Chapter 11

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Excitability

\-responsiveness to chemical signals, stretch, and electrical changes across the plasma membrane

Conductivity

\-electrical excitation setting off a wave of excitation that travels along the muscle fiber

Contractility

\-shortens when stimulated

Extensibility

\-capable of being stretched between contractions

Elasticity

\-returning to its original rest length after being stretched

Skeletal muscle

\-voluntary, striated muscles usually attached to a bone

striations

\-alternating light and dark transverse bands

Muscle fiber length

\-myofibers are as long as 30m

Connective tissue wrappings

\-endomysium: connective tissue around the muscle cell

\-perimysium: connective tissue around muscle fascicle

\-epimysium: connective tissue surrounding the entire muscle

Tendons

\-attachments between muscle and bone matrix

* continuous with collagen fibers of tendons
* in turn, with the connective tissue of the bone matrix

Collagen

\-is somewhat extensible and elastic

\-stretches slightly under tension and recoils when released

* resists excessive stretching and protects muscle from injury
* returns muscle to its resting length
* contributes to power output and muscle efficiency

The muscle fiber section

skip this shit

Sarcolemma

\-plasma membrane of a muscle fiber

Sarcoplasm

\-cytoplasm of a muscle fiber

Myofibrils

\-long protein cords occupying most of the sarcoplasm

Glycogen

\-carbohydrate stored to provide energy for exercise

Myoglobin

\-red pigment, provides some oxygen needed for muscle activity

Multiple nuclei

\-flattened nuclei pressed against the inside of the sarcolemma

Myoblasts

\-stem cells that fused to form each muscle fiber early in development

Satellite cells

\-unspecialized myoblasts remaining between the muscle fiber and edomysium

* plays a role in regeneration of damaged skeletal muscle tissue

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Mitochondria location

\-packed into spaces between myofibrils

Sarcoplasmic reticulum (SR)

\-smooth endoplasmic reticulum that forms a network around each myofibril

* acts as a calcium reservoir; releases calcium through channels to activate contraction

Terminal cisterna

\-dilated end-sacs of sarcoplasmic reticulum which cross the muscle fiber from one side to the other

T tubules

\-tubular infoldings of the sarcolemma which penetrate through the cell and emerge on the other side

Triad

\-a T tubule and two terminal cisternae associated with it

Myofilaments section

switchin it up now muahahahaha

Thick filaments

\-made of several hundred myosin molecules

* each molecule is shaped like a golf club
* two chains intertwined to form a shaft-like tail
* double globular head

Thin filaments

\-Fibrous (F) actin: two intertwined strands

* string of globular (G) actin subunits each with an active site that can bind to the head of the myosin molecule

Tropomyosin molecules

\-each blocking six or seven active sites on G actin subunits

Troponin molecule

\-small, calcium-binding protein on each tropomyosin molecule

Elastic filaments

\-helps stabilize and position the thick filament

\-prevents overstreching and provides recoil

\-runs through the core of thick filaments and anchors it to the Z disc and M line

\-created by titin

Contractile proteins

\-myosin and actin do the work of contraction

Regulatory proteins

\-tropomyosin and troponin

* acts like a switch that determines when fibers can and cannot contract
* activates fiber by releasing calcium into the sarcoplasm and its binding troponin
* Troponin changes shape and moves tropomyosin off the active sits on actin

Dystrophin

\-clinically important protein that links actin in the outermost myofilaments to membrane proteins that link to the endomysium

\-transfers forces of muscle contraction to connective tissue ultimately leading to the tendon

Stiations section

skip

Striations

\-a result from the precise organization of myosin and actin in cardiac and skeletal muscle cells

\-Alternating A-bands (dark) and I-bands (light)

A-band (anisotropic- different way)

\-darkest part is where thick filaments overlap a hexagonal array of thin filaments

\-H-band- not as dark; in the middle of A-band

\-M line- middle of the H band

I-band (isotropic- same way)

\-lighter bands

\-z-disc- provides anchorage for thin filaments and elastic filaments

* forms zig zags in the middle of the I band

Sarcomere

\-segment from Z disc to Z disc

\-THE functional contractile unit of the muscle fiber

\-muscle cells shorten because their individual sarcomeres shorten

* neither thick nor thin filaments change length during shortening
* think only the amount of overlap changes
* during shortening, dystrophin and linking proteins also pull on extracellular proteins
* transfer pull to extracellular tissue

Structural hierarchy of skeletal muscle (this a big one on god)

muscle

fasicle

muscle fiber

myofibril

sarcomere

myofilaments

^^^^largest to smallest^^^^

That nerve muscle relationship section

S K I P

Nerve-muscle relationship

\-skeletal muscles should never contract unless stimulated by a nerve

\-if nerve connections are severed or poisoned, a muscle is paralyzed

Denervation atrophy

\-shrinkage of paralyzed muscle when nerve remains disconnected

Somatic motor neurons

\-nerve cells whose cell bodies are in the brainstem and spinal cord that serve skeletal muscles

Somatic motor fibers

\-their axons that lead to the skeletal muscle

\-each nerve fiber branched out to a number of muscle fibers

\-each muscle fiber is supplied by only one motor neuron

Motor Unit

\-one nerve fiber and all the muscle fibers innervated by it

Muscle fibers of one motor unit

\-dispersed throughout muscle

\-contracts in unison

\-produce weak contraction over wide area

\-provide ability to sustain long term contraction because they take turns contracting

\-effective contraction usually requires contraction of several motor units at once

What is the average amount of muscle fibers in a motor unit?

\-average motor unit contains 200 muscle fibers

Small motor units

\-fine degree of control (hand and eye muscles)

\-three to six muscle fibers per neuron

Large motor units

\-more strength than control

\-powerful contractions supplied by large motor units with hundreds of fibers

\-example: gastrocnemius has 1,000 muscle fibers per neuron

The neuromuscular section

Skip this flashcard. You are doing great :)

Synapse

\-point where a nerve fiber meets its target cell

Neuromuscular junction

\-when the target cell is a muscle fiber

Nerve fibers

\-stimulates the muscle fiber at several points within the neuromuscular junction

Axon terminal

\-swollen end of the nerve fiber

* contains synaptic vesicles wit acetylcholine

Synaptic cleft

\-gap between axon terminal and sarcolemma

Schwann cell

\-envelops and isolated the neuromuscular junction

Nerve impulse

\-causes the synaptic vesicles to undergo exocytosis releasing ACh into the synaptic cleft

Muscle cell

\-has millions of ACh receptors

\-proteins are incorporated into its membrane

\-junctional folds of sarcolemma beneath axon terminal increase surface area holding ACh receptors

\-lack of these ACh receptors causes weakness in myasthenia gravis

Electrically excitable cells section

\-skip it again

Relation between electricity and muscle fibers

\-muscle fibers and neurons are electrically excitable

* their membranes exhibit voltage changes in response to stimulation

Voltage (electrical potential)

\-a difference in electrical charge from one point to another

Resting membrane potential

\-about -90mV in skeletal muscle cells

* maintained by the sodium-potassium pump

Structure of an unstimulated (resting) cell

\-more anions are present on the inside of the cell

\-these anions make the inside of the plasma membrane negatively charges

\-the plasma membrane is electrically polarized (charged) negatively

\-there are excess sodium cells in the extracellular fluid (the outside)

\-there are excess potassium cells in the intracellular fluid (the inside)

Stimulated (active) muscle fiber or nerve cell

\-Na+ opens up the gates and flows into the plasma membrane

\-Na+flows down into its electrochemical gradient

\-these cations override the negative charges

* this depolarizes the cell

\-after this, the K+ comes back into the cell repolarizing it, causing the cell to go back to its resting potential

Action potential

\-the quick up-and-down voltage shift (depolarization and repolarization)

\-once this happens to one cell, it triggers a domino effect to the cells immediately in front of it

Impulse

\-the wave of excitation occurring after the action potential of cells

Neuromuscular toxins and paralysis

\-Toxins that interfere with synaptic function can paralyze muscles

\-some pesticides contain cholinesterase inhibitors

* causes spastic paralysis, which is a state of continual contraction of the muscles leading to possible suffocation

Tetanus (lockjaw)

\-a form of spastic paralysis caused by toxin clostridium tetani

* glycine in the spinal usually stops motor neurons from producing unwanted muscle contraction, but tetanus blocks glycine release in the spinal cord and causes spastic paralysis

Flaccid paralysis

\-a state in which the muscles are limp and cannot contract

* Curare- competes with ACh for receptor sites, but does not stimulate the muscles
* plant poison in blow darts

Botulism

\-type of food poisoning caused by neuromuscular toxin secreted by the bacterium clostridium botulinum

* this **blocks the release of ACh** causing flaccid paralysis

Four major phases of contraction and relaxation

Excitation- process in which nerve action potentials lead to muscle action potentials

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Excitation-contraction coupling- events that link the action potentials on the sarcolemma to activation of the myofilaments, preparing them to contract

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Contraction- step in which the muscle fiber develops tension and may shorten

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Relaxation- when stimulation ends and returns to its resting length

Length-tension relationship

\-the amount of tension generated by a muscle depends on how stretched or shortened it was before it was stimulated

* The most optimal is in the middle (that sweet spot)

Rigor Mortis

\-hardening of muscles and stiffening of body beginning 3 to 4 hours after death

\-happens because the body stops producing ATP

* peaks about 12 hours after death, then diminishes over the next 48 to 60 hours

Myogram

a chart of the timing and strength of a muscle’s contraction

Threshold

minimum voltage necessary to generate an action potential in the muscle fiber and produce a contraction

Twitch

a quick cycle of contraction and relaxation when stimulus is at threshold or higher

Latent Period

**very brief delay between stimulus and contraction**

* **Time required for excitation, excitation–contraction coupling, and tensing of elastic components of muscle (generating internal tension)**

Contraction Phase

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* **time when muscle generates external tension**
* **Force generated can overcome the load and cause movement**

Relaxation Phase

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* time when tension declines to baseline
* SR reabsorbs Ca+2, myosin releases actin and tension decreases
* Takes longer than contraction

Contraction Strength of Twitches

\-below threshold, there is no contraction

\-at threshold produces a twitch

\-above threshold creates a contraction

\-higher voltages excite more nerve fibers

Isometric Contraction

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* Muscle produces internal tension but external resistance causes it to stay the same length 
* Can be a prelude to movement when tension is absorbed by elastic component of muscle
* Important in postural muscle function and antagonistic muscle joint stabilization

Isotonic Muscle contraction

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* Muscle changes in length with no change in tension
* Concentric contraction: muscle shortens as it maintains tension (example: lifting weight)
* Eccentric contraction: muscle lengthens as it maintains tension (example: slowly lowering weight)

ATP sources

\-All muscle contractions require ATP

\-ATP supply depends of oxygen and organic energy sources availability

Two main pathways of ATP

\-Anaerobic fermentation

\-aerobic respiration

Anaerobic fermentation

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* Enables cells to produce ATP in the absence of oxygen
* Yields little ATP and lactate, which needs to be disposed of by the liver

Aerobic respiration

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* Produces far more ATP
* Does not generate lactate
* Requires a continual supply of oxygen

Immediate energy consumption

* Oxygen is briefly supplied by myoglobin but is rapidly depleted
* Muscles meet most ATP demand by borrowing phosphate groups (Pi) from other molecules and transferring them to ADP

Myokinase

transfers Pi from one ADP to another, converting the latter to ATP

Creatine Kinase

obtains Pi from a phosphate-storage molecule creatine phosphate (CP) and gives it to ADP

Phosphagen system

the combination of ATP and CP which provides nearly all energy for short bursts of activity

Short-term Energy

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* As the phosphagen system is exhausted, muscles shift to anaerobic fermentation
* Muscles obtain glucose from blood and their own stored glycogen
* In the absence of oxygen, glycolysis can generate a net gain of 2 ATP for every glucose molecule consumed
* Converts glucose to lactate

Anaeorbic threshold (lactate threshold)

point at which lactate becomes detectable in the blood

Glycogen-lactate system

The pathway from glycogen to lactate

Long-term energy

\-After about 40 seconds, the respiratory and cardiovascular systems start to deliver oxygen fast enough for aerobic respiration to meet most of muscle’s ATP demand

* after 3-4 minutes the rate of oxygen consumption levels off to a steady state where aerobic ATP production keeps pace with demand


* for 30 minutes energy comes equally from glucose and fatty acids
* Beyond 30 minutes depletion of glucose causes fatty acids to become the more significant fuel

Fatigue and endurance shit

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Muscle fatigue

progressive weakness from prolonged use of muscles

Cause of muscle fatigue

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* __**Potassium accumulation**__ in the T tubules reduces excitability
* __**Excess ADP and Pi**__ slow cross-bridge movements, inhibit calcium release and decrease force production in myofibrils

Low-intensity exercise is though to result from:

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* __**Fuel depletion**__ as glycogen and glucose levels decline
* __**__electrolyte loss__**__ through sweat can decrease muscle excitability
* __**Central fatigue**__ when less motor signals are issued from brain
* Brain cells inhibited by exercising muscles’ release of ammonia

VO2 max :))))))

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* the point at which the rate of oxygen consumption plateaus and does not increase further with added workload
* Proportional to body size
* Peaks at around age 20
* Almost always greater in males than females
* Can be twice as great in trained endurance athlete as in untrained person