Muscle Contraction: Steps and Relaxation

• Muscle contraction occurs due to the cross-bridge interaction between actin and myosin, facilitated by the sliding filament mechanism

Relaxation

• Tropomyosin covers the myosin binding sites on actin during muscle relaxation
• ATP is attached to the ATP binding site on myosin and is hydrolyzed into ADP + Pi, but remains attached to myosin
• Myosin heads have potential energy stored, ready to bind with actin
• Sarcomeres are longer during relaxation

Muscle Contraction Steps

• A series of events leads to muscle contraction, starting with an action potential in a somatic nerve
• Acetylcholine is released from the somatic nerve
• This leads to muscle depolarization
• The depolarization spreads through the T tubules
• Calcium is released from the sarcoplasmic reticulum
• Calcium binds to Troponin C, causing Tropomyosin to move and expose actin binding sites
• Actin and Myosin then bind, leading to muscle contraction

Step 1: Neuromuscular Junction

• An action potential travels down a motor neuron to the synaptic knob

Step 2: Neuron to Muscle (Muscle Fiber)

• The nervous system initiates muscle contraction with a conscious decision to move
• Neurotransmitters are released from somatic nerves, specifically acetylcholine
• Acetylcholine binds to nicotinic receptors in the sarcolemma of the muscle fiber
• Acetylcholine receptors are ion channels that allow sodium-potassium movement

Step 3: Depolarization in Muscle

• Acetylcholine binds to its receptors, which are sodium-potassium channels
• Opening of these channels leads to the movement of Sodium-potassium across the sarcolemma with more sodium entering
• The imbalance of charges leads to end plate potential and an action potential

Step 4: Action Potential Spread

• The action potential spreads through the T tubules

Step 5: Sarcoplasmic Reticulum Calcium Release

• Action potentials trigger the release of calcium from the sarcoplasmic reticulum into the sarcomere

Step 6: Calcium Binding to Troponin

• Calcium binds with troponin C
• This causes a conformational change in the troponin-tropomyosin complex
• Troponin and tropomyosin no longer cover actin
• This exposes the actin binding sites

Step 7: Myosin Binding to Actin

• Once the active sites on actin are exposed, myosin heads attach to them
• The myosin heads pull the actin over myosin, causing the actin filaments to slide towards the center of the sarcomere and shorten it
• Phosphate (Pi) is released, allowing myosin to use the stored energy and change shape

Power Stroke

• Myosin heads swivel (bend) towards the center of the sarcomere during the power stroke
• The myosin head moves toward the M line, pulling the actin along
• The actin filaments move approximately 10 nm toward the M line
• Sarcomere shortens and the muscle contracts as the actin is pulled toward the M line
• The power stroke is when force is produced

Sarcomere Length Changes During Contraction

• During contraction, the A band stays the same width while the Z lines move closer together
• The I band gets smaller, and if the ends of a myofibril are free to move, the sarcomeres shorten simultaneously
• The ends of the myofibril are pulled toward its center

Energy for Contraction

• Myosin heads bind ATP and hydrolyze it to get energy
• ATPase activity of myosin heads catalyzes the splitting of ATP into ADP + Pi + energy
• The liberated energy is used in contraction, which is an active process

Relaxation

• No further acetylcholine is released when there are no longer action potentials generated on the motor neuron
• Acetylcholinesterase breaks down acetylcholine at the neuromuscular junction
• The muscle fiber action potential stops, and there is no more release of Calcium from lateral sacs
• Calcium moves back into the sarcoplasmic reticulum
• New ATP is required for the myosin head to release from actin and return to a resting state
• Myosin detaches and moves away from actin
• Troponin and Tropomyosin cover up actin
• Repolarization makes the sarcolemma stable again
• A new ATP molecule binds to the myosin head to detach the cross-bridge from the actin strand

Calcium's Role

• An increase in Calcium starts filament sliding and initiates contraction
• A decrease in Calcium turns off the sliding process

ATP Requirements During Contraction-Relaxation

• During contraction, the splitting of ATP by myosin ATPase provides energy for the power stroke of the cross-bridge
• During relaxation, binding of a fresh ATP molecule to myosin lets the cross-bridge detach from the actin filament at the end of the power stroke, allowing the cycle to repeat
• Active transport of Calcium back into the sarcoplasmic reticulum during relaxation depends on energy derived from the breakdown of ATP

Rigor Mortis

• Rigor mortis is stiffness that develops after death because there is no ATP
• ATP is required for the myosin head to release from actin and return to a resting state
• A lack of ATP results in the constant binding of actin and myosin cross-bridges, causing stiffness
• Rigor mortis begins 2 to 4 hours after death, peaks at 13 hours, and ends after 48-60 hours
• After 48-60 hours, muscle cells begin to autolyze, and the muscle will contract after death due to a lack of Atp.

Key Molecules

• Myosin's function is to pull actin for muscle contraction
• Actin provides the binding site for myosin
• Tropomyosin blocks the myosin binding site on actin
• Troponin I inhibits actin-myosin binding
• Troponin T binds to tropomyosin
• Troponin C binds to calcium
• T-tubules transmit action potential deep into muscle fiber.
• The sarcoplasmic reticulum stores and releases calcium ions.