7.9 Muscle Contraction: Sliding Filament Model

The following notes detail the molecular mechanism of muscle contraction, known as the sliding filament model, which explains how muscle fibers shorten to generate force.

The Sliding Filament Theory

The fundamental principle of muscle contraction is the sliding filament theory. This theory states that muscle contraction occurs not because the myofilaments themselves shorten, but because the thin (actin) myofilaments slide past the thick (myosin) myofilaments. This sliding action increases the degree of overlap between them, shortening the entire muscle cell.

• Relaxed State: In a relaxed muscle, the thin and thick filaments overlap only partially, at the ends of the A band.
• Contracted State: Upon stimulation, myosin heads on the thick filaments attach to binding sites on the actin of the thin filaments, forming cross-bridges. These cross-bridges repeatedly form and break, acting like ratchets to pull the thin filaments toward the center of the sarcomere.

Changes in the Sarcomere During Contraction

As the thin filaments slide, the structure of the sarcomere changes measurably:

Control of Cross-Bridge Formation

The formation of cross-bridges is a tightly regulated process initiated by the nervous system.

1. Nerve Impulse: A nerve impulse arrives at the neuromuscular junction. Neuron→
2. Signal Transmission: The electrical signal (action potential) travels along the muscle cell membrane (sarcolemma), down the T-tubules.
3. Calcium Release: The signal reaches the sarcoplasmic reticulum (SR), triggering the opening of its calcium gates. Calcium ions ($C{a}^{2+}$) are released from the SR into the cytosol surrounding the myofilaments.
4. Role of Regulatory Proteins:
   • At Rest: The protein tropomyosin is positioned over the myosin-binding sites on the actin filaments, blocking them.
   • Upon $C{a}^{2+}$ Release: The released $C{a}^{2+}$ ions bind to another protein, troponin. This binding causes troponin to change shape.
5. Exposure of Binding Sites: The shape change in troponin pulls the attached tropomyosin strand away, exposing the myosin-binding sites on the actin filament.
6. Cross-Bridge Cycle:
   • Myosin heads can now attach to the exposed binding sites on actin, forming a cross-bridge.
   • ATP is hydrolyzed (broken down to ADP and Pi), providing the energy for the myosin head to pivot (the "power stroke"), pulling the actin filament.
   • The cross-bridge is broken, the myosin head re-energizes, and the cycle of attachment, pivoting, and detachment repeats as long as $C{a}^{2+}$ and ATP are present.

Possible Questions/Answers

Q: What is the sliding filament theory? A: It is the theory that muscle contraction results from the sliding of thin (actin) filaments past thick (myosin) filaments, increasing their overlap and shortening the sarcomere. The filaments themselves do not change length.

Q: What is the role of calcium ions ($C{a}^{2+}$) in muscle contraction? A: Calcium ions are the trigger for contraction. They bind to troponin, which causes tropomyosin to move away from the myosin-binding sites on actin, allowing cross-bridges to form.

Q: Which band of the sarcomere does not change length during contraction? A: The A band does not change length because it corresponds to the length of the thick (myosin) filaments, which do not shorten.

Q: What is a cross-bridge? A: A cross-bridge is the physical link formed when a myosin head binds to an active site on an actin filament. The repeated formation and breaking of these bridges generates the force for muscle contraction.

Biological Significance

The sliding filament model is the universal mechanism for muscle contraction in animals, converting chemical energy (ATP) into mechanical force. This process is essential for all forms of movement, from locomotion to the beating of the heart. Phases of Heartbeat→