EXS 320 - Unit 4 Exam

Skeletal muscle is composed of

individual muscle fibers containing myofibrils

myofibrils contain

contractile proteins called actin and myosin

sarcomere

functional unit of skeletal muscle contraction, primary composed of actin and myosin

Structure of skeletal muscle

fascicle, muscle fiber (w/nucleus), sarcolemma, myofibril, protein filaments

actin =

thin filaments

myosin =

thick filaments

Actin & myosin function

Actin molecules form double-helical actin strands, each actin has myosin-binding site, covered by tropomyosin, myosin can only bind to actin after troponin complex removes tropomyosin from actin

myosin structure

has tail and head

- at top of head, a actin-bind site,

-just below binding site is ATPase site

- two myosin molecules bind at their tail ends

sliding filament model

tails of myosin bind to myosin binding sites on actin and pull, allows for sarcomere shortening (muscle contraction)

ATPase =

enzyme that splits ATP releasing energy that goes into the myosin heads

sarcomeres

the functional unit, have Z-lines at each end of myosin heads attached to actin and allow pulling of actin in

Muscle Contraction

1 - following depolarization of sarcolemma, calcium is released from Sarcoplasmic reticulum & attaches to troponin;

2 - tropomyosin moves on actin and uncovers myosin binding sites;

3 - actin-binding sites on myosin heads attach

4 - In presence of ATP, myosin heads "ratchet" and pull actin to the middle of the sarcomere (crossbridge cycle )

Relaxed actin =

when tropomyosin covers binding sites,

contracting actin =

myosin binding site exposed with activation of troponin complex by calcium

When ATP is hydrolyzed to ADP,

creates a high energy configuration of myosin, and attaches to actin releasing phosphate group

Power stroke =

actin gets pulled toward middle of sarcomere

Excitation-contraction coupling

ACH = the NT that binds to Nicotinic cholonergic receptors

- causes channels to open and close allowing sodium and potassium to depolarize & create an action potential in the muscle fibers.

- that action potential travels down T-tubule which triggers the release of Ca2+ from SR ,which allows muscle contraction

muscle twitch -

mechanical response of individual muscle fiber to a single action potential originating in the motor neuron

phases of twitch

1. latent period

2. contraction period

3. relaxation period

isotonic contraction

muscle shortens

types of muscle twitch

determined by the ability of the muscle to produce tension & amount of load

1 - isotonic

2 - isometric

isometric

muscle cannot shorten

isotonic muslce contraction

creates plateaus where the muscle shortens and the load moves

Isometric muscle contraction

happens with a load greater than the tension that the muscle can develop, no shortening occurs

Factors that effect force generation

- frequency of stimulation

- fiber diameter

- fiber length

- recruitment of fibers

- size of motor units recruited

increased frequency =

increased tension

increased fiber diameter =

increased force

maximal tension can develop if

If fiber length is at normal resting length or slightly greater , at beginning of contraction,

treppe

when muscle is stimulated at a high rate, peak tension increases with ever twitch to a higher constant level, till a plateau

Ideal length- tension curve =

between 100-115%

summation occurs

when twitches occur frequently the muscle fibers cannot relax adequately and ____________ _________

then tentanus occurs

when futher increases in stimulus frequency results in increased tension past summation and

maximum tetanic contraction

any further increases past tetanus cause the muscle to generate its maximal force

decreased length of muscle

allows the crossbridges to completely overlap each other

-60-100%

increased length of muscle

not all crossbridges overlap with thin filaments

- 120-170%

Recruitment of fibers

increase in number of active motor units leads to greater # of fibers recruited = greater force generation

type of fiber recruited

Slow twitch vs. Fast twitch, affects force generation

Size of motor unit recruited

- refers to number of fibers in given motor unit

increased size = Greater force

- larger diameter motor neurons are present in motor units w/ larger muscle fibers - HARDer to activate but create greater force

- smaller neurons are activated first to allow for fine motor control

Speed of muscle fiber shortening

1 - latent period of shortening increases as load increases

2 - increasing load results in slower speed of shortening

effect of load on muscle shortening

Smooth muscle

found in internal organs and blood vessels

- under autonomic control

- lack sarcomeres

- actin & myosin are present in parallel configuration but run together in oblique fashion

Smooth Muscle Excitation-Contraction Coupling

utilizes calcium-calmodulin interaction that activates myosin kinase enzyme

Myosin (light-chain) kinase (MLCK)

phosphorylates myosin heads allowing for binding to actin and cross-bridge activity

smooth muscle contraction

contraction squeezes when thick and thin filament overlap past rest

Cardiac muscle

- has striations/sarcomeres

- utilizes calcium-troponin- tropomyosin mechanism for contraction

two areas of cardiac muscle cells

sinoatrial node & AV node

- have "pacemaker" properties

- can contract w/o outside stimulation

via gap junctions

Cardiac cells communicate _____

- allow coordinated contractions of heart

autonomic input

cardiac muscle controlled by

- influences rate and forcefulness of contractions

excitation-contraction coupling in Cardiac muscle

1 - current (AP) spreads through gap junctions to contractile cell

2 - action potentials travel along plasma membrane & T tubules

3 - Ca2+ channels open in plasma membrane & SR

4 - Ca2+ induces release from SR

5 - Ca2+ binds to troponin, exposing myosin binding sites

6 - crossbridge cycle begins

7 - Ca2+ is actively transported back into the SR and ECF

8 - tropomyosin blocks myosin-binding sites (muscle fiber relaxes )

Cardiovascular system

heart, blood vessels, blood

heart

right and left atria, right and left ventricles

blood vessels

arteries, arterioles, capillaries, venules, veins

blood

plasma, erythrocytes, leukocytes, platelets

cardiovascular system functions

- transport of oxygen and nutrients to cells

- transport of metabolic waste products to organs for excretion

- temperature regulation

path of blood flow

- oxygenated blood goes from lungs to pulmonary veins, into left atrium, through left ventricle, into aorta, oxygen levels blood into systemic capillary beds

- deoxygenated blood goes from systemic circuit into venae cavae into right atrium through right ventricle and into pulmonary arteries to pulmonary circuit , where O2 moves into blood and CO2 leaves

primary function of heart

create a "pressure head" for the entire circulatory system

right atrium is

responsible for collecting blood from body (minus lungs), via inferior and superior vena cavae, sending it to the right ventricle pushing it to the lungs for exchange of gases b/w blood and lung air

left atrium is

responsible for collecting blood from lungs and sending to left ventricle which pushes it out to the whole body (except lungs)

left ventricle must

contract with greatest force to be able to distribute blood to such a large area, thus, it has the greatest mass of muscle tissue

atrioventricular (AV) valves

valves b/w the atria and ventricles

- open when atrial pressures exceed ventricular pressures allowing blood to flow from the atria to the ventricles

tricuspid valve

right AV valve

bicuspid valve

left AV valve

pulmonary and aortic semilunar valves

valves b/w ventricles and main blood vessels leaving the heart

- open when pressure inside the ventricles exceeds the pressure in the pulmonary trunk and aorta

valve cusps

serve to seal the heart valves when ventricles relax, and open when ventricles contract, allowing blood to flow into aorta and arteries

electrical conduction in the heart

starts at SA node, spreads through atria, to AV node

- at AV node, slight delay before conduction spreads down the septum through AV bundle, the right/left bundle branches and then up the walls of the ventricles via Purkinje fibers

intercalated disks

where cardiac muscle cells are connected

Within the intercalated disk

- gap junctions allow ions to pass b/w adjacent cells and thus allows current to flow from cell to cell

- desmosomes keep cells from tearing apart during contraction

pacemaker cells

in SA and AV node spontaneously generate action potentials

- SA node cells control overall pace of HR (70 bpm) , if SA node does NOT depolarize, AV node will spontaneously depolarize at rate of 50 bpm

After depolarizing, AV node

will be in refractory state at the SA node rate and will not be able to depolarize at its own intrinsic rate

conduction fibers

associated w/ pacemaker cells and spread AP throughout heart

Conduction moves

in "waves" starting on outside of atria and moving through ventricles in "inside-out" fashion

spread of action potentials through heart

EKG (ECG)

the wave of depolarization through cardiac tissue can be detected and creates 5 waves (P,Q,R,S,T)

P wave

represents atrial depolarization

QRS waves

make QRS complex & represents ventricular depolarization

T wave

represents ventricular repolarization

Normal ECG reading

sinus tachycardia

inverted T wave

cardiac cycle

refers to events that relate to the flow of blood through heart during one complete heartbeat

cardiac cycle includes

- pumping phases (pump cycle )

- valve opening/closing

- pressure changes in atria, ventricle, & aorta

- volume changes in ventricles

- heart sounds associated w valve opening/closing

Phases of cardiac cycle

1. Ventricular filling: mid-to-late diastole

2. isovolulmetric contaction, systole

3. ventricular ejection, systole

4 - isovolumetric relaxation, early diastole

ventricular pressure during cardiac cycle

aortic pressure during cardiac cycle

ventricular volume during cardiac cycle

heart sounds

heard during phase 2 and 4 of cardiac cycle

cardiac output =

heart rate (HR) x stroke volume (SV)

stroke volume =

end diastolic volume (EDV) - end systolic volume (ESV)

Ejection Fraction (EF) =

Stroke volume (SV) / End-diastolic volume (EDV) x 100%

venous return

flow of blood back to the right atrium

preload

amount of stretch of the ventricular wall myocardium

- related to end-diastolic volume (EDV)

afterload

combined load of EDV and arterial resistance during ventricular contraction

- increased afterload = decreased stroke volume (SV)

sympathetic fibers project

to the SA node, AV node, and ventricular myocardium

increases heart rate

stimulation of heart by sympathetic fibers____ ___ ___

Parasympathetic fibers project

to SA node and AV node

decreases HR

stimulation by parasympathetic fibers ____ ___

will increase CO

increased Heart rate ____ ____ __

increases force of contraction (contractility)

sympathetic fibers projecting ventricular myocardium

Epinephrine can

increase contractility & HR

increased contractility

decreases ESV resulting in greater SV

venous return

Stroke volume can be regulated by