flexion is decreasing angle between bones (can only occur at pivot point)

extension is increasing angle between bones

origin: point of muscle attatchment that does not move during an action

insertion: point of muscle attatchment that moves during an action

tendon: linkage connective tissue between bone and muscle (links the mysiums to the bone)

epimysium: irregular dense muscle tissue that is composed of collagen and encapsulates the muscle as a whole

perimysium: fibrous areolar connective tissue inbetween muscle fasicles

endomysium: areolar connective tissue, separates muscle fibers (cell). is looser and less stronger than the other mysiums

multinucleate

1mm to several cm long

excitable (can generate action potential)

contain myofibrils

cords of contractile proteins consisting of actin and myosin

consists of repeated sarcomeres

sarcolemma

vs

sarcoplasmic reticulum

the sarcolemma is the plama membrane of a muscle cell

sarcoplamic reticulum is smoth ER that surrounds myofibrils and stores Ca++

conduct action potentials from sarcolemma to the sarcoplasmic reticulum

deep invagination of the sarcolemma (little holes in the membrane)

labeled diagram of sarcomere

1. A band

2. H zone

3. M line

4. I band

5. Z disk/Z line

Sliding Filament Model of Cell Contration

(What are the steps of this process?)

1. Cell is at rest (uncontracted) free cytosolic Ca++ is between 10^-7 and 10^-9

2. Action potential causes free cytosolic Ca++ to increase (10^-6 to 10^-5)

3. Sarcomeres shorten (thin and thick filaments slide by eachother as a result of repeatedly binding to form actomyosin)

thick=myosin

thin=actin

myofilaments consist of thin (actin) and thick (myosin) filaments

the compination of these filaments make up myofibrils which make up the individual sarcomere units inside the sarcolemma

1. AT REST: atp binds to the myosin head, via atp hydrolysis to form the myosin-ADP complex. This complex also has a Pi attached to it. (It should be called the "myosin-ADP-Pi Complex"

2. acetyl-choline is released from the terminal dendrite of a motor neuron, it then binds to ionotropic ACh receptors on a muscle

3. the action potential spreads across sarcoplasmic reticulum

4. t-tubules conduct the action potential

5. RyR Ca++ channels of sarcoplamic reticulum allow ion diffusion where DHPR proteins are stimulated by action pot'l

6. free cytosolic Ca++ levels attain 10^-5 to 10^-6 concentration

7. Ca++ binds to troponin

8. troponin changes shape and pully tropomyosin away from the actin binding site

9. myosin binds to actin to for the crossbridge

10. the Pi attached to the myosin falls off

11. myosin ADP changes shape causing powerstroke to occur

12. ADP leaves myosin

13. rigor complex is formed

14. myosin hydrolyses ATP to break rigor complex

15. sarcoplasmic reticulum Ca++ pumps increase activity to take away Ca++ and put it back into the sacroplasmic reticulum, thus stopping muscle contraction.

produce a diagram of a muscle twitch. include the following:

1. latent period

2. contraction phase

3. relaxation phse

to cause muscle contraction, the Ca++ channel is unplugged allowing Ca++ to initiate the contraction part of a muscle twitch

during relaxation that free cytosolic Ca++ is gathered up and put back into the sarcoplamic reticulum via a Ca++ pump mechanism

simply unplugging the Ca++ channel and letting loads of Ca++ out during contraction takes less time than pumping it all back during relaxation.

create a graph of an action potential, intracellular Ca++ and a muscle twitch in relation to the time in which they occur

NOTE: in the diagram provided, ignore the red lines

EXPLANATION: An AP occurs first. This is the little spike at the begining of the graph. The AP initiates the increase in Cytosolic Ca++ which causes the muscle twitch.

FINAL NOTE: The more APs there are, the more Ca++ there will be, which causes more tension/twitch force

isometric: "same-length", this is a contraction in which there is no extension or flexion. no movement. no change in muscle length

isotonic: this is when the muscle shortens.

active: tension that results from crossbridge activity

passive: tension that results from muscle ealsticity (due to collagen) this involves the SEEs

what determines how much active and passive tension (relative to one another) contribute to muscle contraction?

describe the different scenarios possible

the initial length of the muscle

initial length of muscle is short: there is low passive tension and high active tension (the SEEs are slacked and therefore not contibuting much passive tension)

initial length of muscle is medium: there is contribution from both passive and active tension, but more from active tension.

initial length of muscle is long: there is high passive tension (SEEs are super stretched out like a stretched rubber band causing high tension) and there is low active tension because the crossbridges can't form b/c there is no myofilament over lap. The thick and thin filaments are stretched to far apart to touch and make crossbridges.

this is an ideal situation in which the initial muscle length is average and a maximal # of crossbridges can form

total tension=active tension+passive tension

where passive tension is a little less than active tenion

make a graph relating muscle length and active/passive tension

NOTE: in the graph provided "contractile" means "active tension" and "parallel elasticity" is the same as "passive tension"

what are preloaded and after loaded muscles?

how does pre and after loading muscles contribute to the latent period and tension

preloaded muscles: a muscle is stretched prior to isotonic contraction

afterloaded muscles: a muscles is made to have a lot of slack prior to isotonic contracion

preloaded muscles have a shorter latent period b/c the SEEs are already stretches out, but they also create less active tension because the myofilaments are stretched so far apart that they can't reach eachother to create crossbridges

afterloaded muscles have longer latent periods b/c they need to decrease all the slack they have. however they also are able to create more tension b/c crossbridge formation can be maximized

after

shortened muscles have maximal active tension

intermediate muscles have middle levels of active tension

lengthened muscles have the lowest levels of active tension

total tension=passive tension+active tension

even though active tension is decreasing with length, passive tension is increasing exponentially. Adding passive tension to active tension creates a total tension that actually increases with muscle length.

"the additaive effects of sequential twitches that result from sequential action potentials"

temporal summation doesn't change the number of motor units involved, but over time it keeps pumping acetycholine in little squirts that causes new muscle contractions before a relaxation can occur

tetanic contraction occurs when a motor unit has been maximally stimulated by it's motor neuron due to multiply impulses stimulating motor unit and not giving time to relax

continuous contraction

prepare a graph of treppe contraction, incomplete tetanic contraction and tetanic contraction

NOTE: in the diagram given the graph of "summation" is the same as a treppe contraction graph

myosin isozymes are proteins with different capacities that accomplish a similary function. they vary in the rate at which ATP is hydrolyzed

=higher ATP hydrolysis,=higher crossbridge cycling=higher degree of sarcomere shortening=increased tension

based on contractility and resistance to fatigue

resistance to fatigue compares oxidative vs. glycolytic activity

what is the oxidative pathway of skeletal muscles used for

what is the benefit of this?

what is the fuel for m. cells at rest?

this is the major metabolic pathway used during sustained activity

oxidative pathways allow for resistance to fatigue

at rest muscle cells use fatty acids for feul (Beta oxidation)

Slow oxidative/type 1

fast oxidative/type IIa

fast glycolytic/type IIb

red meat has tons of myoglobin that has a heme group to bind oxygen and can release when needed

white meat lacks myoglobin

what type of muscle fibers will a bird designed for speed have?

what about a bird that flies long distances?

speed: fast glycolytic

distance: slow oxidative

type 1: slow

type IIa: fast

IIb: fast

what is the fiber diameter of each muscle type?

I: small

IIa: intermediate

IIb: large

I: small

II: intermediate

IIb: large

I: low

IIa: medium

IIb: large

I: low

II: medium

IIb: high

I: high

IIa: intermediate

IIb: low

I: many

IIa: many

IIb: few

type I: hi

IIa: intermediate

IIb: low

I: hi

II: intermediate

IIb: low

I: low

IIa: high

IIb: high

I: low

IIa: high

IIb: high

I: low

II: intermediate

IIb: high

I: low

IIa: high

IIb: high

type I fibers are used for low-level activity

long muscles of back

solues (used for posture, and standing)

what are type IIa fibers used for?

example

used for intermediate activity

vastus lateralis (in thigh)

what are type IIb muscle fibers used for?

examples

rapid and powerful movements

extrinsic eye muscles

finger muscles

latissimus dorsi

gastrocnemius (calf muscle)

when someone starts running quickly, why does pH decrease then after a couple minutes go back to normal?

how does metabolic fuel change during that time?

initially the body is running on anaerobic glycolysis (not very efficient) this creates the byproduct of CO2 which decreases blood pH

after a while there they start breathing more heavily an increasing the O2 delivery by the CV/pulmanary systems. This switches the metabolic pathway to aerobic glycolysis and beta-oxidation

this also starts allowing the body to breath out all the co2 and then restore pH levels

what is the role of creatine during extreme exercise?

what happens to creatine when you stop exercising?

once you hit a certain level of workout, it is impossible to take in enough o2. anaerobic metabolism predominates. the body isn't making enough ATP to keep up.

Creatin phosphate is used as a replacement to ATP. it is creatine with a PO4 and an ADP on it.

Creatine phosphokinase breaks the creatine complex into creatine and ATP when at extreme levels of exertion.

after exersize, creatine hooks back up with the ATP and becomes a creatine-phosphate-ADP complex

myoglobin  binds 02 and releases it when there is not enough 02 in the body.

During extreme exercise the body uses up all the 02 it has and depeletes the 02 that is bound to myoglobin.

after extreme exercise part of the oxygen debt is used to replenish myoglobin

fatigue, in general, is failure to generate tension

rapid fatigue

-muscle units are being used and anaerobic metabolism dominates

-lactic acid increases and therefore pH decreases

-ATP and creatine-phosphate is used up (low levels of each)

-sarcolemma is hyperpolarized and the high stimulation means high extracellular K+

slow fatigue

-occurs during prolonges low level exercise

-liver/muscle glycogen is depleted so beta-oxidation of fatty acids happens

-beta-oxidation of fatty acids procuces half the amount of ATP as glucose

definition: 02 neede following prolonged exercise

needed to:

1. replenish myoglobin/hemoglobin 02

2. replenish ATP/ creatine phosphate

3. exhalation of CO2

4. lactate is converted to CO2 in liver/brain and heart cells so it be released through exhalation