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Biochemistry of Muscle

1) Muscle contraction occurs when calcium ions are released from the sarcoplasmic reticulum in response to an action potential, causing the troponin complex to change shape and expose actin's myosin binding sites. 2) Muscles generate energy through anaerobic glycolysis and aerobic cellular respiration, with the creatine phosphate system helping to rapidly regenerate ATP from ADP. 3) Skeletal, cardiac, and smooth muscles differ in their structure, control, and function, with smooth muscle lacking striations and the troponin complex.

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0% found this document useful (0 votes)
598 views

Biochemistry of Muscle

1) Muscle contraction occurs when calcium ions are released from the sarcoplasmic reticulum in response to an action potential, causing the troponin complex to change shape and expose actin's myosin binding sites. 2) Muscles generate energy through anaerobic glycolysis and aerobic cellular respiration, with the creatine phosphate system helping to rapidly regenerate ATP from ADP. 3) Skeletal, cardiac, and smooth muscles differ in their structure, control, and function, with smooth muscle lacking striations and the troponin complex.

Uploaded by

Wisnu Kuncoro
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
You are on page 1/ 68

Dian Mulawarmanti

Faculty of Dentistry, Hang Tuah University 2013

Body movement (Locomotion) Maintenance of posture Respiration


Diaphragm and intercostal contractions

Communication (Verbal and Facial) Constriction of organs and vessels


Peristalsis of intestinal tract Vasoconstriction of b.v. and other structures (pupils)

Heart beat Production of body heat (Thermogenesis)

1.. Smooth Muscle

2. SKELETAL Muscle

3. Cardiac Muscle

walls of most viscera, blood vessels, skin


not under conscious not striated

usually attached to bones under conscious control


striated control

wall of heart not under conscious control striated

structure
skeletal striated

control
Primarily voluntary

nuclei

Location

Multiple Attached phripheral to bone

cardiac

striated

Involuntary
Nervus & endocrine

1 rarely Heart wall 2 Centrally located


Centrally located Walls of hollow organ

smooth

Non striated

Involuntary Nervus & endocrine

Myofibrils are built of 3 kinds of protein contractile proteins myosin and actin regulatory proteins which turn contraction on & off troponin and tropomyosin structural proteins which provide proper alignment, elasticity and extensibility titin, myomesin, nebulin and dystrophin
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Other protein components of muscle fibrils

sarcolemma sacroplasm sarcoplasmic reticulum transverse tubule triad cisternae of sarcoplasmic reticulum transverse tubule myofibril actin filaments myosin filaments sarcomere

The sarcomere is the functional unit of muscle Contraction

Thin filaments consist of two strands of actin and one tropomyosin coiled about each other
Thick filaments consist of myosin molecules.

I bands A bands H zone Z lines M line

Thick Filaments Myosin

Composed of 6 highly conserved polypeptide chains Two 220 kDa heavy chains that have elongated globlular heads, and long fibrous helical tails. Each head region contains an ATP-binding site/ATPase function Two pairs of light chains, termed essential light chains and regulatory light chains.These interact with the globular heads of the heavy chains, and regulate ATPase functions depending on their phosphorylation status.

As a monomer, termed G-Actin, at low ionic strength and can bind one ATP At physiological ionic strength (plus Mg2+), the Gactin forms fibrous polymers termed F-actin. ATP hydrolysis occurs during this process and ADP remains bound to each F-actin subunit

F-actin is the core of the thin filament, and each monomer is capable of binding one myosin globular head. The coil repeats at roughly every seventh actin unit.

Thick Filaments composed of myosin cross-bridges

Thin Filaments composed of actin associated with troponin and tropomyosin

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Tropomyosin: a two chain fibrous protein that attach to F-actin in the groove between its filaments Troponins: three protein components, troponin C, a calcium binding protein like calmodulin; troponin I, which blocks the myosin binding site on F-actin; troponin T which binds to tropomyosin and the other troponins

also known as myoneural junction site where an axon and muscle fiber meet motor neuron motor end plate synapse synaptic cleft synaptic vesicles neurotransmitters

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When sarcomeres

shorten, thick and thin filaments slide past one another H zones and I bands narrow Z lines move closer together

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muscle impulses cause sarcoplasmic reticulum to release calcium ions into cytosol calcium binds to troponin to change its shape position of tropomyosin is altered binding sites on actin are exposed actin and myosin molecules bind
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myosin cross-bridge attaches to actin binding site myosin cross-bridge pulls thin filament ADP and phosphate released from myosin new ATP binds to myosin linkage between actin and myosin cross-bridge break ATP splits myosin cross-bridge goes back to original position
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acetylcholinesterase rapidly decomposes Ach remaining in the

synapse muscle impulse stops

stimulus to sarcolemma and muscle fiber membrane ceases


calcium moves back into sarcoplasmic reticulum myosin and actin binding prevented muscle fiber relaxes

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The contractile process


The pumping of calcium back into the sarcoplasmic reticulum during relaxation Maintaining the sodium/potassium ion gradients across the sarcolema(membrane potential)

Phosphocreatine Glycolysis from Glycogen or Glucose Tricarboxylic acid cycle (TCA or Krebs cycle) Electron transport chain

It is also known as creatine phosphate or Pcr, that is an important energy stored in the skeletal muscle. Creatine is synthesized in the liver (from Arg, Gly, Met), and transported to the muscle cells, where it is phosphorylated by creatine kinase (ATP is required) to creatine phosphate.

ADP + Phosphocreatine
Creatine Kinase ATP + Creatine

This reaction occurs in the sarcoplasm. ATP broken down during contraction is rapidly restored. Phosphocreatine is subject to depletion during extended periods of contraction (intense effort). Rephosphorylation of creatine occurs at the mitochondrial membrane.

It is the sequence of reactions that converts

glucose pyruvate
with the concomitant production of a relatively small amount of ATP

Glycogen is a polysaccharide of glucose (Glc) which functions as the primary short term energy storage in muscle cells (myofiber).
Glycogen is found in the form of granules in the sarcoplasm, and plays an important role in the glucose cycle.

Glycogen
Glycogen Phosphorylase Glucose 1-Phosphate Glucose 6-phosphate

Summary

1 Glucose + 2ADP + 2Pi +2NAD

2 Pyruvate + 2ATP + 2NADH +2H + 2H2O

It is also known as Citric Acid Cycle Krebs cycle. It is a series of enzyme-catalyzed chemical reactions of central importance in all living cells that use oxygen as part of cellular respiration.

TCA cycle

Summary
Pyruvate

1ATP + 4NADH +1FADH + 3CO2

It is a chemical reaction between an electron donor (such as NADH) and an electron acceptor (such as O2) to the transfer of H+ ions across a membrane
These H+ ions are used to produceATP, as they move back across the membrane.

Summary

NADH

NAD + 3ATP + 4H2O

Process GLYCOLYSIS Pyruvate oxidation (two per glucose) Acetyl-CoA oxidation

Direct product 2 NADH 2ATP 2 NADH (mitochondrial matrix) 6 NADH (mitochondrial matrix) 2 FADH2 2 ATP

Final ATP 4 or 6 2 6 18 4 2

Total yield per molecule of glucose

Release of Ca2+ through voltageor Ca2+-sensitive channel activates contraction Pumps induce relaxation

Ca2+ Channels and Pumps


Release of Ca2+ from the SR triggers contraction Reuptake of Ca2+ into SR relaxes muscle So how is calcium released in response to nerve impulses? Answer has come from studies of antagonist molecules that block Ca2+ channel activity

At rest tropomyosin blocks the myosin binding sites on actin. When calcium binds to the troponin complex a conformational change results in the movement of the tropomyosintropinin complex and exposure of actins myosin binding sites.

Follow the action potential


When an action potential meets the muscle cells sarcoplasmic reticulum (SR) stored Ca2+ is released.

An individual muscle cell either contracts completely or not all. Individual muscles, composed of many individual muscle fibers, can contract to varying degrees. One way variation is accomplished by varying the frequency of action potentials reach the muscle from a single motor neuron.

Graded muscle contraction can also be controlled by regulating the number of motor units involved in the contraction

Recruitment of motor neurons increases the number of muscle cells involved in a contraction
Some muscles, such as those involved in posture, are always at least partially contracted Fatigue is avoided by rotating among motor units

In addition to skeletal muscle, vertebrates have cardiac and smooth muscle Cardiac muscle: similar to skeletal muscle Intercalated discs facilitate the coordinated contraction of cardiac muscle cells. Can generate there own action potentials. Action potentials of long duration.

Smooth muscle: lacks the striations seen in both skeletal and cardiac muscle

Contracts with less tension, but over a greater range of lengths, than skeletal muscle. No T tubules and no SR Ca2+ enters the cytosol from via the plasma membrane. Slow contractions, with more control over contraction strength than with skeletal muscle. Found lining the walls of hollow organs

No troponin complex in smooth muscle

Ca2+ activates myosin light chain kinase (MLCK) which phosphorylates LC2, the regulatory light chain of myosin Ca2+ effect is via calmodulin - a cousin of Troponin C
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12/02/2008

Biochemistry: Muscles

Hormones regulate contraction epinephrine, a smooth muscle relaxer, activates adenylyl cyclase, making cAMP, which activates protein kinase, which phosphorylates MLCK, inactivating MLCK and relaxing muscle

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1) Creatine phosphate

2) Cellular respiration

creatine phosphate stores energy that quickly converts ADP to ATP

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Anaerobic Phase

glycolysis occurs in cytoplasm produces little ATP


Aerobic Phase citric acid cycle electron transport chain occurs in the mitochondria produces most ATP myoglobin stores extra oxygen

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Muscle tissue has two sources of oxygen.


diffuses in from the blood released by myoglobin inside muscle fibers

Aerobic system requires O2 to produce ATP needed for prolonged activity


increased breathing effort during exercise

Recovery oxygen uptake


elevated oxygen use after exercise (oxygen debt) lactic acid is converted back to pyruvic acid elevated body temperature means all reactions

faster
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Oxygen debt amount of oxygen needed by liver cells to use the accumulated lactic acid to produce glucose

oxygen not available glycolysis continues pyruvic acid converted to lactic acid liver converts lactic acid to glucose

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by-product of cellular respiration

muscle cells are major source of body heat blood transports heat throughout body

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Slow oxidative (slow-twitch)


red in color (lots of mitochondria, myoglobin & blood vessels) prolonged, sustained contractions for maintaining posture

Fast oxidative-glycolytic (fast-twitch A)


red in color (lots of mitochondria, myoglobin & blood vessels) split ATP at very fast rate; used for walking and sprinting

Fast glycolytic (fast-twitch B)


white in color (few mitochondria & Blood Vessel, low myoglobin) anaerobic movements for short duration; used for weight-lifting

(angkat berat)
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These differences are due primarily to the male sex hormone testosterone With more muscle mass, men are generally stronger than women Body strength per unit muscle mass, however, is the same in both sexes

With age, connective tissue increases and muscle fibers decrease Muscles become stringier and more sinewy By age 80, 50% of muscle mass is lost (sarcopenia) Decreased density of capillaries in muscle Reduced stamina Increased recovery time Regular exercise reverses sarcopenia

Inability to contract

depletion of creatine phosphate decline of Ca+2 within the sarcoplasm Commonly caused from decreased blood flow insufficient oxygen or glycogen Ion imbalances across the sarcolemma Accumulation of lactic acid insufficient release of acetylcholine from motor neurons Cramp sustained, involuntary muscle contraction
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Rigor mortis is a state of muscular rigidity that begins 3-4 hours after death and lasts about 24 hours After death, Ca+2 ions leak out of the SR and allow myosin heads to bind to actin Since ATP synthesis has ceased, crossbridges cannot detach from actin until proteolytic enzymes begin to digest the decomposing cells.
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