Muscle

Three Main Phases of Skeletal Muscle Contraction:
- Excitation Phase
- Excitation-Contraction Coupling Phase
- Contraction Phase

Definition: The excitation phase involves the nervous system initiating muscle contraction. The neurons release acetylcholine (ACh) to signal muscle contraction.
Key Points:
- Action potential arrives at the axon terminal of a neuron.
- Voltage-gated calcium channels open in the axon terminal, allowing calcium ions (Ca²⁺) to enter the neuron. This is the first instance where calcium is needed.
- The influx of Ca²⁺ causes exocytosis of synaptic vesicles, which release ACh into the synaptic cleft (the space between the neuron and muscle sarcolemma).
- ACh binds to cation channels in the muscle fiber membrane, allowing positively charged ions (primarily Na⁺) to enter the muscle fiber.
- This change in ion concentration generates a new action potential in the muscle fiber.

Definition: This phase translates the electrical signal of muscle fibers into a mechanical response through calcium ion release.
Key Points:
- The end plate potential stimulates action potentials in muscle fibers that propagate along the sarcolemma into the transverse tubules (T-tubules).
- T-tubules are invaginations of the muscle cell membrane that allow depolarization to occur deep within the cell.
- Depolarization of T-tubules opens calcium channels in the sarcoplasmic reticulum, leading to a large influx of Ca²⁺ into the cytosol.
- This rapid release of calcium ions is critical as it enables subsequent muscle contraction by exposing actin active sites.

Definition: The contraction phase is where the physical shortening of muscle fibers occurs as myosin heads interact with actin.
Key Mechanism - Crossbridge Cycle:
- Calcium Binding: Calcium ions bind to troponin, which causes tropomyosin to move and expose the active sites on actin filaments.
- Cross-Bridge Formation: Myosin heads attach to the exposed active sites on actin, forming cross-bridges.
- Power Stroke:
- ATP hydrolysis cocks the myosin head, allowing it to bind to actin.
- When the myosin head pivots and pulls actin toward the center of the sarcomere, this is called the power stroke.
- ADP and phosphate leave the myosin head during this step, returning the head to its low-energy configuration.
- Reattachment: To continue the cycle, another molecule of ATP binds to myosin, causing it to detach from actin.
- This cycle repeats approximately 20 to 40 times for a single contraction, using significant amounts of ATP.

Key Mechanisms:
- Acetylcholinesterase breaks down remaining acetylcholine in the synaptic cleft, ending the signal for contraction.
- Calcium ions are actively transported back into the sarcoplasmic reticulum, which also requires ATP.
- Troponin and tropomyosin return to their original positions, blocking active sites on actin, leading to relaxation.
- The overall process requires both calcium and ATP to reverse the contraction state effectively.

Muscle Spasms: Can occur due to dehydration and electrolyte imbalances, leading to involuntary muscle contractions.
Rigor Mortis: Postmortem, ATP becomes depleted, Ca²⁺ remains bound to troponin, and myosin heads cannot detach, causing muscle stiffness until tissue breakdown.
Myasthenia Gravis: A condition where acetylcholine receptors at the neuromuscular junction are destroyed, leading to decreased muscle contraction ability. Symptoms worsen with disease progression.
Tetanus: Caused by Clostridium tetani, leading to continuous contraction of muscles due to toxins affecting neuromuscular transmission.

ATP Requirements: ATP is essential for muscle contraction; it powers muscle contractions by replenishing spent ATP and ensuring active transport of calcium back into the SR.
Sources of ATP:
- Creatine Phosphate:
- Provides ATP rapidly for about 10 seconds during high-intensity work.
- Useful for short bursts of activity (e.g., sprinting).
- Glycolytic Metabolism (Anaerobic):
- Breaks glucose into pyruvate over approximately 30-40 seconds.
- If oxygen is insufficient, lactic acid is formed as a byproduct.
- Oxidative Metabolism (Aerobic):
- Primary method for long-duration, low-intensity activities; can produce ATP for hours as long as oxygen and fuels are available.
- Myoglobin in muscle fibers binds oxygen, aiding in aerobic respiration.

Function: Involuntary movements such as peristalsis, sphincter formation, and regulation of blood vessel diameter.
Cell Structure: Lacks T-tubules, uses caveolae instead, less organized than skeletal muscle.
Calcium Binding: Calcium binds to calmodulin instead of troponin.
Contraction Mechanism: Functions as a single unit (unitary smooth muscle) or multiple units (multiunit smooth muscle) and can be autorhythmic or respond to nerve stimulation.

Structure: Striated, branched fibers with intercalated discs (gap junctions and desmosomes) that allow synchronized contraction.
Function: Autorhythmic, reliant on pacemaker cells (SA node) for heartbeat regulation.
Oxygen Demand: Contains many mitochondria and myoglobin for constant ATP supply due to the heart's continuous activity.

Muscle contraction involves coordinated electrical signals and mechanical actions, requiring precise interaction between chemical, electrical, and mechanical components.
Understanding muscle physiology is essential for recognizing how muscle contractions can be affected by various physiological and pathological conditions.
Electrolyte Balance: Maintaining proper sodium and potassium levels is crucial for muscle function; depletion can cause significant muscle fatigue and impaired contraction ability.
Applications in Health: Understanding muscle mechanics is important for treating muscle disorders and improving athletic performance through nutrition and exercise regimens.