1.02 Physiology Trans - Muscle Physiology

March 9, 2019 | Author: MineTagra | Category: Muscle Contraction, Neuromuscular Junction, Actin, Muscle, Histology
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1.02 19, June, 2015

Dr. KATHERINE MUNARRIZ | Muscle Physiology

SKELETAL MUSCLE The skeletal muscle is multinucleated, striated and moves voluntarily  Each muscle covered by an EPIMYSIUM  Each muscle is composed of FASCICLES which are covered by the PERIMYSIUM  Each fascicle is composed of several MUSCLE FIBERS (cells) which are covered by an ENDOMYSIUM  A muscle fiber is composed of several MYOFIBRILS which are covered by the SARCOPLASMIC RETICULUM (SR) and invaginated by T-TUBULES (transverse tubules)  SARCOLEMMA is a thin membrane enclosing a skeletal muscle fiber. Through this, the action potential passes towards the T tubules.  The T tubules are extensions or invaginations of the sarcolemma that brings the action potential rapidly to the innermost part of the muscle.  Myofibrils consist of SARCOMERES that contain the Actin (Thin Filament) and Myosin (Thick Filament)  SARCOPLASM is the intracellular fluid between myofibrils that contains large quantities of K, Mg and PO4, plus multiple protein enzymes. Also present are tremendous numbers of mitochondria that lie parallel to the myofibrils. These supply the contracting myofibrils with ATP. Mitochondria also store Ca++ that adds to intracytosolic Ca++ during depolarization.

composition: a. large protein that consists of six diff erent polypeptides b. one pair of large heavy chains c. two pairs of light chain  Thin Filament (Actin) formed by the aggregation of actin molecules (Gactin) into a two-stranded helical filament (F-actin)  – inhibits binding of myosin to actin by covering Tropomyosin – inhibits the binding site

Troponin complex a. Troponin T -Has strong affinity to tropomyosin -Attaches the troponin complex to tropomyosin b. c.

-No. 1 inhibitor of Cross-bridge formation Troponin I- Has strong affinity to actin -Inhibits interaction of actin and myosin Troponin C -Ca ++ protein that once bound permits myosin and actin interaction by the movement of tropomyosin, thereby exposing the myosin binding sites.

*A thin/actin filament is made-up of the following proteins: actin globules, tropomyosin and troponin (T, I, and C).

Parts of a myofibril  Sarcomere - segment of myofibril between two Z lines/disc line – bisects  bisects the I-band; attachment of the actin  Z line – filament (Isotropic)  – contains  contains only actin (thin)  I band (Isotropic) – filaments Zone – light  light are between the A-band contains only  H Zone – myosin (thick) filaments (Anisotropic)  – dark  dark striation of the myofibril  A band (Anisotropic) – that contains both actin and myosin line – bisects  bisects the H zone  M line – *In a normal contraction/ regular contraction, it is the H zone and I band which shorten. *The I band, A band and Z disc/ line  give the skeletal muscles its striated appearance.

Muscle filaments 

Thick Filament (Myosin) tethered to the Z-lines by a cytoskeletal protein called titin

Transcribers: Azarcon, Azarcon, Balucating, Balucating, De Leon, Dela Torre, Pizarras, Pizarras , Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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Neuromuscular Junction Transmission

4. 5.



Ca++ entry triggers the release of Ach from the axon terminals Ach diffuses from axon terminals to the synaptic cleft and attaches to the receptor sites at the motor end plate/sarcolemma of the muscle The binding of the Ach to the receptors opens Ca ++ channels at the end plate and causes and influx of Ca++ and an efflux of K+, depolarizing the membrane (sarcolemma), producing the EPP. EPP depolarizes the adjacent muscle cell plasma membrane to its threshold potential, generating an AP that propagates the muscle fiber surface

Nerve Cell Resting Membrane Potential (RMP): -70 mV Nerve Cell Threshold Potential: -55mV Skeletal Muscle Cell RMP: -90mV Skeletal Muscle Cell Threshold Potential: -75mV 8.

 

SYNAPSE is the area between a nerve and a muscle cell LOWER MOTOR NEURON (LMN) supplies the muscle cell and synapses with the SkM fiber SOMATIC NEURON – supplies the Skeletal  muscle


The AP travels from the sarcolemma towards the Ttubules From the T-tubules, the AP reaches the Ca ++ channel DHPR ( Dihydropyridine Receptor) and activates the RYR (Ryanodine Receptor) which releases Ca++ from the terminal cisternae of the Sarcoplasmic Reticulum (SR) into the myoplasm

AUTONOMIC NEURON – supplies the Smooth muscles END PLATE –the part of the muscle where Ach attaches to the receptor sites ACETYLCHOLINE –the only neurotransmitter found in the NMJ NEUROMUSCULAR JUNCTION (NMJ) -End Plate + Post Synaptic Axon Terminal END PLATE POTENTIAL (EPP) –a localized nonpropagated potential  that could produce an AP in the muscle when threshold is reached 

   

1. 2.


An Action Potential (AP) is received by a neuron and travels down the axon to the a xon terminal The AP causes an influx of Na+ which causes a depolarization while an efflux of K+ will cause a repolarization. The repolarization causes the regeneration of the AP and the next depolarizing event occurs at the Node of R anvier and continues to the next until it reaches the axon terminal. Some Notes: -Upper motor neuron- located in brain cortex -mostly excitatory (Na+ influx) -Interneuron- mostly inhibitory (K+ efflux; Cl- influx) -Lower Motor Neuron-found in spinal cord -Axon Hillock- where action potential is generated. The AP at the axon terminal allows the opening of the voltage-gated Ca++ channels  which causes an influx of Ca++

T-tubules are extensions/invaginations of the Sarcolemma that extends into the muscle fiber, forming a close association with the two terminal cisternae of the SR

This association of the T-tubule with the terminal cisternae is called a triad

The T-tubule and the terminal cisternae are connected by bridging proteins called feet

These feet are the RYR through which the Ca ++ is released in response to an AP At the T-tubule membrane, the RYR interacts with the DHPR which is an L-type voltage gated Ca++ channel with five subunits

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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Dr. MUNARRIZ | Muscle Physiology

One of the subunits of the DHPR appears to be critical for the ability of the AP in the T-tubule to induce release of the Ca++ from the SR

However, influx of Ca++ into the cell through the DHPR is not needed for the ini tiation of Ca++ release from the SR

Instead, release of the Ca++ f rom the terminal cisternae of the SR is thought to result from a conformational change in the DHPR as the AP passes down the T-tubule

This conformational change, by means of a proteinprotein interaction, opens the RYR (like a mechanical opening of a door) and releases the Ca++ into the myoplasm 10. When the Ca++ is released, it binds to Troponin C which promotes the lateral movement of the Troponin-Tropomyosin complex, exposing the myosin-binding site on the actin filament 11. Immediately, myosin heads bind to the sites on the

actin filament and contraction happens 12. The Ca++ that was previously bound to Troponin C is

reabsorbed by the tubules of the SR 13. The reabsorption of the Ca++ causes the

Tropomyosin to cover again the binding sites, releasing the interaction of the myosin head and the actin filament 14. Ca++ uptake in to the SR (Ca++ ATPase) is due to the

a. b. c.


In the relaxed state, ATP is partially hydroyzed by Myosin In the presence of elevated myoplasmic Ca ++, myosin binds to actin Myosin releases ADP and phosphate ion. Hydroly sis of ATP is completed and causes a conformational change in the myosin molecule that pulls the actin filament toward the center of the sarcomere (powerstroke) and contraction occurs. A new ATP binds to myosin and causes release of cross-bridge. Partial hydrolysis of the newly bound ATP recocks the myosin head, returning to the resting state. Myosin head is now ready to bind again and again.

The cycle continues until the SERCA pumps back C a++ into the SR. As Ca++ concentration falls, Ca ++ dissociates from Troponin C, and the troponin-tropomyosin complex moves and blocks the myosin binding site on the actin filament. If myoplasmic Ca++ is still elevated, the cycle repeats, if myoplasmic Ca++ is low, relaxation occurs.

Roles of ATP

  

action of SERCA (Sarcoplasmic Endoplasmic Reticulum Calcium ATPase) 15. From the tubules of the SR, the Ca++ is brought back

to the terminal cisternae where it is stored

Calsequestrin is a low affinity Ca++ binding protein that helps accumulate Ca++ in the terminal cisternae

ECF Ca++: 10-3 mol/L ICF Ca++: 10-8 mol/L resting; 10-5 mol/L contracted Ca++ is more concentrated in the ECF

Cross-Bridge Cycle

Cross Bridge Cycling: 1 Cross bridge = 1 ATP ATP causes both contraction (indirectly) and relaxation (directly) Decreased production of ATP ->Rigor Mortis at death; In living persons, delayed contraction and relaxation

Mechanisms that Prolong Contraction Factors that prolong cytosolic Ca++ a. Increased frequency of AP b. Defective Na+ inactivation: continued Na+ influx ->muscle membrane will be depolarized ->conformational change in DHPR leading to RYR activation ->hyperkalemic periodic paralysis c. Defective Ca++ RYR: continued Ca++ release ->Malignant Hyperthermia Mechanisms for Relaxation: Relaxation occurs by decreasing the cytosolic/intracellular Ca++ or by detaching the myosin head to actin. 1. Via SERCA (sarcoplasmic endoplasmic reticulum calcium ATPase):  Ca++ resequestered to SR due to Ca++ ATPase, an active pump  SERCA is the most abundant protein in the SR of skeletal muscles  Transports 2 Ca++ for each hydrolyzed ATP 2. Decreasing the action potentials  Decreases DHPR and RYR Decreased cytosolic Ca++ 3. Myosin ATPase

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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PHYSIOLOGY Dr. MUNARRIZ | Muscle Physiology

Attachment of ATP to the myosin head  detachment of myosin head to actin  eventually relaxes muscles

Phases of the Muscle Twitch 1. Latent phase  As action potential reaches sarcolemma and down the T-tubules and starts the excitation-contraction coupling  2 ms 2. Contraction phase  Cross-bridge formation (Actin-myosin interaction)  Includes isometric and isotonic phases of contraction  Maximum tension (T M) depends on the number of muscle fibers that are recruited during the contraction  15 ms 3. Relaxation phase  Ca++ reuptake  decreased tension in the sarcomere  25 ms

Phases of Contraction 1. Isometric Phase  No isotonic phase of contraction  No change in muscle length.  Tension  TM is reached at end of the isometric phase of contraction, and is maintained thereafter;  Load (TL)  TM, the muscle does not shorten and the load is not moved; there is simultaneous contractions (co-contraction) of agonist and antagonist muscles  TL TM (+) LENGTHENING and movement of load  TL =TM  (-) shortening and movement of load Muscle Tension

Tension refers to the interaction of actin and myosin. 1. Active tension  Generated when the opposing actin filament is almost equal to myosin filament exerted during the cross-bridge formation.  How to increase the active tension?   Spatial summation: increase number of crossbridges (length of actin-myosin overlap)  Temporal summation: increase number of action potentials by increasing UMN  LMN  sarcolemma stimulation (frequency of stimulus) 2. Passive tension  Tension between connective tissues or cell elements  “Lo” (optimal length), which is between 2.0 – 2.2 m in both skeletal and cardiac muscle, and 90  – 110% of the original muscle length.  Lo = start of passive tension (refer to the picture below)  Change in passive tension is directly proportional to muscle length  Usually the tension measured before muscle contraction.  Refer to the picture below:

Clinical importance of providing passive tension after a n extensive exercise (i.e. cool-down/stretching)  Allows muscle to go back to its L O  Increasing efficiency of muscle length and avoids muscle pain induced after the exercise (delayed-onset muscle soreness/DOMS) Relationships between…


 LO = 2.0 - 2.2 μm for skeletal and cardiac muscles  Active tension:  As stress increases, muscle length also increases up to L O. Beyond this point, contractile force (stress) decreases.

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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PHYSIOLOGY Dr. MUNARRIZ | Muscle Physiology

Passive tension:  When muscle is at rest, stretching of the muscle length initially increases stress slowly, and then more rapidly as the extent of stretch increases.

Length-Tension Relationship 

Optimal length of sarcomere prior to contraction = 2.0 2.2 m

  

initial length # cross-bridges

The Third Law of Newton : When a mass exerts a force on another mass, the second mass simultaneously exerts a force equal in magnitude but opposite in direction to that of the first mass. When all the muscle fibers in the muscle bundle have been recruited to carry the load  the tension generated by that muscle bundle is maximal (see point B of the power-stress curve) Yellow-box region: isotonic concentric contraction Green-box region: isotonic eccentric contraction Point C: isometric contraction (no change in muscle length)

tension in fibers


 Dependent on motor unit activity.  Summation of muscle contractions Spatial summation o  cross-bridges of muscle fibers or increasing the tension twice as its original load Temporal summation (Tetanus) o  number of action potentials or  frequency of stimulation o Results to prolonged cytosolic Ca++ increased number of cross-bridges  increased active tension


Poin t



Velocity of shortening /lengtheni ng


No load

Submaxim al



Submaxim al

Submaxim al

Submaxima l





Max. to decreasin g

**Increasin g from point C/isometric phase (doesn’t



 Increasing the load will increase the cross-bridges: Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

Other notes: No power since no distance was covered Max power No power since work velocity is zero; Maximum tension Velocity of lengtheni ng

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PHYSIOLOGY Dr. MUNARRIZ | Muscle Physiology mean that eccentric contractio n is faster than concentric)

 Recruited later  as more and more force i s needed 

since these fibers are large and more diffi cult to excite. For high-intensity activity that entails great power.

Muscle Fiber Types  Recruitment of muscle  fibers (accdg. to Size Principle of Recruitment):  Simultaneous activation of muscle fibers done to increase force of contraction  Muscle fibers with lower thresholds are stimulated first  Weak stimulus: activates neurons with low threshold (small motor units at the level of UMN)  Strong stimulus:  activates neurons with high threshold

Summary of basic classification of skeletal muscle fiber types

Types of fibers: 1. Type I (Slow-oxidative fibers)  Slow twitch  Uses aerobic respiration (consumes oxygen, glucose, fatty acids, and lastly the 30-32 ATPs)  Less fatigable; hence, good for prolonged activities  Recruited first than fast-twitch fibers since these fibers are small and are easily excited.  For mild-moderate intensity activities that requires control and endurance 2. Type II (Fast twitch)  May be Type IIa (Fast-oxidative) or Type IIb (Fastglycolytic – focus)  Type IIa (intermediate): uses aerobic respiration (consumes oxygen, glucose, fatty acids, and lastly the 30-32 ATPs)  Type IIb: uses anaerobic respiration (ADP and creatine phosphate/CrP)  More fatigable

Muscle Tone  Muscle tone refers to the tautness of a muscle, even at rest.  Mechanisms for Muscle Tone:  At rest, type II afferents  (sensory nerves at the muscle spindle) tonically send afferent proprioceptive impulses towards the spinal cord where they synapse with the lower motor neurons (LMN). 1. The alpha MN synapses with the extrafusal muscle fibers, while the gamma MN synapses with the intrafusal muscle fibers, or the muscle spindles.

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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PHYSIOLOGY Dr. MUNARRIZ | Muscle Physiology 2. The afferents synapse monosynaptically with the alpha MN, and polysynaptically with the gamma MN. *More on this concept, in the Study Guide on the  Autonomic Nervous System, where the myotatic  / stretch reflexes will be discussed.  Muscles are arranged in antagonist pairs  and groups. As one muscle exerts a little contraction in response to the impulses passing thru the reflex arc, it stretches its antagonists,  causing them to send proprioceptive sensory information back to the spinal cord. Thus, a normal state of involuntarily controlled contractions of various skeletal muscle fibers in different muscle groups occurs, which keeps all individual muscles in a state of partial contraction, and ready to contraction more forcefully if voluntary commands are received from the cortical motor areas.

Muscle Fatigue  Prolonged and strong contraction of a muscle  inability of the contractile and metabolic processes of the muscle fibers to continue supplying the same work output  FATIGUE!  Mechanisms of (peripheral) muscle fatigue:  Failure of nerve impulses to release enough ACh  Depletion of ATP, glycogen, creatine PO 4  Build-up of ADP inhibits CB cycling + +  Depletion of ICF K  or accumulation of ECF K ++   Release of Ca ions from SR   protons (  pH) changes protein conformation


    

Cardiac muscle is STRIATED and INVOLUNTARY. Some cardiac fibers are connected by intercalated disks. Cardiac muscle is capable of self-excitation. FASCIA ADHERENS and DESMOSOMES provide mechanical connection. GAP JUNCTIONS in between cells provide electrical connection.

1. Excitation of cardiac muscle results from: a. Primarily by: i. Pacemaker potentials ii. Electrical coupling, or depolarization via gap junctions -these will result in depolarization of the ca rdiac muscle, and activate the DHPR. I n contrast to the skeletal muscle wherein DHPR mechanically changes the RYR to release Ca++ from the SR, activation of the DHPR in cardiac muscle fibers result in a small flux of Ca++ into the sarcoplasm -> small increase in cytosolic Ca++ will open the

RYR channels (Ca++-induced Ca++ release from SR) -> large increase in cytosolic Ca++ -> cardiac muscle contraction. b. Modulation by: -neuromuscular transmission, via autonomic nerves’ release of neurotransmitters. 2.Action Potential a. Fast Response (happens in the atrial and ventricular cardiac cells and in the Purkinje fibers) Phase 0: Rapid Na+ influx caused reversal of polarity from (-) to (+) depolarization. Phase 1: K+ efflux causes an EARLY REPOLARIZATION. Phase 2: Ca++ influx maintains impulse (plateau) Phase 3: continuous K+ efflux makes the cell’s polarity become more (-) than the previous (+) it was (repolarization). Phase 4: Resting state achieved. b.Slow Response (happens in the sinoatrial node and atrioventricular node via cardiac conduction system) Why does the duration of the action potential make tetanic contractions impossible in cardiac muscle fibers? Cardiac muscle and skeletal muscle differ, however, in the level of intracellular [Ca++] attained after an action potential and hence in the number of actin-myosin interactions are high after an action potential. In cardiac muscle, the rise in intracellular Ca++ can be regulated, which affords the heart an important means of modulating the force of contraction without recruitment of more muscle cells or undergoing tetany. Recall that in the heart all the muscle cells are activated during a contraction, so recruiting more muscle cells is not an option. Moreover, tetany of cardiac muscle cells would prevent any pumping action and thus be fatal. Consequently, the heart relies on different means of increasing the force of contraction, including varying the amplitude of the intracellular Ca++ transient.

3.Contraction Events What are the mechanisms for the increase in cytosolic Ca++ in cardiac muscle? -influx through voltage-gated L-type Ca++ channel -Ca++-induced Ca++ release (CICR) from the SR (DHPR -> Ca ++ bind with RYR -through β-adrenergic agonists (activation of β-receptors -> activates adenylyl cyclase -> ^ cAMP -> phosphorylation -> ^ Ca++ in SR 4.Relaxation Events ↓ICF Ca++ through -Ca-ATPase/ SERCA -Ca-ATPase/ sarcolemma -Ca++-Na+ antiporter (secondary active transport: 3Na in, 1Ca out)

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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PHYSIOLOGY Dr. MUNARRIZ | Muscle Physiology

5.Muscle Tension ^muscle tension, contraction force ^cytosolic Ca++ - by β-agonists ^sensitivity of myofilaments to cytosolic Ca++ - ^ stretch by ^preload (Frank-Starling Mechanism)

ii & iii. Anything that ^afterload -> ↓shortening of myocardial fibers during systole -> ↓systolic volume

*Phospholamban- protein which activates SERCA when there is no epinephrine or β-agonist present upon phosphorylation. SERCA- involve in muscle relaxation.

10. Muscle Fiber Type of Cardiac Muscle: Slow-twitch muscle fiber type

Β-1 agonists -> ^rate of contraction -> ^peak tension -> rate of relaxation

There is only ONE PHYSIOLOGICAL MECHANISM for SkM, SmM, CM hypertrophy: ^ AFTERLOAD.

11. Energy Sources of cardiac muscles: Approximately 70-90% of energy is normally derived form oxidative metabolism of fatty acids with abou 10-30% coming from other nutrients, especially lactate and glucose.

6.Summation of muscle contractions: Spatial & temporal summation: seen on individual C ICR events SMOOTH MUSCLES 7. Isometric and isotonic phases of cardiac muscle contractions a. Isometric phase= isovolumic contractions; (-) muscle shortening; ↑T ~ ↑ ventricular pressure b. Isotonic phase= occurs during ejection; muscle shortening occurs here

 Accdg. kay Doc, ang importanteng malaman ditto ay ang contraction-relaxation mechanisms at yung iba ay hindi masyado dahil sa discussion ng ANS pa ang mga ‘yun.

Excitation of smooth muscle results from:  Pacemaker potentials  Electrical coupling, or depolarization via gap  junctions  Neuromuscular transmission, via autonomic nerves’ release of neurotransmitters (further discussed in the Study Guide and Lecture on the Autonomic Nervous System)  Hormone activation of receptors *Signal Transduction mechanisms will be further discussed in the Study Guide for the Autonomic Nervous System.

9. Preload vs. Afterload of Cardiac Muscle a. Preload= load on non-contracting ventricular or atrial muscle -filling of blood in ventricles during diastole -PASSIVE TENSION b. Afterload= load on contracting ventricular or atrial muscle. -ACTIVE TENSION i. What constitutes the afterload on atrial muscle? On ventricular muscle?  Arterial pressure (will be increased by ^cross bridges -> hypertrophy) , aortic impedance to blood f low, ventricular volume Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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PHYSIOLOGY Dr. MUNARRIZ | Muscle Physiology Relaxation Events: 1. Dephosphorylation of light chains by myosin lightchain phosphatase (MLCP) to decrease intracellular Ca++ 2. Stress-relaxation phenomenon  Ability to return to nearly its original f orce of contraction seconds/minutes after it has been elongated or stretched. 3. Reverse stress-relaxation phenomenon  Ability to return to nearly its original force of contraction seconds/minutes after it has been shortened. Relaxation Events:

Contraction Events  Calcium ions bind to c almodulin, instead of troponin C.  MLCK phosphorylates the myosin light chains, and energizes the myosin head to bind with the a ctin filament (crossbridge).



Ligand action  NE, AII, and ET-1  alpha-receptor  stimulation of Gq  PL-C  PIP2 + IP3  increase Ca++ DHPR  CICR  Not as prominent as in cardiac muscle

Must-know concepts (Summary): I talked to Dra. Munarriz at sabi niya ay halos lahat ng nasa table raw na ito ang lalabas sa exam. (Yanna)



Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias




Multinucleated ; Subsarcolemm al (peripheral)

1-2 nuclei; cytoplasmic (central)

Single nucleus; cytoplasmic (central)

DHPR opens channels of RYR to release Ca++ from SR

The DHPR (Ltype) contains the Ca++ channel to release Ca++

(-) DHPR and RYR Ca++ ions are released through the

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PHYSIOLOGY Dr. MUNARRIZ | Muscle Physiology activation of IP3 receptor, the RYR of striated muscles

Regulatory proteins for muscle contraction (for Ca++ binding) Ca++ Source (SR or ECF, or both?)

Troponin C


Troponin C

Both Action potential  opens voltagegated Ca++

Events of Contraction

Action potential  Ttubules Ca++ from SR  inc. Ca++

Hormones and transmitters open IP3-gated Ca++ in SR


Both (sometimes with mitochondria) Influx of Ca++ during plateau of action potential -> calmodulin Activation of MLCK  phosphorylates regulatory MLC Inc Ca++

Events of Relaxation

Main Sources of Energy (glucose or fatty acids, or both?) Motor neuron (somatic or autonomic, or both?) Neurotransmit ters (for cardiac, smooth)

Signal transduction mechanisms (for cardiac, smooth)

Via SERCA, decreasing action potentials, or myosin ATPase

Reaccumulatio n of Ca++ by SR via Ca++ ATPase


Fatty acids





cAMP for adenyl cyclase inhibitition (via beta-2 and alpha-2 receptors)

Mechanisms that increase ICF Ca++

Cross-bridging StressRelaxation mechanism, Dephosphoryla tion of light chains by myosin lightchain phosphatase (MLCP)

Mechanisms that decrease ICF Ca++

Mechanisms or Contraction Force

Depolarization of T-tubules to activate DHPR and RYR

Increase heart rate; Sympathetic stimulation; (+) of cardiac glycosides

Reuptake of Ca++ by the SR  Ca++ released from troponin C  low crossbridge cycling

Parasympatheti c stimutation (Ach) via muscarinic receptors

Summation, recruitment, and preload are varied to varying force

Contractility and preload are varied to varying force; Changing contractility affects speed of contraction

Ligand action; and DHPR activating CICR

Recruitment, summation, preload, and contractility are varied to varying force. Formation of latch-bridges reduces speed of contractility.

Reminders: For the First Long Quiz, 40 questions regarding muscle physiology  15 questions about each specific concept ( with asterisk) in the table below  15 questions about the concepts outlined or discussed above  10 questions for the specific differences between skeletal, cardiac and smooth muscle

Legend: ^- increase “If you don’t go after what you want, you’ll never have it. If you don’t ask, the answer is always no. If you don’t step  forward, you’re always in the same place.” ( Nora Robert

Autonomic Several neurotransmitt ers depending on the location of muscle *See picture of smooth muscle sig. trans. cGMP for smooth muscle relaxation; cAMP for glycogen synthesis

Transcribers: Azarcon, Balucating, De Leon, Dela Torre, Pizarras, Reyes, Serafica, Sierra, Tagra, Tagra, Tobias

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