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EDKP 395 (37)
Lecture 9

Lecture 9 (revised).docx

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Department
Kinesiology&Physical Education
Course
EDKP 395
Professor
Russell T Hepple
Semester
Fall

Description
Cytoskeleton Architecture 12/6/2012 3:48:00 PM Structural proteins provide protection against mechanical stress (hold the muscle structure together)  Endosarcomeric proteins o Inside sarcomere  A-actin  Titin- large protein  Extends from 1 “Z band” to the other  Maintains sarcomere when all other contractile proteins are removed  interacts with actin filament  Maintains the contractile structure  Spring like capacity- important  Force dependent shortening of titin’s spring length  nebulin  Exosarcomeric proteins o Intermediate filament proteins associated with sarcolema (muscle membrane itself)  Desmin  Holds things together  Maintains normal registry of adjacent myofibrils and their relationship to other structures in cell  Can interact with myofibrils within muscle  plectin, synemin, vimentin  Membrane- associated proteins o Dystrophin, ankyrin, spectrin, vinculin, talin  the two above help hold things together  allows the msucel cell to withstand daily stresses and wear/tear that they experience with muscle contractions Predisposing factors  Type of exercise o Ex. eccentric- active lengthening  Typically do during breaking actions- ex. lowering a weight, walking down stairs  Prolonged duration o Increased risk of injury with longer workouts  Especially common in marathon runners  Deconditioning  Aging Clinical Manefestation 12/6/2012 3:48:00 PM After an exercise you typically experience:  Muscle soreness and edema o Max. at 48 hrs post-exercise  Limited range of motion  Weakness, esp. at low stimulation frequencies o Called “low frequency fatigue”  Elevated serum levels of muscle cell proteins o Creatine kinase, myoglobin  Elevated urinary 3-methyhistidine Time line of events  Exercise stimulus o Siginificant Decrease in strength  Loss of force generating capacity  1-12hr POST exercise o significant dec. in strength o significant increases in acute inflammation  24hr post o significant increase in sorness o significant dec. in strength  48hr post o sig. inc. in sorness o in. creatine kinase & T2  start to feel the soreness  5 days post: o peak of CK release into blood o chronic soreness kicks in  due to inflammation Shows that with severe damage (i.e. high intensity exercise) there is a significant decrease in the force generating capacity of the muscles Low frequency fatigue  Due to damage NOT metabolic factors o Force during muscle stimulation recovery depended on the frequency at which you stimulated the muscle  High: force would recover quickly  Low: long time to recover (get back to baseline)  Force is lost in the excitation-contraction coupling mechanism o Problems w/ t-tubules, ryanodine receptors mechanisms that release calcium o During eccentric contractions force is normal so you bypass the excitation-contraction coupling mechanism and go directly to the release of Ca++  Phases 12/6/2012 3:48:00 PM The amount of negative work (work during lengthening) that is done is the major determinant of the severity of muscle injury  Note: positive work = muscle shortening Study: did a stain for intracellular (within cell) albumin content  Shouldn’t be present within the muscle  if it is, it is a signal that there is membrane damage  If a stain is found o Membrane injury  Allows for extracellular calcium to leak in along [] gradient causing  Activation of proteases  Harmful to mitochondrial function  Activate phosphorylase  Can break down membrane Initial phase  Initiating event for injury during exercise o Mechanical stress o Mechanical strain  these two can damage the sarcolemma/sarcoplasmic retirulum resulting in a distruption of calcium homeostasis o Free radical production  eccentric contractions have 2 characteristics that determine how much injury takes place  High level of mechanical stress (i.e. intensity) generate by muscle per unit cross sectional area  Primarily in longitudinal range (myotendinous junction)  Can occur in transverse (points of attachment to membrane)  High level of mechanical strain (muscle being stretched) Autogenetic  Endogenous cellular systems are activated begin degrading cellular structures and attracting inflammatory cells (initial injury leads to further cell injury) o Proteolytic systems o Lipolytic systems o Cytokines and chemokines  Increased intracellular Ca++ is one trigger for autogenetic phase o Phospholipase A2- degrades membrane phospholipids o Activation of proteases  Degrades Z band protein a-actin  Characteristic of eccentric contractions Phagocytic  Infiltration by inflammatory cells o Neutrophils then macrophages  Release is highly regulated  Located in both muscle and blood o Also known as inflammatory phase  Associated with second peak of injury  First spike: release of CPK  Second spike: replenish the stroke????  Removal of damaged cell and extracellular matrix  Max. at about 2 days post injury  interference with this phase will impede subsequent regeneration after acute injury o Produces growth factors that are important for the muscle to regenerate/repair itself  Regenerative  Replacement of damaged muscle fibers via activation of myoblast precursor cells called “satellite cells” o Located b/w basal lamina and plasma membrane o ~50% of hypertrophy (thickness) of muscle cell with increased muscle training is due to satellite cells  Recapitulation of developmental process o i.e. re-expression of embryonic myosin starts to regenerate muscle like it did when it was first building it in urtero  myotubes & small regenerating fibers by 4-6days post injury  injured muscle appears normal by 10-14 days post injury  inflammatory cells are providing the necessary substrates that help with muscle reparations  skeletal muscle regeneration mature fibers are post mitotic cells (cannot divide) it depends on satellite cells  satellite cells are normally quiescent (state of inactivity)  they are activated by injury and enter cell cycle and proliferate  they then undergo differentiation (fusion and expression of muscle specific genes)  soluble factors trigger satellite cell proliferation, migration and differentiation  immune, motor neuron, autocrine, vasculature and other factors play a role  myoD = determinante factors: tells the cell to proliferate and what it will become  myogeninin/MRF-4: help with the transition from proliferating myoblast  myofiber o fuse w e.o to form new fibers o fuse w/ pre-existing fibers to replace damaged segments Growth factors and repair  Fibroblast growth factor o Stimulates satellite cell proliferation and inhibit muscle differentiation  Insulin-like growth factor o Stimulates satellite cell proliferation and differentiation (depends on dose)  Transforming growth factor – beta o Inhibits satellite cell proliferation and differentiation o Stimulates synthesis of extracellular matrix elements o Can be very dangerous if released at the wrong time  muscle fibers can produce these themselves Stem cells and repair  Derived from bone marrow  Cells derived from vasculature have been show to have myogenic potential  Can play a role in muscle regernation o Satellite cells play a more important/predominate role in normal muscle reg
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