoothed further because different motor units fire out of step.

Grading force: recruitment and rate coding

The nervous system controls force in two ways. It changes how many motor units are active, recruitment. And it changes how fast each active unit fires, rate coding.

Recruitment follows an orderly pattern. In 1957 Henneman showed that smaller motor neurons are more easily discharged than larger ones [1]. As effort rises, small units are recruited first and large units last. This is the size principle.

Figure 4 · The size principle

The size principle has a direct training consequence. Small units, which are slow and fatigue-resistant, do the work at low forces. The large, fast, powerful units are brought in only when force demand is high, either with heavy loads or as lighter efforts approach failure.

Energy for contraction

ATP is the only fuel the cross-bridge and the calcium pump can use, yet a muscle stores only enough for a few seconds of hard work. It must be remade continuously. Three systems do this, and Hargreaves and Spriet describe how intensity and duration determine their mix [2].

Figure 5 · Three ways to remake ATP

The systems overlap rather than switch on in sequence. For most hard athletic events, carbohydrate is the main fuel for both anaerobic and aerobic pathways [2]. At rest and in long, gentle activity, fat contributes much more.

Muscle fatigue

Fatigue is a fall in the force or power a muscle can produce with repeated or sustained use. It can arise in the brain and spinal cord (central fatigue) or within the muscle itself (peripheral fatigue).

For decades, lactic acid was blamed. Allen, Lamb and Westerblad reviewed the evidence and concluded that the accumulation of lactate and hydrogen ions is probably of limited importance in mammals [3].

Different activities produce fatigue by different combinations of these mechanisms [3]. Most mechanistic work has been done on isolated animal muscle, so applying it to patients requires care [3].

Adaptation to strength training

Folland and Williams reviewed how strength training increases strength [4]. The gains come from a combination of neural and morphological changes.

Neural factors make their largest contribution early in a programme, but hypertrophy also begins from the start [4]. Strength gains are specific to the trained movement. Training one limb can also increase strength in the untrained one, which points to neural adaptation [4].

Endurance training changes the fibre differently, mainly by building mitochondria and capillaries, as described in Chapter 2.

Clinical relevance for the physiotherapist

• Prescribing load. To train the large, fast motor units, loads must be heavy or sets taken close to failure [1].
• Early strength gains. In the first weeks after injury or surgery, improvement is largely neural; set practice so that it trains the movement the patient needs [4].
• Cross-education. Training the unaffected limb may help preserve strength in an immobilised one [4].
• Fatigue in patients. Fatigue has several mechanisms. Do not tell patients that lactic acid is the cause [3].
• Energy systems in rehabilitation. Interval training with recovery periods lets phosphocreatine recover between efforts [2].
• Electrical stimulation. Evoked contractions fatigue faster than voluntary ones; see Chapter 6.

Assessment and application

Common mistakes

• Saying sodium triggers contraction. Calcium does, released from the SR.
• Forgetting that relaxation needs ATP, both to release cross-bridges and to pump calcium.
• Reversing the size principle. Small units first, large last [1].
• Treating the energy systems as switching on one after another. They overlap [2].
• Blaming lactic acid for fatigue or soreness [3].
• Attributing all early strength gain to hypertrophy [4].

Exam preparation

Long answer

Describe excitation–contraction coupling in skeletal muscle. Add a note on the grading of muscle force.

• Neuromuscular transmission and the muscle action potential (link to Chapter 7).
• T-tubules, voltage sensors, ryanodine receptors and calcium release (Figure 1).
• Troponin, tropomyosin and the cross-bridge cycle (Figure 2).
• Relaxation by SR calcium pumps.
• Grading force: summation and tetanus (Figure 3), recruitment and the size principle (Figure 4) [1].

Short notes

• Energy systems in exercise [2].
• Mechanisms of muscle fatigue [3].
• Adaptations to strength training [4].
• Rigor mortis.

Viva and practical

• “Why do muscles stiffen after death?” — no ATP to release cross-bridges.
• “Which motor units does a light load train?” — mainly small, slow units unless taken near failure [1].
• “Is lactic acid the cause of fatigue?” — probably of limited importance; several other mechanisms dominate [3].
• Practical: measure grip strength with a dynamometer and test repetitions to failure.

Current evidence

Exam and traditional teaching

Fatigue is attributed to lactic acid, and early strength gains are attributed mostly to neural factors before hypertrophy follows weeks later.

What the evidence adds

Lactate and acid are probably minor contributors to fatigue in mammals; ionic changes, impaired calcium release, inorganic phosphate and reactive oxygen species are more important [3].

Neural factors dominate early strength gains, but hypertrophic processes start at the very beginning of training [4].

What the student should understand

Know the classic coupling sequence and energy systems for the exam. When explaining fatigue or early progress to a patient, use the current picture.

Check yourself

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

Quick review

Further reading

References

1. Henneman E. Relation between size of neurons and their susceptibility to discharge. Science. 1957 Dec 27;126(3287):1345–1347. doi:10.1126/science.126.3287.1345 PMID 13495469 Original study
2. Hargreaves M, Spriet LL. Skeletal muscle energy metabolism during exercise. Nature Metabolism. 2020;2(9):817–828. doi:10.1038/s42255-020-0251-4 PMID 32747792 Review
3. Allen DG, Lamb GD, Westerblad H. Skeletal muscle fatigue: cellular mechanisms. Physiological Reviews. 2008 Jan;88(1):287–332. doi:10.1152/physrev.00015.2007 PMID 18195089 Review
4. Folland JP, Williams AG. The adaptations to strength training: morphological and neurological contributions to increased strength. Sports Medicine. 2007;37(2):145–168. doi:10.2165/00007256-200737020-00004 PMID 17241104 Review

Related topics

• Previous: Chapter 7 — The Synapse and the Neuromuscular Junction
• Next: Chapter 9 — Smooth and Cardiac Muscle
• Muscle (Human Anatomy)
• Exercise dose

Reviewed by the Physiotherapist India Team. · Human Physiology contents