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MUSCLE ENERGETICS

MUSCLE ENERGETICS. TETANUS and TETANY. Tetanus Neurological disorder that results from a decrease inhibitory input to alpha motor neurons. Mechanism of Action ---Tetanus. Cause—Bacteria Clostridium tetani Toxin ---- Tetanospasmin

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MUSCLE ENERGETICS

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  1. MUSCLE ENERGETICS

  2. TETANUS and TETANY • Tetanus Neurological disorder that results from a decrease inhibitory input to alpha motor neurons

  3. Mechanism of Action ---Tetanus Cause—Bacteria Clostridium tetani Toxin ---- Tetanospasmin Mechanism of action—Retrograde intraneuronal transport. (Retroaxonally)

  4. Symptoms- -Locked jaw -Opisthotonus -Breathing problems. -Sudden powerful and painful contraction of muscles -Irritability, muscle cramps. -Weakness -Difficulty in swallowing -Sardonic smile

  5. OPISTHOTONUS

  6. TETANUS • Antibiotic to kill the bacteria. • Injecting antibiotics that bind the toxin. • Muscle relaxants. • Mechanically ventilating the lungs Prophylaxsis— Immunization

  7. TETANY • Low serum calcium levels (8.5-10.5 mg/dl) CAUSES– 1-Lack of calcium 2-Excess of phosphate 3-Underfunctioning of thyroid gland.

  8. Mechanism of Action --Tetany • Decrease Calcium ion concentration --- Sodium channels become activated by very little increase in membrane potential.

  9. TETANY SYMPTOMS— 1- Hyperflexia 2- Carpopedal spasm 3-Cramps 4-Laryngospasm Treatment---- 1-I/V calcium 2-Oral calcium +Vitamin D 3-Surgical removal of parathyroid glands

  10. TYPES OF SKELETAL MUSCLE FIBERS • SLOW-TYPE 1 FAST- TYPE II OXIDATIVE GLYCOLYTIC RED WHITE

  11. TYPES OF SKELETAL MUSCLE FIBER

  12. TYPES OF SKELETAL MUSCLE FIBER

  13. Some Diseases related to Muscles • Tetanus • Tetany • Rigor Mortis • Myasthenia Gravis • Dystrophy (Duchenne’s Muscular Dystrophy)

  14. RIGOR MORTIS • Several hours after death all the muscles of the body go into a state of contracture . • Loss of all ATP • Muscle protein deteriorates ----15 to 25 hours later. (Autolysis). • All these events occur more rapidly at higher temperatures.

  15. Function of Skeletal Muscles • Movement • Posture (both agonist & antagonist function together, Co- activation) • Heat Production • Interaction with the Environment (Expression) • Exert Rapidly adaptable force • Voluntary control

  16. Some terms Related to Muscles Disuse Atrophy • Atrophy { Denervation Atrophy • Hypertrophy • Fibrillation • Fasciculation

  17. Atrophy Decrease in the diameter of nerve fiber Decrease in the amount of contractile proteins. Disuse atrophy : Muscle is not used for a prolong period of time. Denervation atropy:1. Neurons are destroyed 2. Neuromuscular junction becomes non functional. (ATP dependent ubiquitin – proteasome pathway)

  18. Hypertrophy Increase in the diameter of nerve fiber. Increase in the amount of contractile proteins Muscle is loaded during the contractile process

  19. Fibrillation Rapid ,irregular and unsynchronized contraction of muscle fiber. • Fasciculation Small local, involuntary muscle contraction and relaxation which may be visible under the skin

  20. Smooth Muscles

  21. Objectives • At the end of this lecture you should be able to know types of smooth muscles and their anatomical location. • Arrangement of myofilaments and sarcoplasmic reticulum • Steps involved in Contraction • Functional differences

  22. SMOOTH MUSCLE • Diameter – 1-5 micrometers • Length --- 20-500 micrometers

  23. Smooth Muscles Generally Divided into Two Types 1. Multi-unit. Composed of : discrete, Independent fibers innervated by separate single nerve ending e.g. iris and piloerector muscles Multi unit Smooth M Fiber

  24. Unitary Smooth Muscle • 2. Unitary: • 100-1000 fibers but contract as a unit. • due to presence of gap junctions • e.g. in most of the viscera

  25. Input Influencing Smooth muscle Contractile activity • Spontaneous electrical activity in the plasma membrane of the muscle cell. • Neurotransmitters released by autonomic neurons. • Hormones • Locally induced changes in the chemical composition of ECF surrounding the cell (acidity, oxygen,osmolarity, ion concentration) • Stretch.

  26. Arrangement of Actin & Myosin Smooth M Fiber

  27. Neuromuscular Junction of Smooth Muscle

  28. Non striated • Dense bodies--- Z-lines • Protein Calmodulin--- Troponin complex. • No Typical branching end feet as in Sk. Muscles • Multiple Varicosities. No Schwann cells at Varicosities. Diffuse junctions. • Contact junctions • Neurotransmitter is released at Varicosities –may be Ach or Noradrenalin.

  29. SarcoplasmicReticulum Smooth Muscle S.R

  30. Action Potential in smooth Muscle • RMP… -50 -60 mv • Action Potential in Unitary Smooth Ms e.g. Viscera • Two forms: • 1. Slow waves • 2.Spike Potential ---10-50 m.sec duration • 3. Action potential with plateau. • 4. Junctional potential

  31. Calcium channels • Far greater voltage gated calcium channels • Few voltage gated sodium channels

  32. Steps involved in the Contraction of Smooth Muscle • Ca++ binds with Calmodulin • Calmodulin-Ca++ combinedly activates Myosin Kinase (phosphorylating Enzyme) • One of the Light chain of Myosin Head (Regulatory chain) is Phosphorylated in response to this myosin kinase. • The head of Myosin gets capability to repetitively attach & detach with active sites of Actin filaments. - Slow cycling of Cross Bridges than skeletal muscles. • Dephosphrylation–Myosin phosphtasein sarcoplasm

  33. Latch Phenomenon • The energy required to maintain full force of contraction , (once developed full contraction initially) in smooth muscles is very negligible (1/300 that of Sk. Muscle) • This phenomenon allows long term maintenance of tone in many smooth muscles without much expenditure of energy.

  34. Comparison of Smooth and Skeletal muscle contraction • Slow cycling of the myosin cross bridges. • Low energy requirement to sustain smooth muscle contraction. • Slowness of onset of contraction and relaxation of the total smooth muscle tissue. • Maximum force of contraction (4-6Kg /cm.sq) • Latch mechanism • Stress relaxation of smooth muscle

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