Muscle – Physiology · FCPS Part 1

Muscle types

Feature	Skeletal	Cardiac	Smooth
Appearance	Striated	Striated	Non-striated
Control	Voluntary	Involuntary	Involuntary
Cell shape	Long, cylindrical	Branched	Spindle-shaped
Nuclei	Multiple, peripheral	Usually 1–2, central	One, central
Sarcomeres	Present	Present	Absent
Intercalated discs	Absent	Present	Absent
Main regulator	Ca²⁺–troponin C	Ca²⁺–troponin C	Ca²⁺–calmodulin–MLCK
T-tubules	Present	Present	Absent; caveolae assist signalling
Main function	Movement and posture	Blood pumping	Visceral movement and vascular tone

Skeletal muscle

The hierarchy is:

Whole muscle → fascicles → muscle fibres → myofibrils → myofilaments

Structure	Description	Function
Whole muscle	Contains multiple fascicles	Produces force and movement
Fascicle	Bundle of muscle fibres	Organises fibres into bundles
Muscle fibre	Long, multinucleated skeletal muscle cell	Contracts in response to stimulation
Myofibril	Repeating series of sarcomeres	Generates contractile force
Myofilaments	Thick and thin filaments	Interact to produce contraction

Connective tissue coverings

Layer	Surrounds	FCPS memory aid
Epimysium	Entire muscle	Epi = entire muscle
Perimysium	Each fascicle	Peri = bundle
Endomysium	Each muscle fibre	Endo = individual fibre

The collagen fibres of these coverings blend with tendon collagen, transmitting muscle force to bone.

Muscle fibre structures

Structure	Function
Sarcolemma	Muscle fibre membrane; conducts action potentials
Sarcoplasm	Cytoplasm containing glycogen, myoglobin, enzymes and organelles
Sarcoplasmic reticulum (SR)	Stores, releases and reaccumulates Ca²⁺
T-tubules	Carry action potentials deep into the muscle fibre
Mitochondria	Generate ATP
Myoglobin	Stores oxygen within muscle
Glycogen	Energy reserve

Sarcomere

The sarcomere is the functional contractile unit of striated muscle, extending from one Z disc to the next.

med.libretexts.org

Sarcomere components

Structure	What it contains / does	During contraction
Z disc	Boundary of each sarcomere; anchors thin filaments	Z discs move closer
I band	Thin filaments only	Shortens
A band	Entire length of thick filaments	Remains constant
H zone	Thick filaments only in the central region	Shortens or disappears
M line	Proteins that hold thick filaments centrally	Remains central
Titin	Elastic protein that stabilises thick filaments	Helps restore resting length

Most tested fact: During contraction, the A band stays constant, whereas the I band and H zone shorten. Actin and myosin filaments slide past each other; they do not themselves shorten.

Thick vs thin filaments

Feature	Thick filament	Thin filament
Main protein	Myosin	Actin
Additional proteins	Myosin light chains	Troponin and tropomyosin
Important function	Generates pulling force	Provides binding sites for myosin
ATPase activity	Myosin head	None in the basic cross-bridge mechanism

Myosin structure

Two heavy chains form the main molecule.
Four light chains are associated with the two heads.
Head: contains ATPase activity and the actin-binding site.
Tail: contributes to the thick filament shaft.
Myosin heads form cross-bridges with actin.

Troponin subunits

Subunit	Function	Memory aid
Troponin C	Binds Ca²⁺	C = Calcium
Troponin I	Inhibits actin–myosin interaction	I = Inhibitory
Troponin T	Binds tropomyosin	T = Tropomyosin

At rest, tropomyosin blocks the myosin-binding sites on actin. When Ca²⁺ binds troponin C, tropomyosin moves and exposes these sites.

Sliding filament mechanism

bio.libretexts.org

Cross-bridge cycle

Step	Event
1. Rigor state	Myosin is tightly attached to actin when no ATP is bound
2. Detachment	ATP binds myosin, causing it to detach from actin
3. Cocking	ATP is hydrolysed to ADP + Pi, energising the myosin head
4. Reattachment	Myosin binds an exposed actin site
5. Power stroke	Pi release triggers the force-generating pivot of the myosin head
6. ADP release	Myosin remains attached until another ATP binds

The cycle repeats while Ca²⁺ remains available and ATP is supplied.

Clinical pearl — rigor mortis: After death, ATP production stops. Myosin cannot detach normally from actin, producing muscle rigidity.

Excitation–contraction coupling in skeletal muscle

This is the link between the electrical signal and mechanical contraction.

quizlet.com

Stage	Event	Key structure
1	Muscle action potential develops	Sarcolemma
2	Action potential travels inward	T-tubules
3	Voltage sensor changes conformation	DHP receptor
4	SR calcium-release channels open	Ryanodine receptor (RyR)
5	Ca²⁺ enters the sarcoplasm from the SR	Terminal cisternae
6	Ca²⁺ binds troponin C	Thin filament
7	Tropomyosin moves, allowing cross-bridge cycling	Actin and myosin
8	Ca²⁺ is pumped back into the SR	SERCA pump

Triad

A skeletal muscle triad consists of:

One T-tubule
Two terminal cisternae of the sarcoplasmic reticulum

FCPS pearl: In skeletal muscle, the DHP receptor acts as a voltage sensor and mechanically couples to RyR1 on the SR to release Ca²⁺.

Relaxation

SERCA pumps Ca²⁺ back into the SR using ATP.
Calsequestrin binds and stores Ca²⁺ inside the SR.
Cytosolic Ca²⁺ falls.
Ca²⁺ dissociates from troponin C.
Tropomyosin re-covers actin-binding sites and contraction ceases.

Skeletal muscle mechanics

Length–tension relationship

Sarcomere condition	Cross-bridge formation	Active force
Optimal resting length	Optimal overlap of actin and myosin	Maximum
Excessive stretching	Reduced overlap	Decreases
Excessive shortening	Filament interference and reduced effective cross-bridge action	Decrease

Term	Definition
Latent period	Time between the muscle action potential and onset of tension
Contraction phase	Tension rises as cross-bridges cycle
Relaxation phase	Tension falls as Ca²⁺ is removed from the cytosol
Wave summation	A new stimulus arrives before complete relaxation, increasing force
Incomplete tetanus	Sustained contraction with fluctuating tension
Complete tetanus	High-frequency stimulation produces fused, sustained tension
Treppe	Progressive increase in twitch force with repeated stimulation after rest

FCPS pearl: Cardiac muscle cannot normally be tetanised because its action potential and refractory period are prolonged.

Types of muscle contraction

Type	Muscle length	Tension	Example
Isometric	Unchanged	Increases	Holding a weight still
Isotonic	Changes	Approximately constant during the movement	Moving a load
Concentric	Shortens	Develops during movement	Lifting a weight
Eccentric	Lengthens while active	Develops during movement	Lowering a weight slowly

ATP sources and fatigue

Energy source	Main role
Stored ATP	Supports only a few seconds of maximal activity
Creatine phosphate	Rapid ATP regeneration during brief, intense activity
Anaerobic glycolysis	Rapid ATP production without requiring mitochondrial oxidative phosphorylation
Aerobic metabolism	Sustained ATP production using oxidative metabolism

Muscle fatigue is multifactorial and may involve metabolite accumulation, ionic changes, altered Ca²⁺ handling and reduced efficiency of excitation–contraction coupling.

Smooth muscle physiology

Structural features

Feature	Smooth muscle
Appearance	Non-striated
Cell shape	Spindle-shaped
Nucleus	One central nucleus
Sarcomeres	Absent
Filament anchoring	Dense bodies and intermediate filaments
Regulatory protein	Calmodulin and MLCK
Troponin	Absent
T-tubules	Absent; caveolae contribute to membrane signalling
Ca²⁺ sources	Extracellular entry and SR release

Single-unit vs multi-unit smooth muscle

Feature	Single-unit (visceral)	Multi-unit
Cell coupling	Many cells connected by gap junctions	Little electrical coupling
Contraction	Coordinated	More independent
Examples	Intestine, uterus, ureter, bladder	Iris and ciliary muscle
Main role	Propulsion and coordinated organ movement	Fine control of specific movements

Vascular smooth muscle has specialised properties and is regulated by autonomic input, local factors and hormones.

Skeletal vs smooth muscle regulation

Feature	Skeletal	Smooth
Ca²⁺ binds	Troponin C	Calmodulin
Main regulatory switch	Exposure of actin-binding sites	Phosphorylation of myosin light chains
MLCK	Not the principal contractile switch	Essential
Ca²⁺ source	Mainly SR in skeletal excitation–contraction coupling	Extracellular entry and SR release
Sustained economical tension	Cross-bridge cycling	Latch state may maintain tension with low ATP use

FCPS pearl: Smooth muscle contraction is controlled primarily through myosin phosphorylation, whereas skeletal muscle contraction is controlled by Ca²⁺ binding to troponin C.

Cardiac muscle physiology

Feature	Key fact
Appearance	Striated, branched cells
Nuclei	Usually one, sometimes two; central
Intercalated discs	Connect adjacent cardiac muscle cells
Gap junctions	Electrical coupling
Desmosomes	Mechanical attachment
Functional syncytium	Electrical activity spreads between cells
Action potential	Prolonged plateau in working myocardium
Plateau mechanism	Sustained inward Ca²⁺ current balanced by outward currents
Excitation–contraction coupling	Extracellular Ca²⁺ entry triggers further Ca²⁺ release from the SR
Regulation	Ca²⁺ binds troponin C
Refractory period	Long, preventing sustained tetanic contraction

Skeletal vs cardiac

Feature	Skeletal muscle	Cardiac muscle
DHP receptor role	Voltage sensor mechanically coupled to RyR1	L-type Ca²⁺ channel allowing Ca²⁺ entry
Trigger for SR Ca²⁺ release	Mechanical coupling to RyR1	Ca²⁺-induced Ca²⁺ release
Extracellular Ca²⁺ entry	Not the primary immediate trigger	Essential trigger
Action potential plateau	Absent	Present in working myocardium
Tetanus	Possible with high-frequency stimulation	Normally impossible due to long refractory period

Cardiac muscle — exam pearls

Question	Answer
Why does cardiac muscle act as a functional syncytium?	Gap junctions
Why can cardiac muscle not be tetanised?	Long refractory period
Main regulator of cardiac contraction?	Ca²⁺–troponin C
What triggers Ca²⁺ release from cardiac SR?	Extracellular Ca²⁺ entry
Major fuel at rest?	Fatty acids are an important major substrate
Does cardiac muscle extract a large proportion of delivered oxygen at rest?	Yes; myocardial oxygen extraction is high

All three muscle types — final comparison

Feature	Skeletal	Cardiac	Smooth
Striations	Yes	Yes	No
Control	Voluntary	Involuntary	Involuntary
Sarcomeres	Yes	Yes	No
Troponin	Yes	Yes	No
Main Ca²⁺ regulator	Troponin C	Troponin C	Calmodulin
MLCK-dependent regulation	Not the main switch	Not the main switch	Yes
T-tubules	Yes	Yes	No
Cell connections	No intercalated discs	Intercalated discs	Gap junctions in many single-unit muscles
AP upstroke	Rapid Na⁺ influx	Na⁺ in working myocardium; Ca²⁺ in nodal cells	Often Ca²⁺-dependent, but varies
Plateau	No	Present in working myocardium	Variable
Contraction speed	Generally fast	Rhythmic and coordinated	Generally slow and sustained
Tetanus	Possible	Not normally possible	Depends on stimulus and tissue