Skeletal Muscle Contraction Overview

Skeletal Muscle Contraction

• Skeletal muscle comprises about 40% of the body's mass, with smooth and cardiac muscle accounting for another 10%.

• Skeletal muscles are composed of numerous muscle fibers, each of which contains smaller subunits.

• Each fiber is typically innervated by a single nerve ending located near its middle.

• Myofibrils are complex organelles within muscle fibers, comprised of myofilaments.

• Sarcomeres are segments of myofibrils; the basic units of muscle contraction.

• Myofilaments, or filaments, are extended macromolecular structures composed of thick and thin filaments.

• The thick filaments are myosin filaments, with globular heads (myosin heads).

• The thin filaments are actin filaments, and associated regulatory proteins (tropomyosin and troponin)

• The sarcolemma is the membrane enclosing a muscle fiber, composed of a plasma membrane and a coat of polysaccharide material containing collagen fibrils.

• Tendon fibers fuse with the sarcolemma at each end of the muscle fiber, forming bundles of tendons that connect muscles to bones.

• Each muscle fiber contains hundreds to thousands of myofibrils.

• Myofibrils are composed of 1500 myosin and 3000 actin filaments.

• Light bands (I-bands) contain only actin filaments, dark bands (A-bands) contain both actin and myosin filaments.

• Small projections from myosin filaments are cross-bridges; interaction between these bridges and actin filaments causes muscle contraction.

• Titin filamentous molecules maintain the side-by-side relationship between myosin and actin filaments.

• Titin molecules hold the myosin and actin filaments in place.

• Sarcoplasm is the intracellular fluid between myofibrils. It contains K, Mg, phosphate, protein enzymes, and mitochondria.

• Mitochondria provide energy in the form of ATP to the contracting myofibrils.

• The sarcoplasmic reticulum regulates Ca storage, release, and reuptake, thereby controlling muscle contraction.

• Action potential travels along a motor nerve to its endings on muscle fibers.

• At each ending, neurotransmitter acetylcholine is released.

• Acetylcholine acts on a muscle fiber membrane to open channels that allow Na+ ions to diffuse into the muscle.

• Local depolarization initiates an action potential along the muscle fiber membrane.

• The action potential depolarizes the muscle membrane; the sarcoplasmic reticulum releases large quantities of Ca2+ ions.

• Ca2+ initiates attractive forces between actin and myosin filaments, causing them to slide past each other (contraction).

• After contraction, Ca2+ is pumped back into the sarcoplasmic reticulum.

• The myosin filament is made up of 200+ individual myosin molecules.

• The protruding arms and heads of myosin molecules are called cross-bridges.

• Myosin head acts as an ATPase enzyme that cleaves ATP and uses the energy to energize contraction.

• A thin filament consists of two strands of actin subunits intertwined with tropomyosin and troponin.

• In the resting state, tropomyosin covers the active sites on the actin filaments, preventing myosin-actin interactions.

• Ca2+ binding to troponin causes a conformational change in tropomyosin, exposing active sites on actin, allowing contraction.

• As soon as actin filaments are activated by Ca2+ ions, myosin heads are attracted to the active sites and initiate contraction (walk-along theory).

• When a myosin head attaches to an active site, intramolecular forces between the head and arm of its cross-bridge change.

• Large amounts of ATP are cleaved to form ADP during contraction; the more work performed by the muscle, the more ATP is cleaved (Fenn effect).

• Cross-bridge formation occurs, energized myosin head attaches to an actin myofilament, forming cross-bridge.

• Energized myosin head pivots and bends, changing to low-energy state.

• As a result, actin filament is pulled towards the M line.

• Cross-bridge detachment occurs after ATP attaches to myosin, which weakens the link between myosin and actin.

• Myosin head detaches and returns to high-energy position (cocking).

• In the absence of ATP, myosin heads will not detach, causing rigor mortis.

• ATP is derived from phosphocreatine, glycolysis, and oxidative metabolism.

• Glycolysis is a rapid source of ATP but is limited by lactate and H+ accumulation.

• Oxidative metabolism is the primary source of energy for sustained contraction.

• Efficiency of muscle contraction is <25%, the remainder is transformed into heat.

• Isometric contractions do not shorten the muscle, while isotonic contractions shorten the muscle in response to a constant tension.

• Isometric system records changes in force of muscle contraction independently of load inertia.

• Whole muscle has connective tissue, sarcomeres in different parts contract differently.

• When muscle is at normal resting length (about 2 micrometers), it contracts with maximal force.

• The maximum tension decreases as the muscle is stretched beyond its normal length.

• Muscle tone results from a low rate of nerve impulses from the spinal cord.

• Nerve impulses are partly controlled by signals from the brain and partly by signals from muscle spindles.

• Prolonged muscle contraction causes muscle fatigue due to depletion of muscle glycogen.

• Nerve signal transmission can diminish with prolonged activity.

• Without blood flow, muscle fatigue occurs rapidly due to loss of nutrients, especially oxygen.

• Body movements result from simultaneous agonist and antagonist muscle contraction, controlled by centers in the brain and spinal cord. Muscle activation ratios determine body positioning.

• Muscle remodeling occurs rapidly (e.g., within a few weeks) in response to function changes.

• Muscle hypertrophy results from increased actin and myosin filament numbers in muscle fibers, causing enlargement.

• Muscle atrophy results from a decrease in muscle mass due to reduced muscle proteins.

• Atrophy occurs rapidly after denervation.

• The muscle fibers are destroyed and replaced by fibrous and fatty tissue during denervation atrophy.

• Daily stretching or appliance use prevents muscle shortening due to atrophy.

• Recovery in diseases like polio involves branching of nerve fibers and formation of macromotor units

• The presence of rigor mortis after death is due to ATP depletion and autolysis of muscle proteins.

• Muscular dystrophy involves progressive weakness and degeneration of muscle fibers due to genetic mutations.

Fast vs. Slow Muscle Fibers

• Every muscle contains a mixture of fast and slow muscle fibers.
• Fast fibers respond quickly, enabling rapid movements, and contain plenty of glycolytic enzymes.
• Slow fibers respond slowly but enable sustained contractions for longer durations; they contain a rich blood supply and high levels of mitochondria.

Muscle Contraction Characteristics

• Skeletal muscles contract by summation of individual twitches - by increasing the frequency of stimulation or the number of motor units activated.
• Muscle force varies based on the number of motor units and their stimulation frequency.
• Frequency summation and multiple fiber summation cause tetanus.

Changes in Muscle Strength at the Onset of Contraction

• A phenomenon called the staircase effect (or Treppe) describes an increase in muscle strength during the first few contractions due to increased Ca2+ levels and sarcoplasmic reticulum.

Other Important Points

• The neuromuscular junction is the synapse between a motor neuron and a muscle fiber.
• At the neuromuscular junction, acetylcholine is released, initiating muscle contraction.
• Acetylcholine is broken down by acetylcholinesterase, ending the signal and allowing relaxation.

Dive into the fascinating world of skeletal muscle contraction. This quiz covers the anatomy of muscle fibers, myofibrils, and the roles of myofilaments in contraction. Test your knowledge on the key structures and processes involved in muscle function.