anatomy & physiology muscles

muscle tissue

muscle cells specialized for contraction

skeletal muscle

organ made of skeletal muscle tissue, connective tissue, nerves, and blood vessels

skeletal muscle functions

1. produce body movement
2. maintain posture
3. support soft tissues
4. guard body entrances/exits
5. maintain body temp
6. store nutrients

skeletal muscle tissue

produce movement by pulling on bone

* voluntary

cardiac muscle tissue

pumps blood and circulates it in vessels

* involuntary

smooth muscle tissue

walls of hollow organs and small arteries

* involuntary

epimysium

dense sheath of collagen fibers around muscle that separates muscle from other tissues/organs

muscle fascicle

bundle of muscle fibers

perimysium

fibrous layer dividing muscle into fascicles

skeletal muscle fibers

individual muscle cells

myofibrls

bundles of protein filaments

endomysium

thin layer of areolar connective tissue around each muscle fiber

myosatellite cells

stem cells that help repair damaged muscle tissue

tendon

attached muscle to specific point in a bone

aponeurosis

broad sheet with broad bone attachments

myoblasts

embryonic cells that fuse to form multinucleate cells that differentiate into skeletal muscle fibers

sarcolemma

plasma membrane

sarcoplasm

cytoplasm

myofibrl

small cylindrical structures arranged parallel inside muscle fiber

sarcomeres

repeating functional units of skeletal muscle fibers

striations

z lines, I band, A band, M line, H band

Z lines

junction of adjacent sarcomeres

* protein connect thin filaments of adjacent sarcomeres (actinins)

I band

lighter band with only thin filaments (actin)

A band

dark/dense region containing thick filaments (myosin)

M line

center of A band where adjacent thick filaments connect

H band

lighter region on each side of M line with only thick filaments

zone of overlap

within A band, overlapping thick/thin filaments

myofilaments

bundles of protein filaments inside myofibrls

thin filament

mostly composed of actin

thick filaments

mostly composed of myosin

transverse tubules

form passageways through muscle fiber and encircle sarcolemma

sarcoplasmic reticulum

similar to smooth ER

terminal cisternae

enlarged sections on either side of T tubule

triad

pair of terminal cisternae and one T tubule

thin filaments structure

attached to z lines by actinin

F-actin

twisted double strand of G-actin

* G-actin molecules have active site for binding myosin

Nebulin

holds two strands of G-actin molecules together

tropomyosin

double stranded protein wrapped around F-actin

* blocks myosin binding sites on G-actin molecules
* prevents actin/mysoin interaction
* blocks muscle contractions

thick filaments structure

* contains \~300 myosin molecules
* titin core

titin core

connects thick filaments to Z lines and recoils after stretching

sliding filament theory

when muscles contract, thin filaments slide over thick filaments

* H & I bands get smaller, zones of overlap get larger
* Z lines move closer together, A band is unchanged
* sliding occurs in all sarcomeres in each myofibrl

membrane potential

unequal distribution of changes on either side of plasma membrane = potential difference

* exists because plasma membrane contains leak channels that are always open (K+ & Na+)

chemical gradient

concentration gradient for an ion across the plasma mebrane

electrical gradient

created by the attraction between opposite charges and repulsion of like charges

electrochemical gradient

chemical & electrical gradient

action potential step 1

small increase in membrane permeability to Na+

* Na+ entering cell moves membrane potential positive to threshold -55mV

action potential step 2

voltage gated Na+ channels open

* rush of positive Na+ ions into cell
* depolarization: change of membrane potential to positive

action potential step 3

membrane potential reaches to +30 mV

* Na+ channels close
* K+ channels open & K+ leaves cells
* repolarization: membrane potential returns to polarized state

action potential step 4

repolarization continues to hyperpolarization

action potential step 5

membrane potential stabilizes

* K+ channels close at resting potential
* Na+/K+ pump restores original distribution
* refractory period: time needed to reach original distribution
* membrane cannot respond to another stimulus until after refractory period

neuromuscular junction

location where motor neuron controls a skeletal muscle fiber

* there’s one NMJ per muscle fiber
* a motor neuron may control multiple muscle fibers

axon terminal (synaptic terminal) of motor neuron

contains vesicles with Acetylcholine (ACh)

motor end plate of muscle fiber

* has junctional folds that increase # of ACh receptors
* contains Acetylcholinesterase (AChE)
* breaks down ACh

synaptic cleft

space between axon terminal and motor end plate

neuromuscular junction action step 1

electrical impulse arrives at axon terminal

* change in membrane permeability causes ACh vesicles to fuse with neuron plasma membrane
* ACh released (exocytosis)

neuromuscular junction action step 2

ACh diffuses across synaptic cleft

* binds ACh receptor membrane channels at motor end plate
* changes sarcolemma Na+ permeability\\
* Na+ enters muscle fiber sarcoplasm

neuromuscular junction action step 3

Na+ influx generates action potential in sarcolemma

* ACh diffuses away or breaks down (AChE)
* ACh receptor membrane channels close

neuromuscular junction action step 4

action potential generated at motor end plate immediately spreads across sarcolemma

* ACh cleared from receptor
* no other stimulus occurs until AP occurs

neuromuscular junction action step 5

action potential moves down T tubules between terminal cisternae of sarcoplasmic reticulum

* changes permeability of SR

neuromuscular junction action step 6

sarcoplasmic reticulum releases stored Ca2+ into sarcomeres and begins contractions

* excitation contraction coupling: action potential is coupled with contraction

muscle fiber contraction cycle step 1

resting sarcomere

* myosin heads are energized or “cocked”
* cocking head requires breakdown of ATP

muscle fiber contraction cycle step 2

contraction cycle begins

* calcium ions arrive from sarcoplasmic reticulum

muscle fiber contraction cycle step 3

active sites exposed

* calcium binds to troponin
* troponin changes position, moves tropomyosin and exposes active sites on actin

muscle fiber contraction cycle step 4

cross-bridges form

* myosin heads bind to exposed active sites on actin
* forms cross-bridges

muscle fiber contraction cycle step 5

myosin heads pivot

* cross-bridge formation causes myosin heads to pivot toward M line (center of sarcomere)
* power stroke
* ADP and P release

muscle fiber contraction cycle step 6

cross-bridges detach

* a new ATP attaches to each myosin head, myosin releases from actin
* released energy used to recock myosin head

troponin

protein or protein complex that assists is skeletal muscle contractions

* promotes muscle contractions

mV

threshold: -55 mV

depolarizatiom: +30 mV

resting: -85 mV

muscle twitch

single stimulus contraction relaxation sequence in a muscle

fasciculation

involuntary muscle twitch under skin

motor unit

group of muscle fibers controlled by single motor neuron

myogram

shows development of muscle tension

muscle twitch phase 1

latent period

* action potential stimulates sarcolemma
* calcium released from sarcoplasmic reticulum
* no tension yet

muscle twitch phase 2

contraction phase

* calcium binds to troponin
* cross-bridge cycling
* start of tension development to peak tension

muscle twitch phase 3

relaxation phase

* calcium drops; cross-bridges detach; active sites covered
* tension returns to resting level
* from peak tension to end of twitch

peak tension

depends on the frequency of stimulation and the number of muscle fibers stimulated

treppe

stimulation of muscle fiber immediately after relaxation phase produces increasing maximum tension

wave summation

addition of one twitch to another

* stimulation of muscle fiber before relaxation phase ends produces increasing maximum tension

incomplete tetanus

rapid cycle of contraction/relaxation producing near peak tension

complete tetanus

higher stimulation frequency eliminates relaxation phase

* results in peak tension
* no calcium ions return to SR

motor unit recruitment

activation of more motor units to produce more tension

* smaller motor units activated first, then large motor units
* smooth, steady increase in muscle tension

asynchronous motor unit summation

motor units activated on rotating basis to maintain sustained contractions

muscle tone

resting tension in skeletal muscle

isotonic contractions

tension rises and skeletal muscle length changes

* concentric contractions
* eccentric contractions

concentric contraction

muscle tension rises until it exceeds load

* as muscle shortens, tension remains constant
* ex: flexing elbow while holding dumbell

eccentric contraction

peak tension produced is less than the load; muscle lengthens

* ex: returning dumbell from flexed position to extended

glycolysis

anaerobic breakdown of glucose to pyruvate

* occurs in cytosol
* oxygen in cytosol
* produces 2 ATP & pyruvate molecules for each glucose

aerobic metabolism

* produces 95% of ATP demands of resting cell
* occurs in mitochondria
* produces 15 ATP for each pyruvate
* ATP comes from electron transport chain

glycogen

the way most energy stored

free ATP

minimal, supports only \~10 twitches

creatine phosphate

* supplies energy for 15 seconds
* creatine assembled from amino acids

muscle metabolism at rest

* low ATP demand
* mitochondria produces surplus ATP
* fatty acids & glucose absorbed from bloodstream
* make ATP to convert creatine to creatine phosphate & glucose to glycogen

muscle metabolism at moderate activity levels

* ATP demand increases
* relies on anaerobic metabolism of pyruvate to make ATP
* increased oxygen consumption

muscle metabolism at peak activity levels

* enormous ATP demands
* mitochondria at max production produces 1/3 ATP needs
* most produced by glycolysis
* excess pyruvates to lactate
* lactate & H+ increase, drops pH (lactic acidosis) and causes muscle fatigue

fatigue

muscle can no longer perform at required level

* major factor is decreased pH
* decreases calcium/troponin binding
* alters enzyme activity

polio

virus that attacks CNS motor neurons causing atrophy and paralysis

tetanus

toxin from bacteria suppresses mechanism that inhibits motor neuron activity; causes sustained and powerful muscle contractions

botulism

toxins from bacteria blocks ACh release at neuromuscular junctions

* paralysis of skeletal muscles
* acquired through bacteria-contaminated food

myasthenia gravis

autoimmune disease causing loss of ACh receptors at neuromuscular junctions

rigor mortis

generalized muscle contractions shortly after death