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