Muscle physio

Which band of a sarcomere is changing while contraction

I band and H b

I band composition of sarcomere

Only thin filaments

H band composition of sarcomere

only thick filaments

A band composition of sarcomere

entire length of Myosin, overlaping parts counted

Acetylcholine is broken down by Ach Estrase to what

Choline and acetate

what is Lambert Eaton Myasthenic Syndrome (LEMS)?

Presynaptic autoimmune disorder of the NMJ - caused by antibodies against Calcium v gated channels - less Ca+2 - less Ach in the synaptic cleft - less action potential

what are common clinical features of Lambert Eaton Myasthenic Syndrome (LEMS)?

Lower extremities affect - waddling gait, upper extremities - difficulty raising arms

what is Latrotoxin and what is clinical importance regarding

Venom of the black widow spider, stimulates the production of presynaptic cation channels, allowing for a massive influx of Ca2+ without the need for presynaptic depolarisation. localised muscular cramps and stiffness to the bite area followed by whole body effects. ANS problems also relate

Whats botulinum toxin

Protein produced by bacteria Clostridium botulinum, It is a protease that interacts with synatobrevin and other proteins to prevent the exocytosis of ACh. Lack of ACh release leads to lack of muscle activation.

whats Myastenia Gravis (MG)

Myasthenia gravis is an autoimmune disease where auto-antibody target nicotinic receptor (Nm) for destruction. Treatment - Ach Estrase Inhibitors - Incerase Ach levels

Whats the test used to confirm the Myastenia Gravis (MG)

Tensilon test - Edrophnium drug used for the confirmation of diagnosis

Whats Tubocurarin drugs and how they work

Curare plant obtained alkaloid used as a poison. Action: blocks ACh action on the NMJ - no action potential - paralysis

What is the role of DHPR in skeletal muscle?

Voltage sensor — it detects T-tubule depolarization and is mechanically coupled to RyR1. It does not conduct Ca²⁺ into the cell.

What is the role of DHPR in cardiac muscle?

It is a voltage-gated L-type Ca²⁺ channel (Cav1.2) that conducts trigger Ca²⁺ into the cell, which then activates RyR2 via CICR.

Which RyR isoform is found in skeletal muscle? In cardiac muscle?

Skeletal = RyR1; Cardiac = RyR2.

What is the coupling mechanism between DHPR and RyR in skeletal muscle?

Mechanical coupling — direct physical interaction; no Ca²⁺ entry required.

What is the coupling mechanism between DHPR and RyR in cardiac muscle?

Ca²⁺-induced Ca²⁺ release (CICR) — trigger Ca²⁺ from DHPR binds RyR2, opening it.

What is the structure of the tubules and cisternae in skeletal muscle? Where is it located?

Triad = 1 T-tubule + 2 terminal cisternae; located at the A-I junction.

What is the structure of the tubules and cisternae in cardiac muscle? Where is it located?

Diad = 1 T-tubule + 1 terminal cisterna; located at the Z-line.

What are the sources of Ca²⁺ for contraction in skeletal vs. cardiac muscle?

Skeletal = SR only; Cardiac = SR (~90%) + extracellular (~10%).

What is preload

The preload is the resting force on the uncontracted (passive)

muscle.

What is contraction?

Contraction = generation of tension/force with or without shortening of a stimulated muscle.

What is afterload

Afterload - load the muscle works against during a contraction

Explain Isometric contraction

Isometric contraction occurs when the muscle is unable to generate

more than specific amount of force, and the muscle will not shorten

Explain Isotonic contraction

If the muscle is able to generate more than specific amount of force, then the weight

moves as the muscle shortens.

What lets the nuscle be the same lenght during isometric contraction even if the muscles still shorten?

Sarcomeres get shorter during the generation of force in isometric contraction. At the same time, series elastic components are stretched by a total amount equal to the

amount of sarcomere shortening.

What is "trigger Ca²⁺" and which muscle type requires it?

Trigger Ca²⁺ is the small Ca²⁺ influx through DHPR (Cav1.2) that activates RyR2. It is required in cardiac muscle only.

What are the phases of the cardiac action potential?

Phase 0 = rapid depolarization (Na⁺ influx); Phase 1 = early repolarization (K⁺ efflux); Phase 2 = plateau (Ca²⁺ influx via DHPR + K⁺ efflux); Phase 3 = repolarization (K⁺ efflux); Phase 4 = resting potential (Na⁺/K⁺ ATPase).

Why can't cardiac muscle tetanize?

The plateau phase (Phase 2) prolongs the refractory period, which almost equals the duration of contraction — preventing summation and tetanus.

What mechanisms mediate relaxation in skeletal vs. cardiac muscle?

Skeletal = SERCA + parvalbumin; Cardiac = SERCA + Na⁺/Ca²⁺ exchanger (NCX) + sarcolemmal Ca²⁺-ATPase.

How does digitalis (digoxin) increase cardiac contractility?

It inhibits Na⁺/K⁺ ATPase → ↑ intracellular Na⁺ → ↓ Na/Ca+2exchanger activity → ↑ intracellular Ca²⁺ → ↑ contractility.

Muscle relaxation - SERCA pump

Within the SR, Ca2+ is sequestered by Calsequestrin to ensure SERCA

operates in required mode.

Cause of Rigor mortis

Rigor mortis is the temporary stiffening of a body's muscles that happens after death

This happens because of the lack of ATP to unbind the myosin heads

what is Malignant Hyperthermia (MH).

myopathy due to genetic mutations or dysregulation of the Ryanodine receptor (RyR: Ca2+ release channel).

Causes: exposure to volatile inhalational anesthetic agents and the muscle relaxant succinylcholine, and in rare cases exposure to high environmental heat or strenuous exercise.

Mechanism of work: high release of Ca2+ from SR into the muscle fiber. Results in sustained muscle contraction and heat production.

Treatment: Dantrolene - directly interferes with muscle contraction by antagonising RyR

receptors.

V max and different types of muscles

Motor units types

Tetanus

The toxin that is released blocks the release of inhibitory

neurotransmitters, such as γ-aminobutyric acid (GABA).

Inotropism

refers to the force or strength of heart muscle (myocardium) contraction

Positive Inotropes: Increase the strength of cardiac muscle contraction and raise cardiac output.

Negative Inotropes: Decrease the force of cardiac muscle contraction and reduce the heart's workload

PDE-3 inhibitor (Milrinone)

prevents cAMP degradation - increase in cAMP - phosphorylation of the v gated Ca+2 channels - more calcium - stronger contraction - positive inotropism

Activation of Myosin & Crossbridge

Cycling in Smooth Muscle

contraction is dependent on the Ca+2 levels

Ca+2 binds to calmodulin - this complex binds and activates Myosin light chain kinase(MLCK)

MLCK phosphorylates myosin and allows it to bind to actin, thus initiating cross-bridge formation and recycling

Structures or organs that have single unit type of innervation

Uterus, GIT

Structures or organs that have multi unit type of innervation

Large blood vessels, large airways, ciliary

muscle & iris

What does phosphodiesterase does

cleaves out cAMP

Millirone drug

phosphodiesterase inhibitor (PDEi) - inhibits cAMP cleavage

Terbutaline

beta-2 agonist used to relax uterine smooth muscles in pregnant women with premature labor

Albuterol

Beta-2 agonist inhaler is used in Asthma for bronchodilation

Control of smooth muscle contraction

Gq-protein-PLC-IP3 pathway

• Norepinephrine, Epinephrine & Dopamine

(via alpha adrenoreceptors) in vascular

smooth muscles

• Acetylcholine (via M2 receptors) in GIT

• Angiotensin II (via angiotensin II receptors)

in vascular smooth muscles

• Endothelin (via ETA receptors)

Control of smooth muscle contraction - cAMP pathway

• Norepinephrine, Epinephrine (via beta2

adrenoreceptor) in bronchial & uterine

smooth muscles

• Dopamine (via D1 receptors) in renal

vascular muscles

• Histamine (via H2 receptors) in skin

blood vessels

Control of smooth muscle contraction

Ca2+ sensitization and desensitization

• Increased MLCK activity and decreased MLCP activity: Can produce a

stronger contraction even with a lower-than-normal calcium. This is

called calcium sensitization.

• Decreased MLCK activity and increased MLCP activity: Can produce a

weaker contraction even with a higher-than-normal calcium. This is

called calcium de-sensitization.

latch state in smooth muscle

Cross-bridge cycling occurs at a slow rate so that each remains in the

attached state for a longer time with least amount of energy and calcium

usage. Example: blood vessels to maintain BP for the entire life