1.02 physiology trans - muscle physiology

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Dr. KATHERINE MUNARRIZ | Muscle Physiology

19, June, 2015

1.02

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

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.

Parts of a myofibril

Sarcomere - segment of myofibril between two Z lines/disc

Z line bisects the I-band; attachment of the actin filament

I band (Isotropic) contains only actin (thin) filaments

H Zone light are between the A-band contains only myosin (thick) filaments

A band (Anisotropic) dark striation of the myofibril that contains both actin and myosin

M line bisects the H zone

*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

composition: a. large protein that consists of six different polypeptides b. one pair of large heavy chains c. two pairs of light chain

Thin Filament (Actin) formed by the aggregation of actin molecules (G-actin) into a two-stranded helical filament (F-actin)

Tropomyosin inhibits binding of myosin to actin by covering the binding site Troponin complex

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

-No. 1 inhibitor of Cross-bridge formation b. Troponin I- Has strong affinity to actin

-Inhibits interaction of actin and myosin c. 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).

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Dr. MUNARRIZ | Muscle Physiology

PHYSIOLOGY 1.02


SKELETAL MUSCLE CONTRACTION

Neuromuscular Junction Transmission

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

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 non-propagated potential that could produce an AP in the muscle when threshold is reached

1. An Action Potential (AP) is received by a neuron and travels down the axon to the axon terminal

2. 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 Ranvier 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.

3. The AP at the axon terminal allows the opening of the voltage-gated Ca++ channels which causes an influx of Ca++

4. Ca++ entry triggers the release of Ach from the axon terminals

5. Ach diffuses from axon terminals to the synaptic cleft and attaches to the receptor sites at the motor end plate/sarcolemma of the muscle

6. 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.

7. 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): -70mV Nerve Cell Threshold Potential: -55mV Skeletal Muscle Cell RMP: -90mV Skeletal Muscle Cell Threshold Potential: -75mV

8. The AP travels from the sarcolemma towards the T-tubules

9. 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

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

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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 initiation of Ca++ release from the SR

Instead, release of the Ca++ from 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 protein-protein 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 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

a. In the relaxed state, ATP is partially hydroyzed by Myosin

b. In the presence of elevated myoplasmic Ca++, myosin binds to actin

c. Myosin releases ADP and phosphate ion. Hydrolysis 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.

d. 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 Ca++ 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

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

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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 (TM) 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 cross-

bridges (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 an extensive exercise (i.e. cool-down/stretching) Allows

muscle to go back to its LO Increasing efficiency of muscle length and avoids muscle pain induced after the exercise

(delayed-onset muscle soreness/DOMS)

Relationships between

MUSCLE TENSION AND MUSCLE LENGTH

LO = 2.0 - 2.2 m for skeletal and cardiac muscles

Active tension: As stress increases, muscle length also increases up to LO. Beyond this point, contractile force (stress) decreases.

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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 tension in fibers

PASSIVE Tension

PHYSIOEX experiments. At 2.2 there is the beginnings of passive tension (0.2 g).

If you dont stretch your muscles prior to exercising them, and you do prolonged exercises, will you cause [contractures, or [power?

MUSCLE TENSION AND FREQUENCY OF STIMULATION

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

MUSCLE TENSION AND VELOCITY OF SHORTENING or LENGTHENING

Increasing the load will increase the 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)

Point

Load Tension

Velocity of shortening /lengtheni

ng

Other notes:

A No load Submaxim

al Maximal

No power since no distance was covered

B Submaxim

al Submaxim

al Submaxima

l Max power

C Maximal Maximal Zero

No power since work velocity is zero; Maximum tension

D Supramax. Max. to

decreasing

**Increasing from point

C/isometric phase

(doesnt

Velocity of lengthening

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mean that eccentric

contraction is faster

than concentric)

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

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 (Fast-glycolytic 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

Recruited later as more and more force is needed since these fibers are large and more difficult to excite.

For high-intensity activity that entails great power.

Summary of basic classification of skeletal muscle fiber types

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.

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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 PO4 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 MUSCLES

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 cardiac muscle, and activate the DHPR. In 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 cells 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 -adrenergic agonists (activation of -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)

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5.Muscle Tension ^muscle tension, contraction force ^cytosolic Ca++ - by -agonists ^sensitivity of myofilaments to cytosolic Ca++ - ^ stretch by ^preload (Frank-Starling Mechanism) *Phospholamban- protein which activates SERCA when there is no epinephrine or -agonist present upon phosphorylation. SERCA- involve in muscle relaxation. -1 agonists -> ^rate of contraction -> ^peak tension -> rate of relaxation 6.Summation of muscle contractions: Spatial & temporal summation: seen on individual CICR events 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

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 flow, ventricular volume

ii & iii. Anything that ^afterload ->shortening of myocardial fibers during systole -> systolic volume There is only ONE PHYSIOLOGICAL MECHANISM for SkM, SmM, CM hypertrophy: ^ AFTERLOAD. 10. Muscle Fiber Type of Cardiac Muscle: Slow-twitch muscle fiber type 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.

SMOOTH MUSCLES

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.

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Contraction Events

Calcium ions bind to calmodulin, instead of troponin C.

MLCK phosphorylates the myosin light chains, and energizes the myosin head to bind with the actin filament (crossbridge).

Relaxation Events: 1. Dephosphorylation of light chains by myosin light-

chain phosphatase (MLCP) to decrease intracellular Ca++

2. Stress-relaxation phenomenon

Ability to return to nearly its original force 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:

1. Ligand action

NE, AII, and ET-1 alpha-receptor stimulation of Gq PL-C PIP2 + IP3 increase Ca++

2. 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)

SKELETAL CARDIAC SMOOTH

Nuclei

Multinucleated;

Subsarcolemmal (peripheral)

1-2 nuclei; cytoplasmic

(central)

Single nucleus; cytoplasmic

(central)

DHPR and RYR

DHPR opens channels of

RYR to release Ca++ from SR

The DHPR (L-type) contains the Ca++ channel to release Ca++

(-) DHPR and RYR

Ca++ ions are

released through the

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activation of IP3 receptor, the

RYR of striated muscles

Regulatory proteins for

muscle contraction (for Ca++ binding)

Troponin C Troponin C Calmodulin

Ca++ Source (SR or ECF, or

both?) SR Both

Both (sometimes

with mitochondria)

Events of Contraction

Action potential T-

tubules

Ca++ from SR inc. Ca++

Action potential

opens voltage-gated Ca++

Hormones and

transmitters open IP3-gated

Ca++ in SR

Influx of Ca++ during plateau

of action potential -> calmodulin

Activation of

MLCK phosphorylates regulatory MLC

Inc Ca++

Cross-bridging

Events of Relaxation

Via SERCA, decreasing

action potentials, or

myosin ATPase

Reaccumulation of Ca++ by SR

via Ca++ ATPase

Stress-Relaxation

mechanism, Dephosphoryla

tion of light chains by

myosin light-chain

phosphatase (MLCP)

Main Sources of Energy

(glucose or fatty acids, or

both?)

Both Fatty acids

Motor neuron (somatic or

autonomic, or both?)

Somatic Autonomic Autonomic

Neurotransmitters (for cardiac, smooth)

ACh Epinephrine

Several neurotransmitters depending on the location

of muscle

Signal transduction mechanisms (for cardiac,

smooth)

cAMP for adenyl cyclase inhibitition (via

beta-2 and alpha-2

receptors)

*See picture of smooth muscle

sig. trans.

cGMP for smooth muscle

relaxation; cAMP for glycogen synthesis

Mechanisms that increase

ICF Ca++

Depolarization of T-tubules to activate DHPR

and RYR

Increase heart rate;

Sympathetic stimulation; (+)

of cardiac glycosides

Ligand action; and DHPR

activating CICR

Mechanisms that decrease

ICF Ca++

Reuptake of Ca++ by the SR Ca++

released from troponin C

low cross-bridge cycling

Parasympathetic stimutation

(Ach) via muscarinic receptors

Mechanisms

or Contraction

Force

Summation, recruitment, and preload are varied to varying force

Contractility and preload are varied to varying force;

Changing contractility

affects speed of contraction

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 dont go after what you want, youll never have it. If you dont ask, the answer is always no. If you dont step forward, youre always in the same place. (Nora Robert

1.02 physiology trans - muscle physiology

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