Histology of Muscle

Skeletal Muscle Tissue

Muscle Histology

• Elongated cylindrical cells = muscle fibers• Plasma membrane = sarcolemma• Transverse (T) tubules tunnel from surface to

center of each fiber• Multiple nuclei lie near surface of cell• Cytoplasm = sarcoplasm

Muscle Histology

• Throughout sarcoplasm is sarcoplasmic reticulum– Stores calcium ions

• Sarcoplasm contains myoglobin– Red pigmented protein related to Hemoglobin that

carries oxygen• Along entire length are myofibrils• Myofibrils made of protein filaments– Come in thick and thin filaments

The Sarcomere

• Filaments overlap in repeating patterns• Unit structure is called sarcomere• Separated by Z discs• Darker area = A band associated with thick

filaments• H zone has no thin filaments• I band has thin filaments no thick filaments

Functional Anatomy

• Thick filament (myosin) has moveable heads (like “heads” of golf clubs)

• Thin filaments (actin) are anchored to Z discs–Contain myosin binding sites for myosin head–Also contain tropomyosin & troponin

• Tropomyosin blocks myosin binding site when muscle is at rest

Sliding Filament Mechanism

• During contraction myosin heads bind actin sites

• Myosins pull and slide actin molecules (and Z discs) toward H zone

• I bands and H zones become more narrow• Sliding generates force and shortens

sarcomeres and thus fibers

Neuromuscular Interaction

• Nerve signal triggers muscle action potential

• Delivered by motor neuron• One neuron can trigger 1 or more fibers at

the same time• Neuron plus triggered fibers = motor unit

Neuromuscular Interaction

• Neuronal ending to muscle fiber = neuromuscular junction (NMJ)

• Synaptic end bulbs (at neuron terminal)–Release neurotransmitter

• Muscular area = Motor end plate• Between is synaptic cleft

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Axon terminal

Axon terminal

Axon collateral ofsomatic motor neuron

Sarcolemma

Myofibril

ACh is releasedfrom synaptic vesicle

ACh binds to Achreceptor

Junctional fold

Synaptic vesiclecontainingacetylcholine(ACh)

Sarcolemma

Synaptic cleft(space)

Motor end plate

Synaptic cleft(space)

(a) Neuromuscular junction

(b) Enlarged view of the neuromuscular junction

(c) Binding of acetylcholine to ACh receptors in the motor end plate

Synapticend bulb

Synapticend bulb

Neuromuscularjunction (NMJ)

Synaptic end bulb

Motor end plate

Nerve impulse

Muscle action potential is produced

Na+

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Action at NMJ

1. Release of acetylcholine (ACh)– Diffuses across cleft

2. Activation of ACh receptors3. Generation of Muscle Action Potential– Repeats with each neuronal action

potential4. Breakdown of ACh

Contraction Trigger

• Muscle action potential → Ca2+ release from Sacroplasmic Reticulum (SR)

• Ca2+ binds to troponin → • Moves tropomyosin off actin sites → • Myosin binds & starts cycle

Contraction Cycle• Myosin binds to actin & releases

phosphate group (forming crossbridges)• Crossbridge swivels releasing ADP and

shortening sarcomere (power stroke)• ATP binds to Myosin → release of myosin

from actin• ATP broken down to ADP & Pi → activates

myosin head to bind and start again• Repeats as long as Ca2+ concentration is

high

Relaxation

• Breakdown of ACh to stop muscle action potentials

• Ca2+ ions transported back into SR lowering concentration →–This takes ATP

• Tropomyosin covers actin binding sites

ACh diffuses acrosssynaptic cleft, bindsto its receptors in themotor end plate, andtriggers a muscle action potential (AP).

Nerve impulse arrives ataxon terminal of motorneuron and triggers releaseof acetylcholine (ACh).

Synaptic vesiclefilled with ACh

ACh receptor Acetylcholinesterase insynaptic cleft destroysACh so another muscleaction potential does notarise unless more ACh isreleased from motor neuron. Ca2+

Muscle action potential

Nerveimpulse

SR

Contraction: power strokesuse ATP; myosin heads bindto actin, swivel, and release;thin filaments are pulled towardcenter of sarcomere.

Troponin–tropomyosincomplex slides back into position where it blocks the myosinbinding sites on actin.

Muscle relaxes.

Ca2+ activetransport pumps

Ca2+ release channels inSR close and Ca2+ activetransport pumps use ATPto restore low level of Ca2+ in sarcoplasm.

Ca2+ binds to troponin onthe thin filament, exposingthe binding sites for myosin.

Muscle AP travelling alongtransverse tubule opens Ca2+

release channels in thesarcoplasmic reticulum (SR)membrane, which allowscalcium ions to flood into the sarcoplasm.

Elevated Ca2+

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Transverse tubule

Muscle Tone

• Even at rest some motor neuron activity occurs = Muscle Tone

• Keeps muscle in a state of readiness• If nerves are cut fiber becomes flaccid

(very limp)

Production of ATP for Muscle Contraction

Aerobic Cellular Respiration

• Production of ATP in mitochondria • Requires oxygen and carbon substrate• Produces CO2 and H2O and heat.

Fatigue

• Inability to contract forcefully after prolonged activity

• Limiting factors can include:–Ca2+

–Creatine Phosphate–Oxygen–Build up of acid–Neuronal failure

Oxygen Use After Exercise

• Convert lactic acid back to glucose in liver

• Resynthesize creatine phosphate and ATP• Replace oxygen removed from myoglobin

Control of Muscle Contraction

• Single action potential(AP) → twitch– Smaller than maximum muscle force

• Total tension of fiber depends on frequency of APs (number/second)–Maximum = tetanus

• Total tension of muscle depends on number of fibers contracting in unison– Increasing numbers = Motor unit recruitment