Ch. 11 skeletal muscle physiology

excitability (responsiveness)

to chemicals signals, stretch, and electrical changes across the plasma membrane

conductivity

local electrical excitation sets off a wave of excitation that travels along the muscle fiber

contractility

shortens when stimulated (muscles only pull)

extensibility

capable of being stretched between contractions

elasticity

returns to its original rest length after being stretched

skeletal muscle

the voluntary, striated muscle usually attached to bones

* should never contract unless stimulated by a nerve
* if nerve connections are severed or poisoned, a muscle is paralyzed

\

striations

alternating light and dark transverse bands (I band and A bands)

* results from the arrangement of internal contractile proteins

H band

not as dark; middle of A band; thick filaments only

(wrap around M line)

M line

middle of H band

voluntary

usually subject to conscious control

what are the connective tissue wrappings

* endomysium
* perimysium
* epimysium

endomysium

connective tissue around muscle cells

perimysium

connective tissue around muscle fascicle

epimysium

connective tissue surrounding entire muscle

* electrical insulation

tendons

attachments between muscle and bone matrix

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

collagen

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

sarcolemma

plasma membrane of a muscle fiber (cell membrane)

sarcoplasm

cytoplasm of a muscle fiber

myofibrils

long protein cords occupying most of sarcoplasm

* bundles in sarcolemma

glycogen

carbohydrate stored to provide energy for exercise

* more stable

myoglobin

red pigment; provides some oxygen needed for muscle activity

* stored oxygen in muscles

multiple nuclei

flattened nuclei pressed against the inside of the sarcolemma

myoblast

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

* building muscles

satellite cells

unspecialized myoblasts remaining between the muscle fiber and endomysium

* reserve adult stem cell
* play a role in the regeneration of damaged skeletal muscle tissue

mitochondria

packed into spaces between myofibrils

sarcoplasmic reticulum (SR)

smooth ER that forms a network around each myofibril

* terminal cisterns: dilated end-sacs of SR which cross the muscles fiber from one side to the other (voltage changes the size of the holes to be bigger)
* acts as a calcium reservoir it releases calcium through channels to activate contraction

T tubules

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

* access ports to the sarcolemma

triad

a T tubule and two terminal cisterns associated with it

* 3 structures together

thick filaments

made of several hundred myosin molecules

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

heads directed outward in a helical array around the bundle

* heads on one half of the thick filament angle to the left, while heads on other half angle to the right
* bare sone with no heads in the middle

thin filaments

* fibrous (F) actin: two intertwined strands
* string of globular (G) actin subunits each with an active site that can bind to head of myosin molecule
* tropomyosin molecules
* troponin molecules

tropomyosin molecules

each blocking six or seven active sites on G actin subunits

troponin molecules

small, calcium-binding protein on each tropomyosin molecule

* changes shape and pulls tropomyosin

elastic filaments

* titin
* run through core of thick filament and anchors it to the Z disc and M line
* helps stabilize and position the thick filaments
* prevents overstretching and provide recoil

Titin

huge, springy protein that makes elastic filament

* beginning and ending of sarcomere

contractile proteins

myosin and actin do the work of contraction

* pulling z disc together

regulatory proteins

tropomyosin and troponin

(actin or myosin contract)

* act like a switch that determines when fiber can (and cannot) contract
* contraction activated by release of calcium into sarcoplasm and it binding to troponin
* troponin changes shape and moves tropomyosin of the active sites on actin

dystrophin

clinically important protein

* links actin in outermost myofilaments to membrane proteins that link to endomysium
* transfers forces of muscle contraction to connective tissue ultimately leading to tendon
* genetic defects in dystrophin produce disabling disease muscular dystrophy

A band

* darkest part is where thick filaments overlap a hexagonal array of thin filaments
* H band
* M line

I band

* The way the bands reflects polarized light
* Z disc
* bisects I band and “zig-zags”

Z disc

provides anchorage for thin filaments and elastic filaments

sarcomere

segment from z disc to Z disc

* ***functional contractile unit of muscle fiber***
* muscle cells shorten because their sarcomeres shorten
* neither thick nor thin filament change length during shortening (**only the amount of overlap changes**)

what is the structural hierarchy of skeletal muscles

* muscle
* fascicle
* muscle fiber
* myofibril
* sarcomere
* myofilaments

muscle

contractile organ, usually attached to bones by way of tendons

* fascicles and muscles fibers
* supplied with nerve and blood vessels
* enclosed in epimysium

fascicle

bundle of muscle fibers within a muscle

* supplied by nerve and blood vessels
* enclosed in perimysium

muscle fibers

a single muscle cell

* enclosed in specialized plasma membrane (sarcolemma) and endomysium
* bundles of myofibrils and sarcoplasmic reticulum

\

myofibril

* bundle of protein myofilaments with a muscles fiber
* fill most of the cytoplasm
* striated appearance due to orderly overlap of protein myofilaments’

\

myofilaments

* carry out the contraction process
* thick and thin filaments
* shortening the entire muscle

denervation atrophy

shrinkage of paralyzed muscle when nerve remains disconnected

* replace fatty tissue and scar tissue
* spinal cord injury

somatic motor neurons

* voluntary
* nerve cells whose cell bodies are in the brainstem and spinal cord that serve skeletal muscles
* info signals to msucle

somatic motor fibers

* their axons that lead to the skeletal muscle
* each nerve fiber branches out to a number of muscle fibers
* **each muscle fiber is supplied by only one motor neuron**
* multiple to the same muscle

motor unit

one nerve fiber and all the muscle fibers innervated by it

function of muscles fibers of one motor unit

* dispersed throughout muscles
* contract in unison
* produce weak contraction over wide area
* provide ability to sustain long-term contraction as motor units take turns contracting
* effective contraction usually requires contraction of several motor units at once

small motor units

fine degree of control (fine motor skills)

* three to six muscle fibers per neuron
* eye and hand muscles

large motor units

more strength than control

* powerful contractions supplied by larger motor units with hundreds of fibers
* gastrocnemius of calf has 1,000 muscle fibers per neuron

synapse

point where a nerve fiber meets its target cell

neuromuscular junction (NMJ)

when the target cell is a muscle fiber

* each terminal branch of the nerve fiber within the NMJ forms a separate synapse with the muscle fiber
* one never fiber stimulates the muscle fiber at several points within the NMJ

axon terminal

swollen end of nerve fiber

* contains synaptic vesicles with Acetylcholine (ACh)

Synaptic cleft

gap between axon terminal and sarcolemma

Schwann cells

envelops and isolates NMJ

* increases surface area

Acetylcholine (ACh)

nerve impulse causes synaptic vesicles to undergo exocytosis releasing ACh into synaptic cleft

* proteins incorporated into its membrane
* junctional folds of sarcolemma beneath axon terminal increase surface area holding ACh receptors
* lack of receptors causes weakness in myasthenia gravis (not enough ACh)

why are 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 -90 mV in skeletal muscles cells

* maintained by sodium - potassium pump

What is in an unstimulated (resting) cell

* there are more anions (negatively charged particles) on the inside of the membrane than on the outside
* these anions make the inside of the plasma membrane negatively charged by comparison to its outer surface
* the plasma membrane is electrically polarized (charged) with a negative resting membrane potential (RMP)
* there are excess sodium ions in the extracellular fluid (ECF)
* there are excess potassium ions in the intracellular fluid (ICF)

depolarization

inside of the plasma membrane becomes positive

steps of depolarization: stimulated (active) muscle fiber or nerve cell

* Na+ on gates open in the plasma membrane
* Na+ flows into the cell down its electrochemical gradient
* these cations override the negative charges in the ICF

steps of repolarization

* immediately, Na+ gates close and k+ gates open
* K+ rushes out of cell partly repelled by positive sodium charge and partly because of its concentration gradient
* known as action potential

repolarization

loss of positive potassium ions turns the membrane negative again

action potential

* point causes another one to happen immediately in front of it, which triggers another one a little farther along as so forth (aka impulse)
* quick up-and-down voltage shift (depolarization and repolarization)
* perpetuates itself down the length of a cell’s membrane

\

resting membrane potential (RMP)

seen in a waiting excitable cell, whereas action potential is a quick event seen in a stimulated excitable cell

spastic paralysis

a state of continual contraction of the muscle; possible suffocation

how does cholinesterase inhibitors work

bind to acetylcholinesterase and prevents it from degrading Ach

tetanus

(lockjaw) is a form of spastic paralysis causes by toxin

* glycine is the spinal cord normally stops motor neurons from producing unwanted muscle contraction
* tetanus toxin blocks glycine release in the spinal cord and causes overstimulation and spastic paralysis of the muscles

flaccid paralysis

a state in which the muscles are limp and cannot contract

* because it can’t get to the sarcolemma
* curare

\

curare

competes with Ach for receptor sites, but does not stimulate the muscle

botulism

type of food poisoning causes by a neuromuscular toxin secreted by the bacterium

* blocks release of Ach causing flaccid paralysis
* no signal to muscles
* botox

what are the 4 phases of contraction and relaxation of muscle fibers

* excitation
* excitation-contraction coupling
* contraction
* relaxation

excitation

process in which nerve action potentials lead to muscles action potential

* signal to muscle fiber

excitation-contraction coupling

events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract

* t-tubules to release calcium to move to sarcomere

contraction

step in which the muscle fiber develop tension and may shorten

* calcium to troponin and tropomyosin and start to contract

relaxation

when stimulation ends, a muscle fiber relaxes and returns to its resting length

* calcium will be pulled and stored in the sarcoplasmic reticulum

length-tension relationship

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

function of length-tension relationship

* if overly shortened before stimulated, a weak contraction results, as thick filaments just butt against z discs
* if too strethed before stimualted, a weak contraction results, as minimal overlap between thick and thin filaments results in minimal cross-bridge formation
* optimal resting length produces greatest force when muscle contract. small overlap between myofilaments
* the nervous system maintains muscle tone (partial contraction0 to ensure the resting muscle are near this length

rigor mortis

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

* deteriorating sarcoplasmic reticulum releases Ca
* deteriorating sarcolemma allows Ca to ender cytosol
* Ca activates myosin-actin cross-bridging
* muscle contracts, but cannot relax

muscle relaxation

muscle relaxation requires ATP, and ADP production is no longer produced after death

fibers remain contracted until myofilaments begin to decay

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

* mechanical depolarization with force can be cramps from a punch

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

time when muscle generated external tension

* force generated can overcome the load and cause movement

relaxation phase

time when tension declines to baseline

* SR reabsorbs Ca, myosin releases actin and tension decreases
* takes longer than contraction
* twitch duration is 7 for fast and 100 for slow

what happens with subthreshold stimuli

no contraction at all

even if the same voltage is delivered, differnet stimuli cause twitches varying in strength, because…

* the muscle’s starting length influences tension generation
* muscle fatigue after continual use
* warmer muscles enzymes work more quickly
* muscles cells hydration level influence cross-bridge formation

stimulating the never with higher volatge produces stronger contractions and…

* higher voltage excite more nerve fibers which stimulate more motor units to contract
* more motor units come pay with stronger stimuli
* occurs according to the size principle: weak stimuli (low voltage) recruit small units, while string stimuli recruit small and large units for powerful movement

low frequency

stimuli produce identical twitches

higher frequency

stimuli produce temporal (wave) summation

* each new twitch rides on the previous one generating higher tension
* only partial relaxation between stimulus resulting in fluttering, incomplete tetanus

unnaturally high stimulus frequencies

(in lab experiments) causes a steady, contraction called complete (fused) tetanus

isometric

* muscles contraction “same length”
* muscles 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
* pushing against the wall, muscles don’t change

isotonic

* muscle contraction “same tension”
* muscle changes in length with no change in tension
* concentric contraction
* eccentric contraction

concentric contraction

muscle shortens as it maintains tension

* lifting weights