Muscle Physiology part 2

Muscle Tissue Types

Three muscle types exist: cardiac (involuntary, heart), smooth (involuntary—intestines, blood vessels, bladder, uterus, eye), and skeletal (voluntary—muscles attached to bones). Each type has unique structure and contraction mechanisms.

Movement Involves Muscle

Muscles generate force to produce movement. Skeletal muscle pulls on bones, smooth muscle changes the shape of hollow organs, and cardiac muscle contracts to pump blood.

Neuromuscular Junction

The functional synapse between a motor neuron and skeletal muscle fiber. Converts electrical signals into chemical signals (ACh), triggering muscle depolarization.

Synaptic End Bulbs

Swollen axon terminal ends containing vesicles filled with acetylcholine (ACh).

Synaptic Cleft

The small extracellular gap between the synaptic end bulb and the muscle fiber's sarcolemma.

Motor End Plate

Folded region of the sarcolemma containing ACh receptors that initiate depolarization upon activation.

Step 1 at Neuromuscular Junction

Nerve impulse arrives at the axon terminal and spreads across the terminal membrane.

Step 2 at Neuromuscular Junction

Voltage-gated Ca2+ channels open, allowing Ca2+ to enter the axon terminal.

Step 3 at Neuromuscular Junction

Synaptic vesicles fuse with the presynaptic membrane and release ACh into the synaptic cleft.

Step 4 at Neuromuscular Junction

ACh diffuses across the cleft and binds to ACh receptors in the motor end plate.

Step 5 at Neuromuscular Junction

ACh receptors open ion channels; Na+ enters and K+ leaves. More Na+ enters than K+ exits, causing depolarization.

Step 6 at Neuromuscular Junction

Acetylcholinesterase breaks down ACh, ending stimulation.

Excitation-Contraction Coupling

Events linking the muscle action potential to contraction, including Ca2+ release and cross-bridge formation.

ECC Step 1

Depolarization spreads from neuromuscular junction across the sarcolemma.

ECC Step 2

Voltage-gated channels open, generating a full muscle action potential.

ECC Step 3

The muscle action potential travels along the sarcolemma and down T-tubules.

ECC Step 4

T-tubule receptors trigger Ca2+ release from the sarcoplasmic reticulum into the sarcoplasm.

ECC Step 5

Ca2+ binds to troponin, shifting tropomyosin and exposing myosin-binding sites on actin.

ECC Step 6

Myosin heads attach to actin, forming cross-bridges initiating contraction.

Sliding Filament Model

Myosin pulls actin filaments toward the M-line, causing sarcomere shortening. H zone and I band shrink; A band remains constant.

Cross-Bridge Formation

Myosin head (ADP + Pi bound) attaches to exposed actin binding site forming a cross-bridge.

Power Stroke

ADP and Pi release; myosin head pivots and pulls actin toward the M-line, generating force.

Cross-Bridge Detachment

ATP binds to myosin, causing it to detach from actin.

Myosin Head Cocking

ATP is hydrolyzed to ADP + Pi, re-energizing the myosin head into its cocked position.

Whole-Muscle Shortening

Thousands of sarcomeres shorten simultaneously, pulling thin filaments inward to produce movement.

H Zone

The central region containing only thick filaments; decreases during contraction.

I Band

Region containing only thin filaments; shrinks during contraction.

A Band

Region containing entire length of thick filaments; remains constant.

Muscle Relaxation Step 1

Acetylcholine broken down by acetylcholinesterase.

Muscle Relaxation Step 2

Ca2+ pumped back into sarcoplasmic reticulum.

Muscle Relaxation Step 3

Low Ca2+ causes troponin-tropomyosin complex to return to original position.

Muscle Relaxation Step 4

Tropomyosin blocks myosin-binding sites; contraction stops.

Cardiac Muscle Structure

Cardiac muscle is striated, branched, interconnected, involuntary, and relies on aerobic respiration. Contains sarcomeres and central nuclei.

Cardiac Cell Branching

Cardiac fibers branch and connect, allowing contraction in one cell to trigger neighboring cells.

Cardiac Cells Pull Against Each Other

Cardiac cells pull against adjacent cells, not bones, relying on strong cell junctions.

Gap Junctions

Connexon protein channels linking cytoplasm of adjacent cardiac cells, allowing rapid ion and electrical signal flow.

Desmosomes

Strong anchoring junctions using cadherins, plaque proteins, and keratin filaments to prevent cells from separating during contraction.

Cadherins in Desmosomes

Transmembrane proteins acting like “Velcro,” attaching cardiac cells firmly together.

Keratin Filaments in Desmosomes

Intermediate filaments anchoring desmosomes and distributing mechanical stress.

Plaque Proteins in Desmosomes

Protein plates reinforcing membrane regions and anchoring desmosomal components.

Intercalated Discs

Specialized regions containing desmosomes, gap junctions, and membrane folds for strong attachment and rapid electrical conduction.

T-Tubules and SR in Cardiac Muscle

One T-tubule per sarcomere paired with SR; coordinates Ca2+ release for contraction.

Cardiac Contraction Mechanism

Depolarization opens Ca2+ channels in SR and cell membrane; extracellular Ca2+ prolongs action potential. Ca2+ binds troponin → contraction begins; relies on aerobic ATP.

Cardiac Self-Excitability

Some cardiac cells spontaneously depolarize, generating rhythmic contractions.

Pacemaker Cells (SA Node)

Self-excitable cells generating regular depolarizations that spread through the atria.

Atrioventricular Node

Delays SA node signal and relays it to ventricles for coordinated contraction.

Conduction Fibers

Fibers that rapidly deliver impulses to ventricular myocardium ensuring synchronous contraction.

Smooth Muscle Arrangement

Smooth muscle forms circular and longitudinal layers around hollow organs, enabling mixing and propulsion.

Smooth Muscle Cell Structure

Spindle-shaped cells with single nucleus, dense bodies, intermediate filaments, caveolae, and gap junctions; lack striations and sarcomeres.

Caveolae

Membrane infoldings containing Ca2+ channels; primary Ca2+ entry sites in smooth muscle.

Dense Bodies

Anchoring points for actin; move closer during contraction, shortening the cell.

Intermediate Filaments

Structural lattice connecting dense bodies and distributing force through the cell.

Smooth Muscle Actin-Myosin Structure

Filaments arranged diagonally; myosin heads along entire thick filament; no troponin present.

Smooth Muscle Contraction

Extracellular Ca2+ enters via caveolae → Ca2+ binds calmodulin → activates myosin kinase → phosphorylates myosin → cross-bridge cycling begins → cell twists and shortens.

Varicosities

Autonomic nerve swellings releasing neurotransmitters broadly across smooth muscle.

Diffuse Junctions

Smooth muscle junctions where neurotransmitters diffuse widely to stimulate multiple cells.

Smooth Muscle Relaxation

Ca2+ pumped into SR and ECF, calmodulin inactivated, myosin dephosphorylated, contraction ends.

Neurotransmitter Regulation

Smooth muscle contraction can be stimulated or inhibited by neurotransmitters like ACh or norepinephrine.

Chemical Regulation

Smooth muscle responds to chemicals such as histamine, high CO2, low pH, and low O2, which alter Ca2+ levels.

Hormonal Regulation

Hormones such as CCK, gastrin, and oxytocin modulate contraction strength and frequency.

Peristalsis

Alternating contraction and relaxation of smooth muscle layers to move substances through lumens (digestive tract, uterus, bladder).