1.

Stimuli and its classification

-Stimuli caused by changes of internal/external environment
-Stimuli causes an Action potential -> depolarization-> contraction or similar
Strength
-Subthreshold weak stimuli causing no response -> no contraction
-Threshold normal stimuli -> leads to contraction
-Supra threshold more than normal but and causes contraction
Receptors
-Adequate acts on receptors, sensitive to this and needs ATP / energy
-Inadequate Acts on receptors, made for receiving msgs
Energy
-Physical, and chemical stimuli
Origins
-Natural comes from the environment like wind or temperature
-Artificial artificially made by medicine, or other research
2. Excitation, Excitability. Excitable Tissue + physiological conditions.
Automaticity
Excitable Tissues
-Tissues able to respond to stimuli leading to an Action potential which in turn
leads to depolarization/hyperpolarization for a contraction or relaxation
1. Muscle tissue - skeletal, smooth, cardiac
2. Neural tissue - nerve cells in CNS/PSN
3. Secretory cells glandular cells
Excitation generalized response to stimuli, non-glandular, process
Excitability the ability to respond to a stimuli, causing an AP -> DP/HP
Physiological conditions of excitable tissues
1. Physiological rest cell doesnt receive stimulus like skeletal muscles cell
mass decreases atrophy
-If stimuli is re applied fully functional skeletal muscles
2. Functional activity Stimulus given to cells excitation contraction for
skeletal muscles, or transmission of impulses of nerve cells.
-cant be used all the time and needs a resting state to re-charge its
batteries by going back to physiological rest state.
3. Inhibition The cell in physiological rest receives an inhibitory stimulus cell
goes into inhibitory state and cannot receive normal stimulus.
-When we are sleeping CNS enters inhibition, a strong stimulus is needed to
wake them up.
-also happens to cells not needed, and has to be refilled with energy/substances
Automaticity ability to go from physiological rest functional activity without
ext. stimuli
-like smooth muscle cells

3. Cell Membrane structure and functions. Chemical Composition.

Differences of extracellular and intracellular fluids
CM
-contains of Lipids, proteins, carbohydrates
-separates intracellular/extracellular compartments
-keeps fluid in different places and shapes the cell
-defense mechanism
-ion/substance transport
-receptor function, by exchange of info btw extra/intracellular compartment
Lipids
-contains of phospholipids, cholesterol and glycoproteins
-needed for permeability of CM to Lipid soluble (C02, 02, fatty acids)
-and low permeability of CM to water soluble (ions, glucose, AA)
-proteins contain of transporters, enzyme and hormone receptors, antigens, ion
and water channels
Phospholipids
-consist of glycerol head and 2 fatty acids tails.
-Head is hydrophilic and it likes the water, while the tails are hydrophobic and
away from the water
-This forms a lipid bilayer used for the transportation of ions btw ECF and ICF
Integral membrane protein
-in CM by hydrophobic interactions
-detergents disrupt and detaches its attachment (detergents)
-some of the IMP are Trans membrane proteins since they are spanned one or more times,
contacts both ICF/ECF (ligand binding receptors, transport protein, pores, ion channels,
cell adhesion, GTP binding protein
Peripheral Membrane proteins
-loosely attached to Intra/extra cellular of membrane by electrostatic interactions
-removed by treatments by disturbing its ionic/hydrogen bonds
Extra cellular fluid
-Contains (Na+), Cl- and high Ca2+
Intracellular fluid
-Contains (K), (Mg2) and low Ca2+
4. Passive transport mechanism across cell membrane (Diffusion, osmosis,
filtration, electro kinetic transport). Ion Channels, classification due to
gating
Passive transport transport of substances in the way of electrochemical gradient.
No need for ATP
Diffusion transport of substances towards the concentration gradient.
-Simple diffusion through phospholipid bilayer/ion channels
-facilitated diffusion Ca2+/K+ potassium channels that requires some kind of
energy to make the diffusion
Osmosis Water transport through cell towards the higher substance concentration
Filtration transport of substances through CM towards pressure gradient
Electro Kinect Transport transport of substance through CM towards electrical
gradient
Ion Channels Allows diffusion through CM
-Voltage gated channels open cus of voltage across CM
-Ligand gated channels open cus of substance binds to protein channels opening

them
-Deformation-gated channels open cus of deformation of CM

5. Active Transport Mechanism across CM (Primary, Secondary)

Endocytosis, Exocytosis
Active transport transport of substances against electrochemical gradient needs
ATP
-Primary active Na/K Pump (pumping Na out from the cell, and K into the cell
-ATP is required for this active transport against the concentration gradient
-Secondary active Multiple Ions/substances transported against the Gradient
(Na/Glucose, Na/AA)
Active Transport mechanism
Uniport one substance is transported in one direction
Symport 2 or more substances are transported in same direction
Antiport 2 or more substances are transported in opposite direction
Endocytosis Particles are absorbed/engulfed into the cell membrane
-Phagocytosis bigger particles are taken in for digestion
-Pinocytosis only small particles/water is engulfed
Exocytosis secretion of vesicles out of the CM
6. Second messengers, formation and functions
-Second messengers are formed by primary messengers binding to its receptors
-used for transmission of information and amplification
1. By opening Ion channels (Calcium-calmodulin complex)
2. By activation of Enzymes in CM
-cAMP cyclic adenosine monophosphate, AC adenylyl cyclase
-cGMP cyclic guanosine monophosphate , CG guanylate cyclase
-IP3 inositol triphosphate, DAG diacylglycerol, PIP2 phosphatidylinositol biphosphate,
PLC phospholipase
7. Membrane potential and measurement. Resting membrane potential
(origination, approximate value). Depolarization, Repolarization,
Hyperpolarization. Action Potential. All-or-nothing principle.
Membrane potential electrical potential difference btw
intracellular/extracellular compartment because of irregular distribution of ions
Resting membrane potential (RMP) Electrical potential difference in outer/inner cell
at Physiological rest
-Influx of K+ and Efflux of Na+ (higher level of Cl-) due to K+/Na+ pumps, 2 in, 3 out.
-established by diffusion potential (-70-90mV)
Changes of Membrane potential
Depolarization sudden change, due to dramatic electrical change
-cell becomes positive from negative state for a short period due to influx of Na+
-needed for organism to function properly
Repolarization occurs after Depolarization
-High levels of Na+ (sodium) and the positive charge -> causes K+ (p) Channels to
open -> efflux of K+ -> RMP
Hyperpolarization K+ keeps getting pumped out from the cell (too much) -> cell
becomes more negative than the Resting Membrane potential, or Influx of ClAction Potential Change of membrane potential when threshold/supra-threshold is
stimulated

All-or-nothing principle AP either happens, or it doesnt.

-if excitable cell is depolarized to its threshold chances of Action potential is very high
and happens
-If excitable cell is depolarized but not to threshold no Action potential will happen
-So stimulus must reach the threshold or no action potential will occur
-stimulus during Refractory period AP happens either way but wont have stereotypical
size/shape
8. The nerve (skeletal muscle) Action Potential. Changes of ion Permeability
of CM during different phases of Action Potential
Nerve Action Potential
-Stimuli causes the threshold to be reached -> AP -> Depolarization ->
Repolarization of MP
-AP only occurs if INWARD CURRENT is higher than OUTWARD current
-basic mechanism for transmission of info to Nerve system in all types of muscles
1. Resting membrane potential no depolarization occurs and membrane potential is
at rest -70mV- -90mV
-Influx of K+ and Efflux of Na+ (higher level of Cl-) due to K+/Na+ pumps, 2 in, 3 out.
2. Upstroke of Action potential Action potential is caused due to higher inward
current than outer
-leading to depolarization at -60mV opens Na+ channels -> Influx of Na+ (more
positively charged)
-Na+ continues until Na+ equilibrium (+65mV) but doesnt reach it
3. Repolarization of Action potential upstroke is terminated and cell moves
towards Resting Membrane pot.
-inactivation Na+ gates are depolarized and closed no upstroke (no AP)
-K+ are effluxes and increases in concentration of K+ than Na+ conductance
membrane repolarized
4. Hyperpolarization after Action potential happens after repolarization, becomes
more negative than RMP
-K+ efflux at rest due to opening its channel and letting K+ flows out
-Cl- Influx
9. Changes of excitability during nerve action potential
-excitability of nerve cells are different and respond to differently to other cells
-able to be stimulated even at low stimuli in some cases
1. Depolarization Threshold next stimuli signal / reaction
Example: 1 person is torturing another one with words other person reacts at
subthreshold, and we keep frustrating the person until he reaches his threshold and starts
to yell
2. Threshold is reached respond to the stimuli by acting (yelling example)
-Excitability 0
-1 more stimuli wont respond to the cell because sodium channels are already open
3.excitability goes back to 100% new stimuli must reach supra threshold to
respond
4. Supernormal period excitability is increased and cell stimulates easier, (sub threshold
stimuli)
-if membrane potential is close to threshold some weak stimuli response
10.Classification of Nerve fibers (Myelinated, direction of propagation of
impulses, ABC and sensory nerve fiber classification + characterization)

-Dendrites part that receives the signal

-Axons transmits the signals taken up by the dendrites cell body
-Cell body part that decides what to do with the information gained, respond or not
Direction:
-Afferent Nerve fibers Up going signals from receptors CNS
-Efferent Nerve fibers down going from CNS muscles, glandular cells, nerve
cells
Myelinated or unmyelinated:
-myelinated axons containing covering sheets that transmits signals faster
-unmyelinated axons doesnt have these sheets slower signaling
Electrophysiological nerve fibers
-Aa Efferent nerve fibers skeletal muscle
-Afferent nerve fibers CNS
-B Afferent nerve fibers from touch, pressure, proprioceptor
-D afferent nerve fibers from touch/pain/temp receptors
-Y efferent nerve fibers muscle spindle
-B autonomic pre-ganglionar
-C Autonomic post-ganglionar
-Afferent nerve fiber from pain/temp
Sensory nerve fiber classification
-1a Afferent nerve fibers from muscle spindle (Aa)
-1b afferent nerve fiber from Golgi tendon receptor (Aa)
-II Afferent nerve fibers from touch/pressure (proprioceptors)
-III afferent nerve fibers from pain/temp receptors
-IV afferent nerve fibers from pain/temp receptors
11.Mechanism of conduction of Action potential in Nerve fibers. Factors
determining velocity of impulse conduction in nerve fibers. Rules of
impulse conduction in nerve fibers.
-at resting membrane potential the cell is negatively charged
-Transmission of AP down nerve fibers occurs due to spread of local currents from active
inactive region
1. Nerve axon becomes stimulated -> threshold -> AP -> depolarized
-Na+ inflow increases cell becomes positively charge
-nearby cells interior are still negatively charged
2. Spread of local current
-positive charges move towards the negative charge threshold -> depolarize
3. Once adjacent cell has caused the depolarization Action potential
-second cell is now positively charged, while first cell repolarized back to RMP
(negative)
-signals are by this way transmitted through axons cell body
Factors determining velocity of impulse conduction in nerve fibers
-how fast a signal is transmitted in the nervous system
Myelination transmits signals along the axon faster than un-myelinated axons
-its a layer of fat/lipid around the axon increasing membrane resistance + decrease
capacitance
-Membrane resistance signal is transmitted by pathway with smallest resistance, rather
than higher
-Decreased membrane capacitance axonal depolarizes faster in response to inward

current faster
-Action potential jumps in long distance from 1 node of ranvier to another
-instead of continuously walking across the axon like in un-myelinated fibers
-Myelin makes fewer areas needed for stimulation faster pathway
Diameter of nerve fiber
-the bigger the faster
-lesser internal resistance easier to bypass faster transmission
Impulse conducting rules in nerve fibers
1. Anatomically healthy no dmg/cuts continuous transmission, without hiccup
2. Physiological healthy contains normal charges, ion concentrations,
membrane permeability
3. Isolated conducting nerve fibers enter bigger nerves for conducting impulses
isolated
4. 2 way conducting Transmission of impulses both ways
-isnt normal, and thats why we divide into afferent/efferent nerve fibers
-if nerve fiber Is stimulated in middle signals both ways
-usually caused by artificial stimulation
5. Impulses doesnt change strength

12.Synapse. Properties of electrical synapses. Structure of chemical

synapse. Classes of neurotransmitters. Co-Transmission
Synapse
-place where information are transmitted from 1 cell to another
-either chemically or electrically transmitted
Electrical Transmitted Signals
-gap junctions btw cardiac muscles and Smooth muscles
-fast, 2 ways conducting, only excitatory, hard to influence by meds
-Moves through low resistance pathways from 1 excitable cell to another
-these are very fast conducting tissues in uterus and bladder
-so contraction happens in coordinated manner when needed and not
Chemical transmitted signals
-Happens in the synaptic cleft btw presynaptic membrane and postsynaptic
membrane
-Stimulation Certain substance is released by presynaptic cleft synaptic cleft binds
to post synaptic terminal
-Action potential opens Ca2+ channels and flows into the synaptic cleft
-neurotransmitters are released by exocytosis post synaptic membrane change of
membrane potential
-either excitatory causes depolarization for contraction
-or inhibitory causes hyperpolarization
Structure
-Presynaptic cell membrane (with neurotransmitters acquire stimuli release of
neurotransmitters)
-Post synaptic cell receptors that binds the Ach example.
Neurotransmitters
Excitatory Dopamine, Epinephrine, Norepinephrine, Acetylcholine
Inhibitory Dopamine, Serotonin, GABA
Co-transmission several neurotransmitters are released at the same time

13.Chemical Impulse Transmission in excitatory Synapse. Excitatory

neurotransmitters
1. A signal/stimuli is initiated sent the presynaptic cell membrane
2. Stimuli reaches its threshold and fires an Action potential -> binding of Ca2+ +
Calmodulin
3. Action potential releases neurotransmitters form the presynaptic cell synaptic cleft
post synaptic cleft
4. Neurotransmitters are bound to its receptors depolarization threshold influx of
Na+ and efflux of K+
Excitatory neurotransmitters Acetylcholine,
Norepinephrine for stimulatory process in body (energy)
Epinephrine regulates heart rate and blood pressure
Dopamine helps depression and focus
14.Chemical Impulse transmission in inhibitory synapse. Inhibitory
neurotransmitters
1. Signal/stimuli is sent presynaptic cell membrane threshold Action potential
2. Action potential releases instead of excitatory, inhibitory neurotransmitters
3. These inhibitory neurotransmitters binds to the receptors at post synaptic cell
membrane
4. Leads to a hyperpolarization instead of depolarization due to inhibitory
neurotransmitters
5. Which takes away the membrane potential away from its threshold and action potential
6. Opens Cl- and K+ channels, allowing influx of Cl + efflux of K+ to the cell
negative charged inhibitory state to avoid excitation
Inhibitory neurotransmitters
GABA fast inhibitory neurotransmitter in synapses of brain
Dopamine helps depression and focus
Serotonin for stable mood and balance of excessive stimulation, (regulates sleep
cycle, pain, digestion)
15.Types of synaptic inhibition (Presynaptic/postsynaptic, direct and
indirect)
-Synaptic inhibition means that the target cell doesnt receive the action potential
needed / no response due to some kind of inhibition/blockage
Presynaptic inhibition
-1 of 2 axons are blocked causing only neurotransmitters to be released from
terminals
1. Stimuli is sent presynaptic cell membrane action potential in 2 of the axon
terminals while one is blocked and no release of neurotransmitters from that specific axon
terminal
Postsynaptic inhibition
-all targeted cells are inhibited equally
-inhibitory neuron inhibits already from beginning, before AP is sent no cell
response
Direct Flexing you biceps causes inhibitory neuron inhibits other neurons to other
muscles
Indirect Motor neuron is stimulated by low frequency or if membrane potential is high
threshold
16.Functional properties of synapse (unidirectional, slow transmission,
facilitation)

Unidirectional one way pathway stimuli presynaptic cell membrane

release of neurotransmitters synaptic cleft postsynaptic cleft (binding to the
receptors)
Facilitation - Too high transmission from presynaptic cleft Ca2+ pump isnt
able to go back to its normal level increase of transduction
Slow Conduction Too low stimuli only causes to reach subthreshold
-in other words there will be no release of neurotransmitters without threshold
-could be caused by diseases to an extreme level (MS)
17.Functional properties of neuronal pools (Convergence, Divergence,
summation)
Convergence several neurotransmitters from presynaptic cell binds to same
postsynaptic receptors
Divergence several neurotransmitters from presynaptic cell binds to different
postsynaptic receptors
Spatial Summation when 2 or more neurotransmitters are bound to postsynaptic
receptors greater depolarization than either one would do alone, could say its a
teamwork of input greater depolarization
-both needs to be of same type either inhibitory or excitatory if not they will + -
cancel each other out
Temporal Summation 2 inputs from presynaptic cell postsynaptic cleft overlap
each other due to their rapid sequence summates (adds to each other)
18.Impulse Transmission in neuromuscular synapse. Neurotransmitters and
corresponding receptors. Role of acetylcholinesterase
Neuromuscular synapse
-Synapses btw motor neuron and muscle fiber
-Its a chemical synapse with release of example Ach for muscle contraction
-facial expression, muscles used while running. Basically important muscles for functional
movement
1. Stimuli presynaptic cell membrane reaches threshold
2.once threshold is reached Action potential opening of Ca2+ channels
3. Influx of Ca2+ in the presynaptic cleft + binds to Calmodulin release of Ach-vesicles
synaptic cleft by exocytosis
4. Acetylcholine binds to Ach-receptors (nicotine receptors) at postsynaptic cell
membrane (motor end plate)
5. Conformational change Na+ and K+ channels open from the postsynaptic cleft
6. Influx of Na+ and Efflux of K+ (post synaptic cleft)
7. The change of ions depolarization of motor end plate (-50mV) spread of local
currents of muscle fibers
8. Which finally leads to a muscle contraction
Role of Acetylcholinesterase
-degrades Ach choline/acetate by on the receptors at motor end plate
-half of choline is returned by Na+ cotransport presynaptic terminal and used again
-if not degrade continuous muscle contraction death (WW1, snap gas)
19.Possibilities to affect impulse transmission at neuromuscular synapse.
Myorelaxants
-Botulinum toxins Blocks the Ach from being released from the presynaptic
membrane no muscle contraction paralysis death due to not being able to
breath
-Curare competes with Ach and binds to nicotine receptors, too much = death

-D-Tubocurarine used to relax muscle during anesthesia

-Acetylcholine esterase inhibitors prevents degradation of acetylcholine
continuous muscle contraction
-Hemicholinium blocks uptake of choline back to presynaptic cleft decrease of
Ach synthesis
20.Impulse transmission from nerve fibers to smooth muscle cells.
Neurotransmitters + corresponding receptors
1. Binding of Ca2+ to calmodulin
2.release of neurotransmitters from Varicosities (enlargement on nerve fibers)
3.binds to Nicotine receptors depolarization Action potential muscle
contraction
-no synapses, but the enlargement instead that releases the Ach vesicles, that binds to
nicotine receptors
21.Structure of skeletal muscle (Muscle fiber, myofibrils, protofibrils). Motor
units. Functions + properties of skeletal muscles
-Causes the voluntary muscle contraction of the body
-Stimuli action potential -> depolarization release of ACh binding to post synaptic
membrane depolarization T-tubules release of Ca2+ binding to Troponin C
release of tropomyosin from actin-myosin binding site actin-myosin binds filaments
are moved on each other contraction
Structure
Thick filament
-myosin - Contain 6 polypeptide chains
-1 pair of heavy chain, 2 pairs of light chains (Head and tail of the myosin)
-binds to actin for cross-bridge formation hydrolyze ATP
Thin filament
-Actin contains actin-myosin binding site
-tropomyosin covers the actin-myosin active site doesnt let binding occur
-if occurred must be released
-Troponin I inhibits actin + myosin interaction
-Troponin T binds to troponin to tropomyosin
-Troponin C binds to Ca2+ conf. change removes tropomyosin allows actinmyosin binding contraction
Properties
Elacticity, Passive (Stretch), Contraction, Plasticity, Excitability
Function
Movement causes voluntary movement such as facial, movement of position of body,
extremities
Receptive tells the CNS how our body is situated and how we should respond to it
Protective function protects the inner organ, and hold the bone together
Heat production produces heat due to physical activity sweat
Facilitates venous blood support the venous blood from going from down upward.
Else would be hard due to gravity
Specific function speech, eat, drinking
22.Contractive filaments of skeletal muscle. Mechanism of contraction +
relaxation of skeletal muscle
Contractile filament of skeletal muscle
Thick filament
-known as myosin

-contains 6 polypeptides 1 set of heavy chain and 2 set of light chains

-head contains binding spot for actin-myosin for their interaction contraction
-bound to Z-lines of sarcomere double helix
Thin filament
-Actin filament with binding site to myosin
-Troponin I inhibits the binding of actin-myosin
-Troponin T binds troponin to tropomyosin
-Troponin C binds to Ca2+ conf. change tropomyosin is de-attached actinmyosin can interact contraction
Mechanism of contraction
-Stimuli threshold action potential influx of Ca2+ release of ACh binding to
post synaptic membrane depolarization Action potential towards the T-system
opens Ca2+ channels and sarcoplasmic reticulum Ca2+ binds to troponin C conf.
change tropomyosin is detached actin-myosin binds together forming a complex
myosin pulls actin sarcomere shortens (Z-line pulled) energy produced filament
slide on each other contraction
-ATP is needed to detach myosin from actin filament, else muscle stiffness
-No ATP = rigor mortis
Mechanism of relaxation
-Muscle relaxation happens when the process of contraction is over
-troponin C detaches from Ca2+ -> Ca2+ decreases from the cytoplasm
-troponin regains its normal form tropomyosin binds again and covers the
binding site of actin-myosin
23.Effect of strength of stimuli on muscle contraction
Sub-threshold no sufficient stimuli is given no depolarization no Ap no release
of Ach no cont
Threshold sufficient stimuli is given depolarization action potential release of
ach binding of Ach to its receptors etc etc
-increase stimuli strength increased contraction force
Optimal stimuli all muscles are maximally stimulated + contracted
24.The effect of frequency of stimuli on muscle contraction (single
contraction; incomplete/complete tetanic contraction). Summation of
contractions
Single contraction
1. Latent phase preparation phase before contraction of skeletal muscle (5-7ms)
2. Contraction phase contraction time of muscles, due to actin-myosin interactions
(50-100ms)
3. Relaxation phase force of contraction decreases due to Ca2+ decrease in
cytoplasm no binding to troponin C regains its normal state tropomyosin
covers actin-myosin site no contraction (50-100ms)
Incomplete tetanus obtained by giving stimuli to excitable tissue increase of
contraction, and as its going towards relaxation phase stimuli again maximal
contraction
Complete tetanus continues stimuli given, one after another no time for relaxation
phase
Summation of contraction
-happens if the Ca2+ isnt decreased completely in the cytoplasm
-new Ca2+ is pumped cytoplasm binding to troponin C removal of tropomyosin

and binding of actin-myosin shortening of sarcomere energy sliding of filaments

contraction
25.Types of contractions (isometric, Isotonic, auxotonic)
Isometric Iso = same, metric = length.
-Contraction doesnt lead to a change of length length is same as it was before
contraction
-happens if we want to lift something too heavy
Isotonic iso = same, tonic = tension
-contraction doesnt lead to a change of tension tension is the same as it was before
contraction
-isnt really visible unless we take a muscle and simulate it by adding no load to it
Auxotonic mixed contraction change of length + tension
-most common
26.Effect of length of sarcomere on muscle contraction
Relaxed state no length change of muscles due to no contraction
-maximal force is generated if stimuli is added, due to recharge of batteries
Contraction state changes muscle length by decreasing the length (biceps)
-occurs because Ca2+ binds to troponin C detaches tropomyosin actin-myosin binds
myosin pulls actin backwards shortens sarcomere (shortens Z-line) energy
produced filament sliding on each other contraction
Surgery important to remove dmg muscle tissue fix it re add it exactly as it was or
else no proper function
27.Energy sources for muscle contraction. Efficiency of muscle contraction
-Relaxed state myosin splits ATP ADP + P ready for actin to be bound for
contraction
-ATP is important for contraction changes position of head towards actin
Energy Sources
ATP is short time energy (1-3 sec) is continuously generated by citric acid cycle
Phosphocreatine (5-8 sec) donates Phosphate for ATP
Anaerobic glycolysis no oxygen present
-40sec- 1 min energy
-happens fast, but gives little energy molecules with limited time
-Skeletal muscles could be running for 1 minute, but brain wont keep up
without Oxygen
-feeling of fatigue is usual
Aerobic energy production
-By breathing a lot splitting of pyruvate a lot of ATP
-they are in-toxic waste products (C02 + water), not dangerous
-usage of glucose, free fatty acids and proteins ATP
-not sufficient for running fast
28.Types of muscle fibers (I, IIa, IIb). Composition of skeletal muscles
Type I (red) - contains a lot of capillaries, myoglobin, mitochondria
-contraction for long period of time with little force
-supports aerobic activity by using fats/carbs into ATP
Type II anaerobic, short bursts of speed/strength
Type IIa uses both anaerobic/aerobic metabolism to form energy
Type IIb anaerobic, has the highest rate of contraction and occurs very fast

Composition of skeletal muscle

-75 % H20, 20% protein, 5% electrolytes, carbs and fats

29.Motor units; Types (due to size and type of muscle fibers), their
recruitments in contraction
Motor units considered a motor pool
-containing motor neuron, skeletal muscle fibers innervated by neurons + terminals
-Muscles with more motor unit controls force output better (ocular vs thigh muscle)
-CNS recruits motor neurons, from smallest largest (depending on size of load)
Spatial recruitment activation of 1 more motor unit greater force
Temporal recruitment frequency of activation of muscle fiber contractions
Consecutive stimulation of motor unit from motor neuron frequent muscle twitch
greater force than single contraction (by decrease of interval stimuli into larger force
with same number of motor units)
30.Strength of muscle contraction and factors affecting it
-How often, strong the stimuli is
-how many/size muscle fibers are affected
-degree of muscle strength
31.Difference btw Smooth and skeletal muscles. Unitary and multi-unitary
smooth muscle
Smooth muscles
-doesnt have thick or thin filaments like skeletal/cardiac muscles
-since they are not organized in the sarcomeres
-found in the walls of GI, bladder, uterus, ureter, bronchioles and eye
-production of motility and to maintain tension of BV
-mixed is a mixed of unitary, and multi-unit
Unitary smooth muscle
-contains gap junctions btw cells spread of electrical activity through organs
-low resistance pathway easier flow
-Action potential occurs same time contraction + emptying of bladder at same time
-In GI tract, bladder, uterus, ureter
Multi-unit smooth muscle
-in iris, cilia muscle of lends, vas deferens
-each muscle fibers acts as separate motor unit (similar to skeletal muscle)
-no coupling btw cells
-highly innervated by parasympathetic and sympathetic nervous system
32.Mechanism of contraction and relaxation of smooth muscles
Smooth muscles Doesnt have troponin C
1. Stimuli -> Threshold -> AP -> Depolarization opens Ca2+ channels from SR
influx of Ca2+
-Hormones, + (IP3) + Neurotransmitters also opens Ca2+ Channels from SR
2. Ca2+ binds to calmodulin activates myosin-light chain kinase -> Increase of
Myosin ATPase activity -> Myosin binds to Actin -> Cross-bridge formation ->
tension
-high level of Ca2+ is needed -> else no Phosphorylation of Calponin + Caldesmon
= no actin-myosin binding

Relaxation of Smooth muscles

1. Decrease of Ca2+ from Cell (back to Sarcoplasmic Reticulum or out of the cell)
2. Ca2+ unbinds from Calmodulin
3. Myosin Phosphatase removes Phosphate from Myosin -> Decrease Myosin
ATPase activity
4. Less myosin ATP -> decreased muscle tension

33.Reflex. Classification or reflexes (due to somatic or vegetative Nervous

system, due to level of realization, due to number of synapses, due to
elicited response)
Reflex A response to stimulus organized through CNS
Classification
Somatic Connected with skeletal muscles
Autonomic helps to activate/inactivate smooth muscles/cardiac muscles
Due to lvl
Spine, Bulbar, Mesencephalic, Diencephalic and cortical
Due to synapses
Monosynaptic single synapse
Polysynaptic 2 synapses in CNS
Due to elicited response
-motor muscle contraction
-Secretory autonomy reflexes -> secretion of glands
34.Somatic reflex arc through spinal cord. Reflex time and factors affecting
it

Reflex time the time until a response occurs after sent stimuli
Factor affecting
-Amount of synapses (more synapses = slower)
-velocity of impulse-> faster = faster
-Strength of stimulus stronger = better
-Inhibition in CNS -> slower reflex (sleep)
-Fatigue slows down the reflex time
35.Proprioceptors. Muscle spindle; Nerve fibers connected with it and their
functions

Proprioceptors receptors in bone, muscles, tendon, ligaments (informs our body

of movement + position)
Muscle Spindle
-Stretch receptor btw skeletal muscle
-senses stretch (corrects muscle length after being contracted/stretched)
Function
-Stretch = intra/extra fusal fibers are lengthened (detected by 1a and 2a afferent
fibers)
-1a fiber detects velocity of length change
-2a fiber detects length of muscle fiber
36.Stretch Reflexes (Phasic and tonic) their characteristics. Tendon reflexes
that are used in clinic and their corresponding segmental levels

Phasic tendon reflex -> triggered when muscle is stretched fast (monosynaptic)
Tonic Reflex Muscle tonus -> if we stretch muscle slowly by gravity force
37.Muscle tonus; its cause and regulation
Muscle Tonus continues/passive contraction of muscles
-or muscle is resistant to passive stretch when at rest
-maintains posture
Sudden pull body tenses and gives us posture due to sudden movements
-if someone pushes u, ur body reacts and we tend to make our self stiff to maintain
balance
38.Reflex from receptors in muscle tendon; its role
Golgi tendon organs
-stretch receptors in tendons (senses contraction of muscles)
-activated due to stretch made by a strong muscle contraction -> wants to relax
the muscle
-has a high threshold and isnt easily stimulated

39.Innervation of muscles antagonists, its role

40.Nociceptive reflex. Crossed extensor reflex

-aka flexor reflex caused by painful signals
1. Pain receptor -> CNS -> Activates flexor muscle -> flexing of extremities while extensor
muscle is inhibited
-for protection of falling on painful objects
41.Functional anatomy of the spinal cord. Functions of the spinal cord

42.Early and late consequences of spinal shock

Spinal shock dmgs to the spinal cord
-Above C5 -> death
-Below C5 -> spinal shock
Immediate effects lack of spinal cord functions
Late Effects (2 months) spinal cord becomes more excitable (tries to function by its
own without the CNS)
Consequences of spinal shock
-Anesthesia permanent loss of sensation of legs or other body parts
-Paralysis the inability to make own movements
-Hypertonia if spinal cord is cut -> all functions are lost (reflex arent working)
-loss of autonomic reflexes affecting blood pressure, organs cant evacuate
themselves
43.Difference between autonomic and somatic nervous system
Somatic nervous system
-higher centers - cortex of the brain
-lower centers - thoracolumbar + sacral part
-controlled by free will conscious control
-afferent pathway + receptors of the reflex arch (same as somatic/autonomic nervous
system)
-efferent pathway CNS -> Synapses -> Skeletal muscle, (ACH binds with Nicotine
receptor)
-reflex time is faster in somatic than autonomic due to being voluntary and only 1
neuron skeletal muscle
Autonomic nervous system
-high centers hypothalamus (impulses doesnt reach cortex)
-low centers - spinal cord (anterior horn)
-isnt controlled by will, its automatic hence auto-nomic subconscious control
-afferent pathway - receptors of the reflex arch are the same as somatic/autonomic
nervous system
-efferent pathway Both Sympathetic + Parasympathetic pathways
-divided in sympathetic and parasympathetic regulation of organ system functions
44.Sympathetic nervous system: centers and efferent part. Transmitters and
corresponding receptors. Sympato-adrenal system
Sympathetic starts in the thoracolumbar regions
-function prepares the human body in a stressful moment for either fight or flight
situation
-increase of blood pressure dilation of pupil, heartbeat, adrenaline, glucose
concentration, metabolic activity which all sharpens our alertness become
quicker
-higher centers Hypothalamus (anterior region)
-lower centers thoracolumbar part (T1-L3) innervation of all organs
-Efferent Pathway: - 2 pre preganglionic c -> synapse -> 2 post ganglia (ACH + Nicotine
receptor) -> Synapses with A/B Receptor of effector organ (NE + Alfa / Beta receptor)
-Effector organ: Smooth/Cardiac muscle, Endocrine/exocrine glands, adipose
tissue
Sympato-adrenal system
-formed by Sympathetic nerve + Adrenal medulla
-Adrenal medulla specialized ganglion in sympathetic part of autonomic nervous
system

-Efferent pathway - Preganglion -> adrenal medulla -> release of Epinephrine -> BV
-> binds to B1 + B2 receptors

45.Parasympathetic nervous system: centers and efferent part

Parasympathetic
-part of the autonomic nervous system
-starts in the brainstem + sacral spinal cord (cell bodies in pons, medulla, midbrain)
-increases during resting and digestion once body has relaxed (sleeping, lying, relaxing)
-function conserving energy
-higher centers hypothalamus
-lower centers spinal cord (S2-S4), 3, 7, 9, 10 cranial nerves
-efferent pathway Preganglion synapses with Post ganglion (Ach + Nicotine receptor)
-> synapses with Effectors (ACH + M receptor)
-Smooth/Cardiac muscle, Endocrine/exocrine glands, adipose tissue
46.Adrenergic receptors; types, their affinity and activation effects
Adrenergic receptors
-divided in alpha and beta
-Norepinephrine binds best to alpha receptors (could bind to Beta 1)
-Epinephrine binds best to beta receptors,(in some cases binds to alpha receptors)
Norepinephrine binds best to alpha receptors in the blood vessels
-narrows BV and Smooth muscle contracts increases resistance of blood flow
increase of blood pressure
-to high blood pressure negative feedback cardiovascular system wants to
lower it
-reduced blood pressure circulation
Epinephrine binds best to beta2 and alfa1 receptors
-both effects of cardiovascular system
-Dilates BV increased heart rate (due to dilation of BV)
47.Cholinergic receptors; Types and their activation effects
Cholinergic receptors
-Divided in Nicotinic (N) and Muscarinic (M)
-N Neuromuscular (Nm) and Nn (Autonomic ganglion)
-ACh binds to both Nicotine receptors in case of skeletal muscle contraction
-and M-receptors in case of parasympathetic and sympathetic
-M1 receptor neuronal receptor in CNS
-M2 cardiac receptor in the heart decrease of AMP decrease heart rate
-M3 glandular/smooth muscle receptors for relaxation and gland secretion
-M4/M5 CNS receptors found in smooth muscle cells, and glandular cells

48.Sympathetic effects in organisms (in cardiovascular, respiratory,

digestive and urogenital system, in skin, eyes, metabolic effects)
Sympathetic effects-Activated in case of stress fight or flight situations
Heart - increase of heartrate, force of contraction, excitability, faster
conduction/signaling
Arterioles
-constriction of abdominal cavity, skin, mucous, cerebral, sex organs
-dilation of coronary, pulmonary, skeletal muscles
Veins constricts
Bronchi dilates less secretion
GI Less movement, contraction less secretion
Bladder wall relaxes and sphincters contract
Eye Pupil narrows = sharper sight, and the ciliar relaxes
Skin contracts increase of sweat secretion
Liver Glucogenolysis, Gluconeogenesis
Fat tissue - Lipolysis
49.Parasympathetic effects in organism (in cardiovascular, respiratory,
digestive and urogenital system, in skin, eyes, metabolic effects etc)
Parasympathetic effects
-Happens when the body is in a relaxed state (no more fight or flight situation, when
sleeping, or lying, eating)
Heart lower heartrate, less force contraction, less excitability and less signaling
Arterioles dilation of sex organs/coronary
Veins stays the same
Bronchi constricts increases secretion
GI relaxed movement of food increases increased secretion
Bladder contraction relaxed
Skin increased of lacrimal secretion
Liver / fat tissue - nothing special
50.Pharmacological influences on autonomic system: cholinergic and
adrenergic substances
Adrenergic substances (A&B receptors)
-Alpha And Beta receptors or mixed in cardiac muscles
-Neurotransmitters like Epinephrine, Norepinephrine
-found in organs stimulated by the sympathetic fibers
-Atropine blocks parasympathetic effects inhibit salivation/respiratory secretion
+ dilation of pupil
-Neostigmine inhibits cholinesterase treatment of skeletal muscle due to lack of
ACh
-Tricyclic antidepressants longer NE effect makes u feel better
Cholinergic substances
-Nicotine(skeletal muscles) or Muscuranic receptors (cardiac muscles)
-ACH binds to both receptors and is either inhibitory or excitatory depending receptor
-Usage of ACh in somatic nervous system
-M1 receptor neuronal receptor in CNS
-M2 cardiac receptor in the heart decrease of AMP decrease heart rate +
contraction
-M3 glandular/smooth muscle receptors for relaxation and gland secretion
-M4/M5 CNS receptors found in smooth muscle cells, and glandular cell