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Muscle Contraction: A Comprehensive Guide to Physiology and Mechanisms, Lecture notes of Physiology

All about Physiology in paragraph form

Typology: Lecture notes

2019/2020

Available from 09/11/2021

arianeleconte
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Skeletal muscle
-Made of fascicles made of muscle fibers. Muscle fibers are
multinucleated induvial muscle cells. Myofibrils are
comprised of myofilaments composed of sarcomeres.
-H zone (helle zone) is spilt down the middle by M line. H
zone disappears as the sarcomere contracts and actin does
not overlap myosin. I bands (isotropic band) are spilt down
the middle by Z discs.
-Thick filaments contain myosin and extend across the A
band (anisotropic band) connected at the M line. Myosin is a
large molecule that has a tail region named light
meromyosin and headgroups named heavy meromyosin.
The tail and head region connect to actin.
-Thin filaments contain actin extending across the I band and
into the A band.
-Titin, a protein involved in sarcomere organization, are
elastic filaments spanning from the Z disc to the thick
filament involved in storing energy. They help increase the
total tension in filaments.
-Heads are site of activity because of ATP and actin binding
sites for cross bridges
-Creatine phosphokinase is a type of protein found in the
sarcomere for energy metabolism. This converts ADP to ATP
for muscle contraction.
-Sarcoplasmic reticulum: surround microfibrils to regulate
calcium storage and calcium includes t tubules.
Sliding filament model
-When nervous system stimulates muscle fibers, myosin
heads interact with binding sites on actin. Thick and thin
filaments pull z disc towards mline. I bands shorten and H
band disappears. A bands get closer together which
produces a muscle contraction
-The muscle contracts when myosin and actin glide over each
other shortening the muscle. Z lines come together towards
the sarcomere.
Cross bridge cycle
-Four steps are involved in the cross-bridge cycle. The first of
them being the crossbridge attachment. Energized myosin
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Skeletal muscle

  • Made of fascicles made of muscle fibers. Muscle fibers are multinucleated induvial muscle cells. Myofibrils are comprised of myofilaments composed of sarcomeres.
  • H zone (helle zone) is spilt down the middle by M line. H zone disappears as the sarcomere contracts and actin does not overlap myosin. I bands (isotropic band) are spilt down the middle by Z discs.
  • Thick filaments contain myosin and extend across the A band (anisotropic band) connected at the M line. Myosin is a large molecule that has a tail region named light meromyosin and headgroups named heavy meromyosin. The tail and head region connect to actin.
  • Thin filaments contain actin extending across the I band and into the A band.
  • Titin, a protein involved in sarcomere organization, are elastic filaments spanning from the Z disc to the thick filament involved in storing energy. They help increase the total tension in filaments.
  • Heads are site of activity because of ATP and actin binding sites for cross bridges
  • Creatine phosphokinase is a type of protein found in the sarcomere for energy metabolism. This converts ADP to ATP for muscle contraction.
  • Sarcoplasmic reticulum: surround microfibrils to regulate calcium storage and calcium includes t tubules. Sliding filament model
  • When nervous system stimulates muscle fibers, myosin heads interact with binding sites on actin. Thick and thin filaments pull z disc towards mline. I bands shorten and H band disappears. A bands get closer together which produces a muscle contraction
  • The muscle contracts when myosin and actin glide over each other shortening the muscle. Z lines come together towards the sarcomere. Cross bridge cycle
  • Four steps are involved in the cross-bridge cycle. The first of them being the crossbridge attachment. Energized myosin

molecule will attach to actin which will produce a steric shift in the molecule. ADP is then released from the headgroup and goes through a power stroke by pulling the actin over the myosin. The third is a detachment in the cycle. To get the headgroup to detach, add an ATP molecule. As long as regulatory proteins allow attachment and ATP allows for detachment, the cycle will continue.

  • Or in other words, muscle contraction is initiated when muscle fibers are stimulated by a nerve impulse and calcium ions are released
  • The troponin units on the action myofilaments are bound by calcium ions. The binding displaces tropomyosin along the myofilaments which expose the myosin binding sites
  • The head of each myosin unit is bound to an ADP and phosphate molecule. The myosin heads then release the phosphates and bind to the actin myofilaments thru the myosin binding sites, forming a cross bridge
  • The two filaments glide against one another while releasing the ADP molecules
  • Once ATP is bounded to the myosin heads, the binding stops Excitation contraction coupling
  • An action potential runs down and gets to the neuromuscular junction releasing neurotransmitter, acetylcholine which binds to the receptors on the sarcolemma triggering the generation of actional potential. As action potential spreads along the sarcolemma, it is carried along the myofiber with the help of transverse tubules. Dihydropyridine receptors (DHP) are depolarized changing and pulling on ryanodine receptors of the sarcoplasmic reticulum triggering the response of calcium channels and the release of calcium from the sarcoplasmic reticulum into the cell membrane. As calcium diffuses it binds to the troponin regulatory protein which thus makes a change in the displacement of tropomyosin and troponin exposing the myosin binding sites on actin allowing myosin to bind forming a cross bridge and initiating the power stroke cycle in muscle contraction

receptors which depolarizes the membrane. The electrical impulse travels down the T-tubules and allowing calcium to flow in and bind to the myofibrils to trigger a muscle contraction. The sarcomere contracts as a whole and the zlines draw closer to the mline Chapter 6 Single fiber contractions

  • The total tension produced by the muscle is a summation of tension produced by induvial fibers. Total tension is influenced by the number of motor units activated
  • Three different types of contraction that could take place o Isometric contraction: muscle contracting under the same length o Isotonic contraction: same resistance or load on the muscle o Lengthening contraction: when load is greater than the force generated by the muscle Individual twitches
  • Time period before contraction starts
  • Tension is produced depending on how many cross bridges are formed
  • The latent period is the time period of excitation contraction coupling
  • Generate tension to go to contractile phase, calcium is reclustered in SR, fewer cross bridges so relaxation state muscle. Relaxation time is longer than excitation time Isotonic contraction
  • Occurs when there is a constant load on the muscle enabling it to shorten.
  • With a light load = much greater distance shortened
  • All stimulated at the same point but as you get heavier, the latent period increases. Takes more time to move the load so latent period increases.
  • The rate of shortening changes. If there is a light load, muscle moves quickly. Shortening velocity decreases as you

get a heavier weight. As we increase the load, the latent period gets increased as well. While decreasing the shortening velocity and duration of contraction because it takes more force to move the load, so there is less energy left to maintain the contraction and shorten the muscle. Change activity of muscle depending on how we activate the muscle Frequency effects

  • Tetanus: maximum amount of force that can generated. 3-5x as much than a twitch produces A combination of the series elastic component, storing energy and the increase in calcium that we release Length vs tension curve
  • Length that produces the greatest tension is known as the rust length or the else of 0. As the length gets increased, the z lines get pulled further apart, the myosin and actin have been separated and the number of cross bridges and tension gets decreased. The shorter the z line, the further myosin gets pushed back from actin eliminates tension production
  • Length of the muscle shows us how we are changing the number of cross bridges which changes the tension produced Load velocity relationships
  • A muscle will contract or shorten more rapidly when there is no load on the muscle and shorten
  • A muscle will achieve Maximum velocity when there is no load
  • As load increases or you cross the 0 access you get an isometric contraction because muscle is no longer shortening and lengthening contractions as you geta. Negative shortening

Whole muscle contraction

  • Recruitment is a change in tension. Starts firing with a few neurons then upgrades if needed. There is a graded response on amount of tension to perform movement. Adaptations to exercise
  • Atrophy: decrease muscle size if not used
  • Denervation atrophy: motor neuron malfunction
  • Hypertrophy: muscle mass increases if stimulated often. ATP forming capacity increases and vascularization for the production of red fibers Types of fibers Velocity of shortening and formation of ATP pathway
  • Isozymes: a fast and slow myosin isozyme. Differ in how fast they transfer ATP
  • Oxidative muscle fibers: red muscle fibers dark because of myoglobin (oxygen storage to make ATP)
  • Glycolytic muscle fibers: uses glycolysis as main energy formation pathway. Have little myoglobin little basculation. Large glycogen storage. Larger in diameter, last to be activated because cannot work for very long. Fatigue very rapidly o Slow oxidative fibers: dark red large concentration myoglobin. Produces lost of ATP thru aerobic respiration. Store low amounts of glycogen. Slower contraction cycle. High fatigue contractions o Fast glycolytic fibers: contain larger concentrations of myoglobin. Produce ATP. Can store more glycogen through anerobic glycolysis. Fatigue resistance “fast twitch” o Fast oxidative fibers: lowest concentration of myoglobin, = more pale color. Store large quantities of glycogen. Second type of fast twitch stronger contraction speed. Low fatigue resistance Smooth muscle
  • Uses calcium to regulate contractions and is involuntary using autonomic system
  • Lacks sarcomeres but instead uses actin directly for tension to be formed. Actin anchors to dense bodies to work over greater length changes.
  • Rare length is greater than cardiac giving the greatest tension
  • Smooth muscle can inhibit and activate its muscle unlike skeletal that can only activate.
  • Shorter than skeletal muscle and is uninucleate meaning it can divide muscle cells Smooth muscle contractions (smooth muscle excitation contraction coupling)
  • Calcium from extracellular fluid in the sarcoplasmic reticulum innervates an action potential. Calcium then binds to calmodulin to a form a calcium calmodulin complex. The complex binds to an MLC (myosin like chain kinase) enzyme and becomes activated
  • Enzyme then takes energy from ATP and phosphorylated MLC so a contraction occurs. Myosin molecule will be activated to regulate the contractions as cross bridges are forming and muscle is shortening. To stop the contraction, remove phosphatase to come back to MLC to decrease the cross bridges to enter relaxation How cells transfer information
  • Spontaneous electrical activity: pacemaker potential in cells slowly depolarize until action potential reaches giving spontaneous activity
  • Nerves and hormones can influence contractions: neurons innervate smooth muscle at swellings if varicosities. Both sympathetic and parasympathetic innervation on a single cell through neural and hormonal stimulation.
  • Local factors: ph of extracellular concentration leads to changes in tension. We have a localized response based on the conditions in that area

Heart

  • Cardiac muscle is Mostly composed of myocardial cells jointed by intercalated disc or specialized junctions. They are a combination of desmosomes and gap junctions
  • Valves create a unidirectional flow in a passive process. There are four valves in the heart.
  • The right atria ventricular valve or atrioventricular valve also called the tricuspid valve. Lies in the right atrium and right ventricle with three cusps.
  • On the left side, the left atria ventricular valve also called the bicuspid valve or mitral valve consisting of two flaps. Lies between the left atrium and left ventricle. The atrioventricular valves allow blood flow from the atria to the ventricle and prevents backflow.
  • The semilunar valves located at the origin of pulmonary artery and aorta. These valves open during ventricular contraction or close when pressure in the arteries is greater than ventricles. Can be subdivided into aortic semilunar valve and pulmonary semilunar valve as semilunar valves separate ventricles from arteries. Heartbeat coordination
  • Pacemaker cells have pacemaker potentials and are autorhythmic. Whichever group of cells depolarize fastest are the pacemaker cells
  • Sinoatrial node (SA node) : a normal pacemaker as it has the fastest rate of depolarization. Generates impulses in the right atrium to produce a heartbeat. Actional potential spreads through the atria to form a simultaneously contraction.
  • Atrioventricular node (AV node): conducts cardiac impulses to ventricle by AV bundle.
  • Atrioventricular bundle (of his) : begins in AV node and runs along of intraventricular septum. Conducting impulses from atria to ventricles
  • Right and left branches of bundle of his: high speed conduction branches of AV bundle
  • Purkinje fibers: branches of right and left branches of bundle of his. Conduction system of the heart
  • SA node initiates impulses that spread to atria to contract. AV picks single from atria to conduct it to AV bundle and its branches. Papillary muscles and Purkinje fibers contracts to cause contraction of ventricular muscle and fibers Cardiac action potential (ventricle action potential)
  • A maintained depolarization is also called a plateau phase with the continuing of release of calcium by inhibiting potassium channels and opening sodium channels Excitation contraction coupling
  • Once a depolarization occurs, extracellular calcium channels are open for the flow of calcium to come in to bind to myosin once tropomyosin rotates out. Actin and myosin form cross bridges which initiates a contraction.
  • Begins when extracellular calcium comes in through a calcium dependent voltage and is released with the help of ryanodine receptor. Calcium that is released from the sarcoplasmic reticulum bind to the actin thin filaments initiating contraction of the sarcomeres. At the end of the contraction, calcium comes off the myofilaments and is actively transported out of the cell. Interactions with the actin thin filaments and myosin cross bridges comes from the binding of calcium and troponin C which shifts troponin complexes and tropomyosin to enable the actin to interact with myosin. Myosin ATPase then hydrolyzes ATP for myosin and actin to pull to the center of the cell and start the activation again. Electrocardiograph
  • Measure electrical activity of heart. Wave forms differ depending upon where the electrons are placed
  • P wave: atrial depolarization ( SA node fires and atria contracts)

Cardiac output

  • CO = HR x SV Regulation of heart rate
  • In sympathetic system: norepinephrine is released to increase permeability of the membrane to sodium and calcium so there leads to a depolarization to reach an action potential. Thee SNS increases the speed of contractions by decreasing the end systolic volume to get a greater stroke volume.
  • In parasympathetic nervous system, by releasing acetylcholine, potassium’s permeability increases to slow the rate of depolarization Regulation of stroke volume
  • End diastole volume – end systolic volume
  • SV = EDV – ESV
  • End diastole volume: how much blood we have at the end of diastole
  • End systolic volume: how much blood is left over in the ventricle after a contraction Starling law:
  • a law which define how well cardiomyocytes work well to increase the volume
  • End diastolic volume: volume of blood in ventricles before contraction
  • Preload: end diastolic pressure stretching the walls of ventricles to their greater
  • Stroke volume: volume of blood ejected from heart per heartbeat
  • A greater end diastolic volume would increase the contractile strength of the ventricles and will increase the stroke volume
  • The myocardium will be more stretched due to a greater volume therefore increased sarcomere length resulting in increased sensitivity to calcium ion therefore having a stronger contraction Contractility for heart rate contraction
  • Decrease end systolic volume (ESV) to increase stroke volume (SV)
  • norepinephrine will bind to a membrane receptor because of its water solubility composition.
  • The receptor will activate the G stimulatory protein which will activate adenylate cyclase that will then make clyic AMP with ATP.
  • The cAMP will then activate protein kinases which will influence the activity of the cardiac muscle
  • In the four pathways it contains, the first thing it will do is open calcium channels to come in. The second protein kinase goes to a promiscuous sodium channel allowing calcium to go through instead of sodium.
  • The third protein kinase works on calcium making it go faster, shortening the contraction to maintain time for ventricular filling
  • The fourth protein kinase will phosphorylate myosin to use the ATPase more rapidly so this increases the speed of the contraction to generate the greater amount of tension. Because of the greater amount of calcium channels being released.
  • To increase heartrate: cut into time ventricular ejection to make the contraction happen faster to maintain EDV when ESV is decreased we get a greater stroke volume Chapter 8 Arterial compliance
  • Change in volume/ change in pressure

Blood

  • The blood is composed of three layers the top, most abundant plasma layer, the middle containing leucocytes and thrombocytes and bottom including erythrocytes. Blood is used for substance distribution such as oxygen and metabolic waste and protection maintaining the total pH, fluid volumes, infections and much more. Plasma
  • Plasma proteins can be synthesized by the liver and lymphocytes. Three types of plasma proteins are albumins, fibrinogen, and globulins. The most abundant, albumin, maintains osmotic pressure by forcing fluid out and

o Eosinophils pick up acidic stains and are found in our respiratory mucosa. These bind to antigen and antibody complexes

  • Agranulocytes lack cytoplasmic granules o Monocytes are the largest of white blood cells and differentiate into macrophages to eat pathogens much easier. These activate lymphocytes o Lymphocytes are b and t cells. B cells differentiate into plasma cells to make antibodies and T cells are the cell to cell killing cells.
  • Thrombocytes produce a megakaryocyte going through mitosis but not cyto-kinases Decrease oxygen tension in kidney
  • Renal erythropoietin factor activates erythropoietin to activate red bone marrow to activate the production of red blood cells. The Renal erythropoietin factor transports oxygen better Vascular system
  • Five different types of blood vessels
  • Arteries leave heart. It is composed of single layer endothelium o Has a tunica media made of smooth muscle allowing for basal constriction of the blood vessels and compliance allowing arteries to stretch when ventricle contracts
  • Arterioles determine where the blood goes within organs. It is the major sire of resistance as there is a greater drop in pressure. It has the ability to direct flow. Blood vessels can self regulate blood flow coming to them. If lumen gets smaller or decreasing diameter it is known as vasoconstrictions and larger, vasodilation
  • Vasoconstriction decreases volume and increases pressure Capillaries
  • Velocity of blood vessels decrease as the cross sectional area increases
  • Precapillary sphincters slow regulations of amount of blood flow into the capillary network Net filtration pressure
  • NFP = (pressure in capillary – pressure of interstitial fluid) – (plasma osmotic pressure – pie interstitial fluid) Venules
  • Increase velocity and decrease total area to get blood to heart Veins
  • lowest pressure is found here so uses pumps to function
  • skeletal muscle pump: brings blood to heart
  • respiratory pump: helps in breathing. Movement of air is based on pressure differences Lymphatics
  • made up of blind capillaries
  • lymph: excess fluid that is returned to circulatory system. Lymph’s avoid swelling of the tissue by forcing fluid in when fluid pressure is greater out and vice versa Ch 9.
  • Highest pressure is the ventricular ejection or systolic pressure where the lowest pressure is the isovolumetric contraction just before the valves open again or diastolic pressure
  • Pulse pressure: systolic – diastolic mmHg
  • Pulse pressure determines MAP (mean arterial pressure)
  • MAP: 1/3(pulse pressure) + diastolic pressure mmHg (93.33mmhgin an average person) Two factors to calculate cardiac Output: heart rate and stroke volume
  • TPR x CO = MAP
  • Delta P = CO x R (heartrate x stroke volume) Factors affecting blood pressure
  • F = delta P/ R

Baroreceptor reflux

  • Baroreceptors are special pressure receptors found in the aortic arch directing an increase or decrease in pressure to reply information to the medulla depending on what unput is the response will influence the TPR to either vasoconstrict or dilate.
  • Baroreceptors sense overall bp around the body. With an increasing arterial pressure, so will the baroreceptors sending that information to the medullar cardiovascular control center to determine that bp is rising sending out signals to decrease bp by decreasing sympathetic activity and simultaneously increasing parasympathetic activity and decreasing the heart rate. Because of the decreased sympathetic activity any contractility effects such stroke volume, vasoconstriction and pressure in veins will be decreased as will. The decrease in stroke volume and heart rate leads to a decrease in cardiac output. The decreased vasoconstriction leads to a decrease in the total peripheral resistance which indeed decreases blood pressure.
  • If bp is decreased, the stimulation of the release of hormones is activated. The baroreceptors in the hypothalamus will then trigger a signal to the posterior pituitary to release ADH to resorb as much water to maintain blood volume and vasoconstriction. Another system is the renin angiotensin system
  • Renin is released in the kidneys when there’s a decrease in blood pressure. The renin converts angiotensin to angiotensin 1. A converting enzyme converts angiotensin1 to angiotensin 2 to get a vasoconstriction as it is a vasoconstrictor to lead to a increase in bp. Angiotensin 2 also stimulates the release of aldosterone release from the adrenal cortex for sodium and ADH reabsorption in the kidney tubules to occur for reabsorption of water to increase the blood volume thus increasing the blood pressure.

Other responses in blood pressure

  • Chemoreceptors are important in intrinsic responses. They provide information about blood flow in a particular region to feed that information to the Medullar Control Center to eventually maintain the flow
  • Higher brain centers such as the cerebral cortex and hypothalamus changes the vasomotor activity in the body
  • Chemical controls such as the adrenal medulla hormones and atrial natrieutic factor determine blood pressure as well. The adrenal medulla hormones releases epinephrine and norepinephrine for vasoconstriction or dilation. Norepinephrine increases the cardiac output, heartrate and contractility. Epinephrine in skeletal muscle causes vasodilation because of the beta receptors found. ANF produced by the atrial cells of the heart are stretched as blood pressure increases. The ANF goes to the blood pressure for vasodilation to decrease it. ANF also decreases reabsorption of sodium in kidneys leading to a decrease in blood volume and blood pressure.
  • Alcohol influences blood pressure by vasodilation and decreasing ADH to cause a decrease in blood pressure Exercise leads to more blood to the heart and muscle. CO2 will increase by vasoconstruicting organs not begin used such as the kidneys Active herima: eliminate heat through mucles to tlimate through skin so blood flow pattern changes Increase cardiac output increase MAP , systolic pressure pulse pressure, amount of blood flowing around the body while decreasing peripheral resistance Increase venus return = increase EDV Hypertension: cronic increase 140/ 120/80 normal bp