What does skeletal muscle do?
- Posture & movement
- Respiration
- Glucose metabolism & temperature
- Peripheral nervous system
Neuropathic changes in muscle
Effect or absence of nerve supply
Myopathic changes in muscle
Primary disease is in the muscle cell
Neuromuscular changes in muscle
Disease that include muscle cells & neurons
Satellite cell
Involved in muscle repair
“Resting myoblast”
Myocyte
Muscle cell
Muscle fiber classification
- Rate of contraction
- Rate of fatigue
- Type of metabolism
Type 1 fibers
Lots of mitochondria "Light color" Oxidative metabolism Slow contraction & slow fatigue Maintaining posture
Type 2 fibers
Few mitochondria "Dark color" Glycolytic 2A = oxidative & glycolytic 2B = anaerobic Fast contracting & fast fatigue Sprinting
Skeletal muscle metabolism
Energy = ATP
Type 1 & 2A = oxidative glycogen & fat
Type 2B = anaerobic
What is rigor mortis?
Absence of fresh ATP after death prevents the relaxation of muscle
Myosin heads to not release
What does necrosis in injured muscle look like?
Segmental hypercontraction
Eosinophilia
Pallor of the cytoplasm
Floccular or granular cytoplasm
What enzymes are elevated in the plasma when there is muscle damage?
Creatine kinase (CK) Aspartate animotransferase (AST)
How does muscle regenerate after injury?
Triggered by increased intra-cellular calcium
Macrophages invade necrotic area
Activation of satellite cells
What determines the outcome of muscle regeneration?
Whether or not the basal lamina in intact
Keeps nuclei in and fibroblasts out
How does muscle regenerate with an in tact basal lamina?
- Macrophages clean up
- Satellite cells enlarge and divide
- Damaged cell disappears
- Satellite cell moves into vacant area
- Differentiation into myoblast
- Myoblasts increase in numbers
- When myoblasts’ membranes fuse differentiation into mature muscle
How does muscle regenerate with an in damaged basal lamina?
- Satellite cells and damages fiber are NOT contained
- Nuclei from damaged ends divide
- Ends of fiber bulge
- Muscle giant cells form
- Large gaps heal by fibrosis
What happens when there are no satellite cells to repair damaged muscle?
Healing by fibrosis only
Atrophy of muscle
DECREASE in size of fiber diameter
Causes = denervation, cachexia
Can be seen grossly
NOT hypoplasia = underdevelopment
Hypertrophy of muscle
INCREASE in muscle fiber diameter
Addition of myofilaments
Physiologic hypertrophy
Normal process
Exercise conditioning
Compensatory hypertrophy
Nonspecific process
Secondary to:
1. Decreased number of functional myofibers
2. Problem with normal metabolic processes
Downer syndrome
Degenerative disease
Cause = muscle ischemia by external pressure
External pressure exceeds venous & arterial pressure
Acute gross = dark & hemorrhagic
Chronic gross = pale
Nutritional myopathy
What nutrients are deficient?
Selenium
Vitamin E
What is the pathologic process in nutritional myopathy?
- Loss of antioxidant defense mechanisms
- Muscle is very sensitive to oxidative injury
- Loss of ability to maintain ion gradients
- Calcium induced hypercontraction
Basal lamina is left INTACT
Who is most affected by nutritional myopathy?
Pigs & herbivores
Young animals = esp in utero
Clinical signs may worsen with physical activity
What do lesions look like in nutritional myopathy?
Pale muscle = "white muscle disease" Mineralization of tissue Thigh & shoulder Young animals = tongue & neck Bilaterally symmetrical May have myoglobinuria
Names for Nutritional Myopathy
White muscle disease
Stiff lamb disease
Mulberry heart disease (swine)
Toxic degenerative diseases of muscle
Difficult to distinguish from nutritional
Do NOT act on Vit E or Selenium
MORE lethal than nutritional deficiencies
Mineralization of tissues is common
Monensin Toxicity
Antibiotic fermentation produce (Streptomyces) Growth promotion in ruminants Coccidiostat in birds, etc Monogastrics (horses) = toxic Ruminants = toxic at HIGH doses
How is Monensin toxic?
Distorts membrane transport of Na and K
Calcium overload
Death of skeletal & cardiac muscle
Clinical signs of Monesin Toxicity
Lethargy Stiffness Muscle weakness Recumbency Horses = colic symptoms Pale STREAKS in muscle tissue NO mineralization!
Exertional mypoathy
Buildup of lactic acid Coagulation of contractile proteins Water is lost to intersitium = pressure & ischemia Myoglobinurua Metabolic acidosis
Other names for exertional myopathy?
Exertional rhabdomyolysis (necrosis)
“Monday morning disease”
“Tying up”
Two types of exertional rhabdomyolysis
- Sporadic
2. Recurrent
Sporadic exertional rhabdomyolysis
Following exercise with prior good performance
Stiff stride, sweating, elevated RR
Reluctance to move
Myoglobinuria = affects kidneys!
Painful cramps
Muscles = gluteal & lumber regions
Histo = swollen vacuolated disrupted myofibers
Why does sporadic exertional rhabdomyolysis occur?
Exercise exceeded the horse’s underlying state of training
Need 4-8 weeks of rest to repair muscles!
Maybe affected by viral infections
Recurrent exertional rhabdomyolysis (RER)
Occurs even with light exercise
Recovery is rapid
NO gross lesions
Autosomal dominant trait
Pathogenesis of RER
Alteration in muscle Ca regulation
DECREASED threshold for contracture
Disorder in carbohydrate storage and utilization
= Polysaccharide storage myopathy (PSSM)
= Insufficient energy production by fibers