Learning Objective

Explain why cardiac muscle cannot undergo tetanus by comparing calcium handling, electrical properties, and refractory periods in skeletal and cardiac muscle.

Why Skeletal Muscle Can Tetanize, But Cardiac Muscle Cannot

Both skeletal and cardiac muscles are striated and use the same contractile proteins (actin, myosin, troponin, tropomyosin, and titin). In both tissues, contraction begins when cytosolic Ca²⁺ rises and binds to troponin-C, allowing cross-bridge cycling.

However, the source and handling of calcium during contraction are fundamentally different — and this difference determines whether summation and tetanus can occur.

Activity

Skeletal Muscle Contraction

In skeletal muscle, calcium required for contraction comes only from the sarcoplasmic reticulum (SR).

• An action potential travels down the T-tubule and activates the dihydropyridine (DHP) receptor, which mechanically opens the ryanodine receptor (RyR) on the SR. This releases a fixed amount of Ca²⁺ into the cytosol.
• Because the action potential is very short, the muscle membrane repolarizes before contraction is complete.
• This means another action potential can arrive before relaxation occurs → additional Ca²⁺ is released → force increases.

This produces:

Summation → Tetanus

Cardiac Muscle Contraction

In cardiac muscle, calcium required for contraction comes from two sources:

• Extracellular fluid
• Sarcoplasmic reticulum

During depolarization, voltage-gated L-type calcium channels open and allow extracellular Ca²⁺ to enter the cell. This incoming calcium then triggers further calcium release from the SR via calcium-induced calcium release. This process also creates a prolonged action potential due to the plateau phase. Because of this prolonged depolarization, the absolute refractory period lasts almost as long as the contraction itself. While the muscle is contracting, the cell is still in its refractory period and cannot be stimulated again.

Therefore:

• Summation cannot occur
• Tetanus cannot occur

This is essential for maintaining rhythmic cardiac pumping.

Clinical Relevance

Mutations in titin impair myocardial elasticity and are associated with dilated and restrictive cardiomyopathies due to reduced contractile efficiency.

Activity