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Neuromuscular Junction

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Motor Unit

one motor neuron all the skeletal muscles it stimulates

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Fine Muscle Control

few muscle fibers stimulated by one motor neuron

single motor neuron may supply very few fibers (eye)

Result:

- finer control of muscle fibers

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Coarse Muscle Control

many muscle fibers stimulated by one motor neuron

single motor neuron may supply many fibers (large muscle)

Result:

- less control of muscle fibers

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Neuromuscular Junction

contact or junction between motor neuron and a skeletal muscle

- thread-like extensions of neuron branch into many axonal terminals

- each branch forms a junction with sarcolemma (one muscle fiber)

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Nerve Endings

individual branches of axon near muscle fiber loose myelin sheath

divide into several bulb-shaped structures (synaptic end bulb)

- bulbs contain neurotransmitter acetylcholine (ACh)

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Nerve Endings

extremely close to muscle but never touch

space is called synaptic cleft

- filled with interstitial fluid

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Motor End Plate

portion of muscle fiber membrane adjacent to synaptic end bulb of motor neuron

contains receptors for acetylcholine

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Polarization

muscle fiber relaxed (resting sarcolemma) outside sarcolemma + charge

(predominant extracellular ion is Na+) inside sarcolemma - charge

(predominant intracellular ion is K+) sarcolemma is relatively impermeable to

both ions

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Depolarization(generation of the action potential)

stimulation of sarcolemma by motor nerve patch of sarcolemma becomes permeable to

sodium ions (sodium gates open) + sodium ions rush into cell inside sarcolemma + charge outside sarcolemma - charge this rush upsets electrical currents causing

action potential

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Propagation of the Action Potential

+ charge inside sarcolemma changes permeability of adjacent patches on sarcolemma

depolarization is repeated

- therefore action potential spreads along entire length of sarcolemma

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Repolarization

events occur in reverse sarcolemma permeability changes Na+ gates close K+ gates open allowing diffusion of K+ ions

out of cell activation of sodium-potassium pump

restores ionic resting state concentrations

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Repolarization (cont.)

occurs in same direction as depolarization

must occur before muscle can be stimulated again

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Sequence of Events of Muscle Stimulation

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Muscle Stimulation

muscle fibers are stimulated by motor neurons

impulse arrives at axon terminal of motor neuron

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Muscle Stimulation (cont.)

impulse depolarizes plasma membrane opening voltage-sensitive calcium channels (Ca+2)

calcium ions diffuse from extracellular fluid into the axon terminal

- triggers release of acetylcholine from synaptic end bulb

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Muscle Stimulation

ACh diffuses across synaptic cleft ACh interacts with receptors in the motor

end plate of the muscle fiber, thus altering its permeability to sodium ions (Na+)

sodium ions diffuse from extracelluar fluid into muscle fiber, producing local depolarization called end-plate potential

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Muscle Stimulation(power stroke)

end-plate potential generates flow of ions or current to bring adjacent sarcolemma to threshold

current spreads in both directions triggering action potentials

action potential initiate wave of contraction by way of transverse tubules

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Muscle Stimulation (power stroke) (cont.)

action potential triggers release of Ca+2 from sarcoplasmic reticulum

Ca+2 ions bind to troponin molecules on the thin filaments

tropomyosin moves, uncovering cross-bridge binding sites on actin

binding of actin and myosin causes ATP to split releasing energy for the power stroke

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Muscle Stimulation (power stroke) (cont.)

rotational movement of a myosin cross-bridge

one power stroke of a cross-bridge results in a small movement of the thin filament

each cross-bridge produces many cycles of movement during a single twitch contraction

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Muscle Stimulation (power stroke) (cont.)

acetylcholine is quickly decomposed by cholinesterase

its decomposition prevents generation of further end-plate potentials

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Sliding Filament Mechanism

during muscle contraction, neither the thick nor the thin filaments decrease in length

the actin (thin) filaments slide like pistons inward among the myosin (thick) filaments

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Sliding Filament Mechanism

(cont.) in the resting state, the ends of the actin

barely overlap the myosin during contraction, these ends overlap

considerably while the two Z membranes approach the ends of the myosin filaments

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Myosin

has globular bridges

Ca+2 ions help cross bridges react with actin

Actin

ADP molecules on surface act as sites for linkages with cross bridges

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Sources of Energy

phosphate system glycogen-lactic acid system aerobic system

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Phosphate System

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Phosphate System

ATP and creatine phosphate together they provide energy for

muscles to contract maximally for approximately 15 seconds

this system is used for short bursts of energy

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Energy Source for Muscle Contraction

immediate source is ATP (adenosine triphosphate)

supplied by mitochondria near myofibrils enzyme ATPase splits a phosphate group

from ATP, forming ADP (adenosine diphosphate) and P (phosphate group)

energy released when P is split from molecule of ATP activates myosin cross-bridges

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Energy Source for Muscle Contraction

very little ATP present in muscle fibers if exercise is to continue for more than a

few seconds, additional ATP must be produced

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primary energy source available to regenerate ATP from ADP and phosphate is creatine phosphate

contains high-energy phosphate bonds cannot directly supply energy to a cell 3-5 times more abundant in muscle fibers

than ATP

Energy Source for Muscle Contraction

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Creatine Phosphate

stores energy released from mitochondria when sufficient ATP is present, creatine

phosphokinase (enzyme) promotes synthesis of creatine phosphate

energy is stored in its phosphate bonds when ATP is being decomposed, energy

from CP is transferred to ADP and then quickly converted back to ATP

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Glycogen-Lactic Acid System

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Glycogen-Lactic Acid System

with continued activity, muscles require energy after the supply of creatine phosphate is depleted

glucose must be catabolized to generate ATP

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Glycogen-Lactic Acid System

glucose passes into contracted muscles via blood (facilitated diffusion)

glucose is also produced by glycolysis (breakdown of glycogen in muscles)

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Glycolysis

series of ten reactions splits glucose into two molecules of

pyruvic acid and two molecules of ATP anerobic process (no oxygen)

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Glycogen-Lactic Acid System

pyruvic acid formed by glycolysis enters mitochondria

- its oxidation produces large quantities of ATP from ADP

some activities do not supply enough O2 to completely break down pyruvic acid

pyruvic acid is then converted to lactic acid

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Glycogen-Lactic Acid System (cont.)

most lactic acid diffuses from skeletal muscles into the blood

heart muscle fibers, kidney cells and liver cells use lactic acid to produce ATP

liver cells can convert lactic acid back to glucose

some lactic acid is accumulated in blood and muscles

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Glycogen-Lactic Acid System (cont.)

can provide energy for about 30-40 seconds of maximal muscle activity, e.g., a 50 meter swimming race

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Aerobic System

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Aerobic System

reactions that require oxygen carried by the blood

oxygen is bonded to molecules of hemoglobin

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Cellular Respiration

when energy is exhausted, muscles become dependant upon cellular respiration of glucose as a source of energy for synthesis of ATP

muscle activity longer than 30 seconds requires an aerobic process

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Aerobic System

conversion of pyruvic acid into CO2, H20, and ATP

yields 36 molecules of ATP from each glucose molecule

provides energy for muscular activity lasting longer than 30 seconds

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Recovery Oxygen Consumption (oxygen debt)

elevated oxygen use after exercise above resting oxygen consumption elevated oxygen necessary to restore

metabolic conditions to resting state

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Recovery Oxygen Consumption

converts lactic acid back into pyruvic acid

reestablishes glycogen stores in muscle and liver cells

resynthesizes creatine phosphate and ATP

replaces O2 removed from myoglobin

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Recovery Oxygen Consumption (cont.)

ATP production for metabolic reactions (increased rate due to increased body temperature)

ATP production for continued elevated activity of cardiac and skeletal muscles

ATP production needed for an increased rate of tissue repair

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Muscle Fatigue(inability of a muscle to contract)

Condition may result from:

- insufficient O2 delivered to muscle cells

- depletion of glycogen stored in muscle cells

- buildup of lactic acid in body fluids

- insufficient acetylcholine