PHGY 502 Lecture Notes - Lecture 4: Shock Absorber, Growth Factor, Myod
29 Jun 2018
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1. Exercise Induced Muscle Injury and Repair
Cytoskeletal Architecture
-Muscle has evolved to contain structural proteins that give protection against
mechanical stress
oEndosarcomeric (within the sarcomere) proteins
Alpha-actinin, titin, nebulin
oExosarcomeric (outside the sarcomere) proteins = intermediate filament proteins
Desmin, vimentin, plectin, synemin, paranemin)
oMembrane associated proteins
Dystrophin, Ankyrin, spectrin, vinculin, talin)
-Endosarcomeric Skeleton
oTitin = being a very large protein, goes from one Z band to the other
Spring like molecule
Dissolve other proteins in the sarcomere and just leave titin, the Z bands
would be maintained
oAlpha Actinin = major component of the Z band
Mechanical reinforcement property
oNebulin = another large protein
Z band to the thick filament
-Exosarcomeric Skeleton and Membrane Associated Cytoskeleton
oExo - Squigly connecting – connects myofibrils to muscle membrane, some
connect to the nucleus, some to the mitochondria, run in parallel to the
myofibrils
Complex network – trying to hold things in their proper locations
Not just muscle cells but in muscle, very important because of the
amount of movement and forces exerted
oMembrane
Ankyrin – anchors membrane proteins
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Spectrin – also important in RBC (hereditary spirocytosis – lack spectrin in
RBCs)
Dystrophin – resembles spectrin in many aspects; defective in muscles =
hyperfragile – susceptible to membrane breakage during contraction
-Low frequency fatigue is due to damage and not metabolic factors
oVigorous exercise of a muscle = muscle becomes weaker = fatigue (loss of force
under contraction = REVERSIBLE)
oGenerally, we think of fatigue as a metabolic phenomenon
oBUT difference here with LOW frequency exercise – with strenuous exercise
(especially lengthening contractions), loss of force (that eventually recovers)
takes a LONG time (>24 hours and the muscle still hasn’t fully recovered)
Very transient drop in force and recovers but still low
= some form of injury taking place in the muscle
oLow frequency fatigue (20Hz) vs. High Frequency fatigue (100Hz) – high
frequency overcomes but low frequency shows this slower recovery
Predisposing Factors:
-Type of exercise (i.e. eccentric = active lengthening – most associated with contraction-
induced muscle injury; bias in the literature towards this type of contraction)
-Prolonged duration
-Deconditioning (don’t do anything and then BOOM – vigorous exercise = very sore)
-Aging
-Other factors???
Diagram:
-Difference between shortening, isometric and lengthening contraction
-Measure length, force and stimulus (same in all cases)
oShortening Contraction
Initial portion of contraction = isometric (no change in length); force
increases but as the muscle shortens, the force decreases
oIsometric Contraction:
No change in length, no change in force
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oLengthening contraction
Opposite; muscle shortens = force decrease but as muscle lengthened =
force increases
Highest peak force achieved – reason why more damaged is caused
Clinical Manifestations
-Muscle soreness and edema (maximal at about 48hrs post exercise)
-Limited ROM
-Weakness (especially at low stimulation frequencies = low frequency fatigue)
-Elevated serum levels of muscle cell proteins (creatine kinase and myoglobin)
oMuscle fibres have broken open and these proteins have leaked into the blood
-Elevated urinary 3-methylhistidine (similar reasoning to above – leak)
-Sore after vigorous exercise
oSoreness is usually worse going downhill, down stairs etc.
oMuscle is injured – imposing further stress but doing ECCENTRIC contractions
-Diagram shows what he said:
oLooking at time course in terms of soreness (SOR), creatine kinase (CK), T2 (index
of edema), strength (STR) and inflammation
-Another diagram showing that there is a direct relationship between magnitude of
damages determined histologically and the loss of force
Stages of exercise-induced muscle injury
-Kind of artificial – they are not distinct as they overlap in time
-Initiating Phase
oTriggers the injury during exercise
oMechanical stress – stress = force through the CSA
oMechanical strain – strain = lengthening component
oFree radical production = can use anti-oxidants to block the injury
oMost important for eccentric contractions
oLongitudinal – at the myotendinous junction
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Muscle has evolved to contain structural proteins that give protection against mechanical stress: endosarcomeric (within the sarcomere) proteins. Alpha-actinin, titin, nebulin: exosarcomeric (outside the sarcomere) proteins = intermediate filament proteins. Desmin, vimentin, plectin, synemin, paranemin: membrane associated proteins. Endosarcomeric skeleton: titin = being a very large protein, goes from one z band to the other. Dissolve other proteins in the sarcomere and just leave titin, the z bands would be maintained: alpha actinin = major component of the z band. Mechanical reinforcement property: nebulin = another large protein. Exosarcomeric skeleton and membrane associated cytoskeleton: exo - squigly connecting connects myofibrils to muscle membrane, some connect to the nucleus, some to the mitochondria, run in parallel to the myofibrils. Complex network trying to hold things in their proper locations. Not just muscle cells but in muscle, very important because of the amount of movement and forces exerted: membrane. Spectrin also important in rbc (hereditary spirocytosis lack spectrin in.
