Difference between revisions of "Muscles - Anatomy & Physiology"
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+ | <big><center>[[Musculoskeletal System - Anatomy & Physiology|'''BACK TO MUSCULOSKELETAL ANATOMY AND PHYSIOLOGY''']]</center></big> | ||
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− | + | ===Introduction=== | |
− | + | *Skeletal muscle includes muscles of: | |
+ | **Posture | ||
+ | **Movement | ||
+ | **Respiration | ||
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− | + | *Two basic types of skeletal myofibre: | |
− | + | **<u>'''Type I'''</u> | |
− | + | ***Grossly '''red''' | |
+ | ***'''High''' myoglobin level | ||
+ | ***'''Slow''' rate of contraction | ||
+ | ***High '''oxidative''' activity | ||
+ | ***Function - postural | ||
+ | **<u>'''Type II'''</u> | ||
+ | ***Grossly '''white''' | ||
+ | ***'''Low''' myoglobin level | ||
+ | ***'''Fast''' rate of contraction | ||
+ | ***High '''glycolytic''' activity | ||
+ | ***Function - exercise | ||
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− | ''' | + | *Each muscle is composed of multiple '''fascicles''' |
+ | **Each fascicle is composed of multiple polygonal '''myofibres''' | ||
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− | === | + | ===Regeneration=== |
+ | [[Image:Muscle regeneration.jpg|right|thumb|100px|<small><center>Muscle regeneration (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
− | + | *Skeletal muscle myofibres have substantial regenerative ability | |
+ | *Success depends on: | ||
+ | **An intact '''sarcolemmal tube''' - to act as a support and guide | ||
+ | **Availability of '''satellite cells''' - to act as progenitor cells for new sarcoplasm production | ||
+ | **Macrophages to clear up cell debris | ||
+ | **If these conditions are not met (e.g. severe thermal damage) '''fibrosis''' will occur | ||
+ | *Stages: | ||
+ | #Nuclei in [[Muscles - degenerative#Necrosis|necrotic segement]] disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or [[Muscles - degenerative#Calcification|mineralise]] | ||
+ | #Monocytes from capillaries -> macrophages in necrotic portion, satellite cells swell -> vesicular with prominent nucleoli -> mitosis (within 1-4 days after initial injury) | ||
+ | #Satellite cells move to centre | ||
+ | #Macrophages clear the sacrolemmal tube, plasmalemma disappears, shape maintained by basal lamina | ||
+ | #Satellite cells -> myoblasts (contain myosin) -> fuse forming myotubes with row of central nuclei; cytoplasmic processes fusing | ||
+ | #Growing and differentiating fibre, striations appear - formation of sarcomeres | ||
+ | #Nuclei move to peripheral position (2-3 weeks after initial injury) | ||
+ | *Regeneration by '''budding''' | ||
+ | **When conditions are not optimal, disrupted sacrolemma | ||
+ | **E.g. injection of irritating substance, trauma, [[Muscles - degenerative#Ischaemia|infarction]] | ||
+ | **Myoblasts proliferate -> sacrolamma bulges from cut part -> club-shaped with numerous central nuclei = muscle giant cells | ||
+ | *Monophasic lesions - all at same phase above | ||
+ | **Damage occured at one time, e.g. trauma or one toxin exposure | ||
+ | *Multiphasic lesions - different stages as described above | ||
+ | **Ongoing damage, e.g. vitamin E - selenium deficiency, continuous exposure to toxin | ||
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− | + | ===Rigor Mortis=== | |
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− | + | *Muscles remain biochemically active after the death of an animal | |
− | [[ | + | *Following a period of relaxation, contraction and stiffening occurs |
+ | *Due to deficiency of ATP releasing myosin heads from their binding sites at end of power stroke | ||
+ | *Onset faster in ATP deprived animals (starvation, hunting, tetanus...) | ||
+ | *May be absent in cachetic animals | ||
+ | *Disappears due to autolysis or putrefaction | ||
+ | *See [[General Pathology - Post-Mortem Change#Rigor Mortis|general pathology]] | ||
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− | + | <big><center>[[Musculoskeletal System - Anatomy & Physiology|'''BACK TO MUSCULOSKELETAL ANATOMY AND PHYSIOLOGY''']]</center></big> | |
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Revision as of 11:09, 18 July 2008
Introduction
- Skeletal muscle includes muscles of:
- Posture
- Movement
- Respiration
- Two basic types of skeletal myofibre:
- Type I
- Grossly red
- High myoglobin level
- Slow rate of contraction
- High oxidative activity
- Function - postural
- Type II
- Grossly white
- Low myoglobin level
- Fast rate of contraction
- High glycolytic activity
- Function - exercise
- Type I
- Each muscle is composed of multiple fascicles
- Each fascicle is composed of multiple polygonal myofibres
Regeneration
- Skeletal muscle myofibres have substantial regenerative ability
- Success depends on:
- An intact sarcolemmal tube - to act as a support and guide
- Availability of satellite cells - to act as progenitor cells for new sarcoplasm production
- Macrophages to clear up cell debris
- If these conditions are not met (e.g. severe thermal damage) fibrosis will occur
- Stages:
- Nuclei in necrotic segement disappear, hyalinased sarcoplasm due to loss of normal myofibrillar structure, may separate from adjacent normal myofibrils and/or mineralise
- Monocytes from capillaries -> macrophages in necrotic portion, satellite cells swell -> vesicular with prominent nucleoli -> mitosis (within 1-4 days after initial injury)
- Satellite cells move to centre
- Macrophages clear the sacrolemmal tube, plasmalemma disappears, shape maintained by basal lamina
- Satellite cells -> myoblasts (contain myosin) -> fuse forming myotubes with row of central nuclei; cytoplasmic processes fusing
- Growing and differentiating fibre, striations appear - formation of sarcomeres
- Nuclei move to peripheral position (2-3 weeks after initial injury)
- Regeneration by budding
- When conditions are not optimal, disrupted sacrolemma
- E.g. injection of irritating substance, trauma, infarction
- Myoblasts proliferate -> sacrolamma bulges from cut part -> club-shaped with numerous central nuclei = muscle giant cells
- Monophasic lesions - all at same phase above
- Damage occured at one time, e.g. trauma or one toxin exposure
- Multiphasic lesions - different stages as described above
- Ongoing damage, e.g. vitamin E - selenium deficiency, continuous exposure to toxin
Rigor Mortis
- Muscles remain biochemically active after the death of an animal
- Following a period of relaxation, contraction and stiffening occurs
- Due to deficiency of ATP releasing myosin heads from their binding sites at end of power stroke
- Onset faster in ATP deprived animals (starvation, hunting, tetanus...)
- May be absent in cachetic animals
- Disappears due to autolysis or putrefaction
- See general pathology