Skeletal Muscle Contraction Notes


Skeletal Muscle Contraction

Motor Neuron

Nerve cell that innervates skeletal muscle tissue

Dendrite - 

Receives information

Axon - 

Transmits information, 

Has vesicles containing neurotransmitter that will stimulate or inhibit muscle contraction

Neuromuscular Junction -

Site where branch of motor neuron (motor nerve ending) comes in contact with sarcolemma of skeletal muscle fiber 

A type of synapse

Neuromuscular Junction

Motor end-plate

Sarcolemma of muscle fiber directly beneath motor nerve ending

Contains an abundance of mitochondria and nuclei


Junction between the axonal end of one neuron and the dendrite of another neuron OR membrane of another cell type

Synaptic cleft - Separation that exists between the axonal ending of the motor nerve and the sarcolemma of the muscle cell fiber

The axon ending contains vesicles of neurotransmitter


Chemical substance released from vesicles in the motor nerve ending (axonal ending)

Acetylcholine (Ach) is the neurotransmitter released by motor neurons

When stimulated by a nerve impulse, Ach is released, travels across the synaptic cleft and binds receptors on the motor end plate

Stimulates contraction

Sliding Filament Theory

A sarcomere is the functional unit of skeletal muscle

When a skeletal muscle contracts, sarcomeres shorten

This is described by the sliding filament theory

Sarcomeres shorten because thick and thin filaments slide past one another 

Thin filaments move towards the center of the sarcomere from both ends

Physiology of Skeletal Muscle Contraction: Neurotransmitter Release

Motor impulse is initiated in the brain

Travels through the brain and spinal cord to a motor nerve ending

Motor nerve endings (axons) depolarize

Calcium enters the axonal endings

Calcium causes the release of acetylcholine into the neuromuscular junction (synaptic cleft)

Physiology of Skeletal Muscle Contraction: Depolarization

ACh binds receptors on motor end plate

Depolarizes skeletal muscle fibers

Reverses charge of membrane

Impulse travels through transverse tubules to reach all of the muscle fibers

Muscle depolarization causes release of calcium from the sarcoplasmic reticulum into the sarcoplasm

Physiology of Skeletal Muscle Contraction: Power Stroke

Calcium binds troponin (which is attached to tropomyosin

Moves tropomyosin from the myosin binding sites on actin

Myosin crossbridges (heads) bind to actin

ATP hydrolysis supplies energy

Actin is pulled inward towards the center of the sarcomere = POWER STROKE

Sarcomeres shorten as muscle contracts

The Sliding-Filament Mechanism

With exposure of the myosin binding sites on actin (the thin filaments)—in the presence of Ca2+ and ATP—the thick and thin filaments “slide” on one another and the sarcomere is shortened

Muscle Relaxation Mechanism

1. Acetylcholinesterase present in the NMJ destroys ACh (preventing continual stimulation)

2. Calcium ions are transported from the sarcoplasm back into the SR

3. Linkages between myosin and actin are broken - Requires ATP binding

THEN: The muscle fiber relaxes 

Contraction in the Sarcomere

A band stays the same 

I band gets smaller

H zone gets smaller

Sarcomere shortens

Energy for Contraction

Muscle cells require huge amounts of ATP energy to power contraction

The cells have only a very small store of ATP

Three pathways supply ATP to power muscle contraction

ATP initially supplied from cellular respiration

If ATP is abundant, is converted to creatine phosphate and stored in skeletal muscles

When ATP is low, creatine phosphate supplies phosphate to ADP making ATP

CP & ATP stores only good for about a 10 second maximal contraction

ATP must then come from cellular respiration or glycolysis

Oxygen & Muscle Contraction

Myoglobin of muscle (similar to hemoglobin) binds to and stores oxygen

Supplies O2 needed to make ATP for contraction 

Exercise and Skeletal Muscles

Prolonged, moderate exercise

ATP supplied through cellular respiration

Once glycogen stores are depleted in muscle, glucose and fatty acid deliveries from blood are used as fuel source

Intense, strenuous exercise

Muscles exceed capacity of respiratory and cardiovascular systems to deliver oxygen for contraction

ATP supplied anaerobically through glycolysis

Pyruvate is converted to lactic acid

Lactic acid builds up in muscles

Causes muscles to fatigue

Exercise and Contraction

In intense strenuous activity, oxygen can be depleted

Contraction of skeletal muscles decreases blood delivery to muscles

Nutrient and O2 levels in contracting muscles decrease

Oxygen Debt

Amount of oxygen needed by liver cells to use the accumulated lactic acid to produce glucose

Oxygen not available

Glycolysis continues

Pyruvic acid converted to lactic acid

Liver converts lactic acid to glucose

Also the amount of oxygen needed to replace O2 levels in skeletal muscle to pre-exercise levels

Heat Production

Cellular respiration is only about 40% efficient

About 60% of the energy found in a glucose is lost as heat during cellular respiration

Muscle contraction generates heat because muscles use large amounts of nutrients to make ATP, generating large amounts of heat

Heat is used to maintain body temperature


Glycogenolysis is the breakdown of glycogen into glucose molecules

Epinephrine can trigger this pathyway too

Depends upon the presence of an enzyme – glycogen phosphorylase

McArdle’s Disease

Absence of the muscle glycogen phosphorylase enzyme

Individuals must rely on blood-transported fuels

Fatty acids, protein, glucose from the liver

These reserves take 5-10 minutes to arrive to the mitochondria

Muscles stop functioning until these fuels arrive

Autosomal Recessive Disorder

Symptoms of McArdle’s Disease 

Premature muscle fatigue and weakness and pain during exercise

Muscles can become injured during exercise

The Muscular System & Skeletal Muscle Contraction Notes PDF

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