Muscle Physiology Quiz

Physiology of Muscle

• Muscles are tissues that shorten and develop tension, leading to movement.
• Muscles are categorized into:
  • Striated muscles (skeletal and cardiac), characterized by alternating light and dark bands.
  • Smooth muscles, lacking distinguishing surface features.
• Skeletal muscles make up approximately 40% of the body, smooth muscles 10%.

Muscle Cells

• Skeletal, cardiac, and smooth muscles are depicted in Fig 35.

Skeletal Muscles

• Skeletal muscles are connected to bones, over 400 in the human body.
• Their contraction is controlled by nerve supply.
• Major functions of skeletal muscles:
  • Force production for locomotion and breathing.
  • Force generation for posture maintenance and stabilizing joints.
  • Heat production
  • Assisting in venous return.

Morphology of Skeletal Muscle

• Skeletal muscle is made of muscle fibers bundled by connective tissues, arranged in parallel.
• Each muscle fiber (a single cell) is encased by a sarcolemma.
• Myofibrils, composed of thick myosin and thin actin filaments, comprise muscle fibers.
• The arrangement of these protein filaments creates the striated appearance.
•  Sarcomeres are functional units within the myofibrils. They are divided by transverse protein sheets called Z lines.

Muscle Protein: Myosin

• Myosin is a protein comprised of two heavy chains and four light chains.
• The terminal portions of the heavy chains, along with light chains, form cross-bridges.
• Cross-bridges have hinge points for flexibility.

Muscle Protein: Actin

• Actin is a protein formed by two coiled chains.
• Tropomyosin molecules cover the active sites on actin at rest.
• Troponin molecules are globular proteins that attach tropomyosin to actin.
• Troponin is comprised of three components: Troponin I (affiinity for actin), Troponin T (affinity for tropomyosin) and Troponin C (affinity for Ca²⁺).
• Ca²⁺ binding to troponin C initiates the contraction process.

Neuromuscular Transmission

• Definition: Transmission of nerve impulses from alpha motor neurons to skeletal muscle fibers.
• Physiologic anatomy of neuromuscular junction: the alpha motor neuron branches as it approaches the muscle, sending axon terminals to several skeletal muscle fibers.
• Acetylcholine (Ach): transmits impulses across the synaptic cleft, the space between axon terminals & the muscle membrane.
• Motor-end plate (MEP): the muscle membrane under the nerve terminals is thickened with numerous receptors.
• Synaptic cleft: the extracellular space between the nerve terminals and the muscle membrane, containing basal lamina with acetylcholinesterase.

Sequence of Events during Neuromuscular Transmission

• Arrival of nerve impulses at nerve endings opens voltage-gated Ca²⁺ channels.
• Ca²⁺ entering the nerve endings triggers the release of acetylcholine into the synaptic cleft.
• Acetylcholine binds to its receptors on the motor end plate (MEP), initiating sodium influx and depolarization, creating the end-plate potential (EPP).
• EPP triggers action potentials in the muscle fiber, leading to muscle contraction.
• Acetylcholinesterase in the synaptic cleft hydrolyzes acetylcholine, preventing multiple muscle contractions.
• New vesicles are formed from presynaptic membrane invaginations to be refilled with acetylcholine for future use.

Properties of Neuromuscular Transmission

• Unidirectional: it travels only from nerve to muscle.
• Delay of about 0.5 milliseconds (msec): represents time for acetylcholine release, membrane permeability change, sodium influx and depolarization to the firing level.
• Fatigued easily: due to repeated stimulation and exhaustion of acetylcholine vesicles.
• Effect of ions (Ca²⁺ and Mg²⁺): Ca²⁺ entry into end feet triggers acetylcholine release, while Mg²⁺ competes with Ca²⁺ reducing acetylcholine release.

Effect of Drugs on Neuromuscular Transmission

• Some drugs stimulate neuromuscular transmission like methacholine, carbachol, and nicotine (in small doses).
• Others (neostigmine, physostigmine, di-isopropyl fluorophosphate) block acetylcholinesterase, allowing acetylcholine to accumulate and excessively stimulate the muscle.
• Curare-like drugs block neuromuscular transmission by competing with acetylcholine for receptor sites.

Myasthenia Gravis

• Autoimmune disease causing skeletal muscle weakness and fatigue.
• Antibodies against acetylcholine receptors impair neuromuscular transmission.
• Treatment involves anticholinesterase drugs to increase acetylcholine levels.

Miniature End-Plate Potential

• At rest, spontaneous rupture of few vesicles containing acetylcholine occurs at the motor end plate, producing a minute depolarization.

Changes Following Skeletal Muscle Stimulation

• Electrical events in skeletal muscle are similar to nerve but with slight differences. The resting membrane potential is −90 mV, and action potentials last 2-4 milliseconds.
• Action potentials precede contraction by about 2 milliseconds.
• Excitability changes during action potentials temporarily make the muscle refractory to restimulation until excitability has been regained.

Mechanical Changes Following Skeletal Muscle Stimulation:

• Molecular mechanism of muscle contraction (excitation-contraction coupling): Action potentials initiate the contractile process.

Release of Calcium

• Action potential propagation into T tubules opens Ca²⁺ channels in terminal cisternae.
• Ca²⁺ flows into the cytoplasm.

Activation of Muscle Proteins

• Ca²⁺ binds to troponin C on actin, which induces a conformational change in tropomyosin, exposing myosin-binding sites on actin.
• Myosin cross-bridges attach to actin, leading to sliding filaments and contraction.

Generation of Tension

• Muscle contraction generates tension.
• Binding of actin and myosin is followed by bending of cross-bridges and sliding of actin filament past myosin.
• ATP hydrolysis provides energy for this process.
  • Detachment of cross-bridges from actin happens when new ATP molecules bind to myosin.

Relaxation

• Removal of Ca²⁺ from the cytoplasm by the Ca²⁺ pump in the sarcoplasmic reticulum.
• Troponin returns to its normal shape.
• Tropomyosin resumes blocking the myosin-binding sites on actin and cross-bridge cyclin stops as a result, the muscle relaxes.

All-or-none and Twitch Relationship

• The all-or-none law states that a single muscle fiber contracts maximally or not at all upon stimulation.
• A twitch is a brief contraction followed by relaxation resulting from a single action potential.
• The twitch begins about 2 milliseconds following membrane depolarization.

Types of Skeletal Muscle Contractions

• Isometric contractions: generate tension but there is no change in muscle length (e.g., holding a heavy weight).
• Isotonic contractions: cause a change in muscle length while the tension stays constant (e.g., lifting a weight).

Factors Affecting Skeletal Muscle Contraction

• Muscle types: Type I (slow-twitch) and type II (fast-twitch) fibers have varied properties which affect how they perform.
• Stimulus factors(grading of muscle contraction): the frequency and strength of stimulus affects the intensity of contraction.

Smooth Muscles

• Smooth muscles function involuntary in organs like blood vessels, viscera, and other internal passageways regulating material movement.
• There are two types of smooth muscle: single-unit smooth muscle and multi-unit smooth muscle.
• The characteristics of smooth muscle differ from skeletal muscle structure. For example, smooth muscle lacks striations (or sarcomeres).

Structure of Smooth Muscle

• Filaments are arranged without sarcomeres and lack striations (or sarcomeres).
• The sarcoplasmic reticulum is poorly developed (compared to skeletal muscle) Smooth muscle cells have relatively few voltage-gated calcium channels.
• No troponin; instead, calmodulin protein is present.

Electrical Activity of Smooth Muscle

• Membrane potentials in smooth muscle are unstable, averaging -50 to -60 mV with fluctuations (slow waves).
• Action potentials can occur in two forms: spike potentials (similar to the form in skeletal muscle) and action potentials with plateaus (prolonged depolarization phase used for prolonged muscle contraction).
• Depolarization primarily results from changes in intracellular Ca²⁺ concentrations, which is slower compared to skeletal/cardiac muscle activity.

Role of Calcium in smooth muscle Action Potentials

• Ca⁺² influx is usually responsible for the smooth muscle action potential.
• Ca²⁺ binds to calmodulin, which activates myosin light-chain kinase (MLCK).
• MLCK phosphorylates myosin and this results in ATP hydrolysis and cross-bridge cycling, triggering muscle contraction. 
• Relaxation occurs when intracellular Ca²⁺ concentration decreases, allowing for dephosphorylation of myosin and ending the cross-bridge cycle.

Role of Nerve Supply in Smooth Muscle

• Smooth muscle has a dual autonomic nerve supply.
• The nerve supply does not initiate smooth muscle activity but rather modulates it through influences on spontaneous activity and sensitivity to chemical agents.

Factors Affecting Contraction of Smooth Muscles

• Stretch
• Local factors (e.g., acids, alkalis, pH fluctuations, oxygen availability)
• Temperature influences contraction
• Chemical mediators.

Test your knowledge on muscle physiology and functions with this quiz. Explore various aspects such as muscular hypertrophy, types of muscles, and electrical activity in muscles. Challenge yourself with specific questions related to muscle fibers and their components.