muscle lecture 5
TRANSCRIPT
![Page 1: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/1.jpg)
STAIRCASE EFFECT OR TREPPE
• The graduated series of increasingly vigorous contractions that results when corresponding increase series of identical stimuli is applied to rested muscle
• Muscle contraction after a long period of time
• Initial contraction become only half as strong as those occur in later in response to stimuli of same strength
![Page 2: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/2.jpg)
STAIRCASE EFFECT OR TREPPE
• Increased Ca ions in cytosol
• Failure of sarcoplasm to pump back to sarcoplasmic reticulum
• Warm up period by athletes
![Page 3: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/3.jpg)
SKELETAL MUSCLE TONE• Tautness occurs in muscles in relaxed condition
• In case of skeletal muscles •
• CAUSES• Generation of low rate of nerve impulse coming from spinal
cord
• Unconscious nerve impulses
• Tone enables the muscles to go quickly in action
![Page 4: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/4.jpg)
SKELETAL MUSCLE TONE
• Tendons are toned
• Controlled partly signals transmitted from brain and partly by signals originate in muscle spindles
• Example• Maintain posture, prevents from injury from sudden
pull
![Page 5: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/5.jpg)
MUSCLE FATIGUE• Prolonged and strong contraction
• Depletion of muscle glycogen
• Inability of metabolic machinery
• Inability contractile machinery
• Diminishing nervous signal
![Page 6: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/6.jpg)
MUSCLE FATIGUE
• Diminishing muscle contraction
• Interruption of blood flow to contracting muscles
• Complete muscle fatigue
![Page 7: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/7.jpg)
CO-ACTIVATION
• Simultaneous contraction of agonist and antagonist muscles on opposite side of joints
• Controlled by motor control centers of brain and spinal cord
• Nervous system directs the position of muscles
![Page 8: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/8.jpg)
Remodelling of muscle• Reorganization or reconstruction or renovation of
old structure
• Muscles are remodeled• Alteration in their lengths• Alteration in their diameters• Alteration in their strengths• Alteration in their types of fibers• Alteration in their vasular supply• Process in weeks
![Page 9: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/9.jpg)
MUSCLE HYPERTROPHY• Increase in total mass of muscles
• Mechanism• Increase in number of actin and myosin filaments in
each muscle fiber• Enlargement of individual muscle fiber
• Simple fiber hypertrophy• Loading of muscles during contractile phase
![Page 10: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/10.jpg)
MUSCLE HYPERTROPHY
• Reasons• Rate of synthesis of muscle protein is greater• Increase in number of actin and myosin
filaments to almost 50%• Splitting of myofibrils• Rapid supply of energy • Increase in number of enzymes especially for
glycolysis
![Page 11: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/11.jpg)
MUSCLE ATROPHY
• Muscles remain unused for many weeks• Decay of contractile proteins• More rapid
![Page 12: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/12.jpg)
Hypertrophy
• Examples• Weight training• Steriod use• Enabling these cells to mature in size
![Page 13: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/13.jpg)
Adjustment of muscle length
Another type of hypertrophy Stretching of muscles to maximum length Adding of new sarcomeres• Shortening of muscles to maximum• Disappearance of sarcomeres at end
![Page 14: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/14.jpg)
HYPERPLASIA
• Hypergenesis• Proliferation of cells• Gross enlargement of organ• Physiological phenomenon• Microscopically visible as normal• Normal regulatory control mechanism• In addition to hypertrophy increase in number of
fibers• Linear splitting of enlarged fibers
![Page 15: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/15.jpg)
REASONS OF HYPERPLASIA
• Increased demand• Chronic inflammatory response• Compensation for damage and tissue injury• Harmless• Occurs at particular tissue
![Page 16: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/16.jpg)
HYPERPLASIA
• Example• Growth and multiplication of milk secreting
glandular cells in the breast in response to pregnancy
• Artificially produced by injecting hormones such as IGF-1
• Human growth hormone
![Page 18: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/18.jpg)
Abnormal Hyperplasia
• Cushing syndrome• Congenital adrenal hyperplasia• Benign prostatic hyperplasia• Endometrial hyperplasia • Breast hyperplasia• Compensatory liver hyperplasia
![Page 19: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/19.jpg)
PLASIA
• Anaplasia; Dedifferentiation• Neoplasia; Abnormal proliferation• Dysplasia; Maturation abnormality• Metaplasia; Cell type conversion• Desmoplasia; Connective tissue growth
![Page 20: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/20.jpg)
NEOPLASIA
• Genetically abnormal cells proliferate in non-physiological manner
![Page 21: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/21.jpg)
EFFECT OF MUSCLE DENERVATION
• No nerve supply, no signal• No contractile signals to maintain normal size• Atrophy occurs• Appearance of degenerative changes• after 2 months• If nerve grows rapidly• Return of muscle within 3 months• Incapability of muscles after three months
![Page 22: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/22.jpg)
EFFECT OF MUSCLE DENERVATION
• At final stage of denervation• Fibers are destroyed• Replacement by fibrous and fatty tissue• STRUCTURE• Long cell membrane• Nuclei in series• No contractile apparatus• No regeneration of myofibrils• Capability to continue shortening• Contracture
![Page 23: Muscle lecture 5](https://reader036.vdocuments.net/reader036/viewer/2022062503/589983221a28abb97c8b5bc3/html5/thumbnails/23.jpg)
Recovery of muscle contraction in poliomyelitis
Some nerve fibers are destroyed• Remaining nerve fibers branch off to form
new axons• Innervation into paralyzed muscles• Formation of large motor units• Macromotor units• Decrease in fitness of control