Building Skeletal Muscle and Neuromuscular Control Systems IB
Building Skeletal Muscle and Neuromuscular Control Systems IB Sports and Exercise Medicine -1 Metro High School Winter 2020 Stan Misler (stan. misler. il@gmail. com)
Human Biology of Sports and Exercise *Essential Body Systems 1. 2. 3. 4. Neuromuscular : central motor systems and skeletal muscle (movement analysis, skill development) Skeletal: bone, tendon Energy Supply (metabolites): organ stores, ATP Energy Distribution (including O 2/CO 2 exchange): Circulatory, Respiratory *Auxiliary Systems 1. Endocrine 2. Renal 3. Gastrointestinal 4. Thermoregulatory All under variable control by brain *However, too much exercise can produce deleterious effects on all organ systems of body in part due to hijacking brain control centers
Part 1: Functions of Skeletal (axial) Muscle 1. 2. 3. 4. 5. 6. 7. Muscle fibers divided into functional bundles each innervated by nerve fibers of a single spinal motor neuron (motor units) Contraction excited by impulses down nerve fiber reaching muscle fiber surface at synapse (the end-plate) when chemical release (acetylcholine) -> initiation of muscle action potential (electrical impulse) Muscle action potential spreads down muscle fiber -> releases Ca from cellular stores Contractility: increased Ca in the cytoplasm unlocks the “breaks” allowing sliding of interdigitating actin and myosin filaments in functional contractile units of myofibrils (= sarcomeres) -> sarcomere shortening and generation of force of contraction Passive properties of muscle aid contractility and restoration of resting length : (a) Extensibility = stretched beyond resting length; (b) Elasticity = return to original length Fascia around myofibrils grow out of muscle body as tendons that attach to bone. Proximal attachment (origin) stays fixed while distal attachment (insertion) into moveable bone Muscle plasticity = (a) Exercise -> inc # myofibrils either length-wise or thicknesswise and (b) muscle self-repair: new muscle fibers develop from local stem cells; return of nerve endings to specialized end-plate regions of muscle fiber surface (endplate)
1. Motor Units: how nerve drives muscle a. Muscle fibers divided into functional bundles each innervated by nerve fibers of a single spinal motor neuron (motor units) b. Muscle contraction is excited by impulses traveling down nerve fiber and reaching muscle fiber surface at synapse (the end-plate) where chemical release (acetylcholine) -> initiation of muscle action potential (electrical impulse)
2. Excitation-contraction coupling in muscle fibers a. Transmission across neuromuscular junction: Nerve impulse at nerve terminal releases neurotransmitter chemicals stored in vesicles. These molecules cross cleft between nerve and muscle, bind to receptors on muscle endplate region setting off an electrical impulse along membrane of muscle fiber (Chemical transmission)
Electrical activity is the action potential AP = Jumping wave of electrical activity. At regions of membrane the electrical polarity across the cell membrane is transiently reversed (from -70 mv inside to +40 mv inside), as Na rapidly enters the cell and as K more slowly leaves. Buried in this is the entry of small amount of Ca
b. Action potential releases neurotransmitter Synaptic vesicles at tip of nerve terminal just opposite the specialized muscle membrane (end-plate region) release their chemical contents by their fusion with plasma membrane, the latter promoted by entering Ca
c. Spread of electrical impulse along muscle fiber, the surface muscle membrane and the T tubules that dip deep into the body of the muscle and contact sacs of interior membrane, the sarcoplasmic reticulum (SR), containing Ca stores
d. The sarcoplasmic reticulum releases Ca that binds to molecules on the actin proteins (Tn. C) allowing actin to interact with myosin
3. Muscle Contractility Parallel actin and myosin filaments, able to slide past one when a non-excited, relaxed muscle fiber is stretched (A ->B) , now hook onto one another (to form a “tiltable” cross-bridge) with myosin pulling actin along (the powerstroke). The muscle fiber contracts and force is generated. Force can be transmitted to the muscle tendon thereby pulling a joint between two bones Relaxed fiber Thin exterior filaments = actin Thick central filaments with projections = myosin Actin Myosin Relaxed fiber Contracting fiber
Detail: How The actin/myosin “cross bridge” undergoes a “powerstroke” (a) myosin, under influence of increased cytosolic Ca, form cross-bridges with actin (b) Cross-bridges go through power stroke with myosin head (lever arm) tilting; tension and displacement are generated. (c) At end of power stroke, through which ADP + PO 4 have been bound, myosin head exchanges ATP for ADP + PO 4 and dissociates from actin. If ATP is lacking actin and myosin will not dissociate and there will be constant force generated (the rigor complex, as in rigor mortis in a cadaver, where the muscle can only be relaxed by injecting ATP into it. (d) Myosin undergoes a “repriming” state during which it hydrolyses ATP.
Experiment showing connection between muscle impulse (the action potential =AP), Ca release from SR ([Ca]i, hv) and muscle tension and contraction (i) Mount fiber on microscope slide, (a) attach one end of muscle fiber to strain gauge to measure tension; (b) insert electrode into fiber to record AP; and (c) inject fiber with Ca sensing dye. (ii) Stimulate muscle -> AP, followed by rise in [Ca]i, (spark seen in vicinity where T tubule and SR contact each other), followed by development of contractile tension
4. Mixing function (physiology) with microanatomy a. The length – tension curve If the contractile unit of muscle (or the sarcomere) is stretched to a length that provides optimal actin/myosin filament overlap (and presumed cross -bridging opportunity) the sarcomere will generate the greatest possible force (or tension) when stimulated. Fall off of tension at smaller (A) or larger (C) sarcomere lengths where fewer usable cross-bridges can form. (Note in A that cross bridges are cramped together
b. The force - velocity curve The lower the load that the sarcomere must support, the faster it can contract (higher velocity) That is (i) the smaller the average number of cross-bridges needed to support the load, and (ii) the faster the dissociation of actin – myosin cross bridge (less resistance to head tilting)
5. Modes of muscle contraction a. Muscle can generate lots of force but hardly change length (isometric contraction, as in holding up dumbbell) vs. b. Muscle can shorten a great distance when hardly bearing a load (isotonic contractions, as in quickly flexing arm at elbow) vs c. Muscle can do something in between (generate some force and shorten some distance)
• • 6. Muscle Energetics Muscles that exert a force do work (W = force X distance) Doing work requires expenditure of energy In living things the ultimate source of energy is high energy bond in ATP (A-P-P~P) Muscle needs ATP to (i) break A-M cross-bridge and allow formation of a subsequent one as well as (ii) pump out Na that enters during AP so that electrical activity may be maintained. • In brief exercise (the sprint), the source of ATP is creatine~P (Cr~P +ADP -> creatine + ATP). In somewhat longer exercise source is aerobic glycolysis (break down of glycogen stores to glucose and metabolism of glucose with O 2 to CO 2 +H 2 O). In prolonged exercise the source of ATP is aerobic metabolism of glucose provided by blood supply. The need for breakdown and transport of stored glucose recruits much of the rest of the body into action: heart to pump more blood; blood vessels to carry blood to active muscle; the liver to provide source of circulating glucose from breakdown of glycogen; fat stores to release fatty acids that cells can also metabolize as backup for glucose; increased gas exchange (O 2 for CO 2) by lungs to provide adequate O 2; and brain to direct increased ventilatory function of lungs as well as pick the order of smooth, sequential activation of motor units. • Since chemical reactions are not 100% efficient, breakdown of glucose produces heat which the body must dissipate by radiating it through evaporation of skin sweat
7. Passive properties of muscle These aid contractility and restoration of resting length : (a) Extensibility = stretching of muscle beyond resting length; (b) Elasticity = passive recoil (return) to original length
Tension is passive, as in relaxed fiber by way of collagen, as well as active, by way of cross bridges in sliding filaments
8. Muscle Attachment to bone: Fascia around myofibrils grow out of muscle body as tendons that attach to bone. Proximal attachment (origin) stays fixed while distal attachment (insertion) is into moveable bone
9. Muscle plasticity (a) Muscle remodeling with exercise: increased # myofibrils (actin and myosin filaments) either length-wise for fast exercise or thickness-wise for sustained lifting; and (b) Muscle self-repair after injury: new muscle fibers develop from local stem cells (satellite cells); return of nerve endings to specialized end-plate regions of muscle fiber surface
(a) Changes in # sarcomeres in series (-> longer fiber) or in parallel (-> thicker fiber) Aging without exercise: decreased average fiber diameter (fewer sarcomeres wide)
(b) Effects of exercise training: need to choose type of exercise for type of muscle adaptation (thickness or lengthwise) sought
c. Muscle Satellite Cells and Muscle fiber regeneration vs degeneration Satellite cells were first identified in 1961 by electron microscopy. In his brief communication, Mauro reported “[…] the presence of certain cells, intimately associated with the muscle fibre, […] which we have chosen to call satellite cells […]. ” Owing to their close association with the myofibers, satellite cells soon became good candidates for the solution of what Mauro defined “the vexing problem of skeletal muscle regeneration. ” Indeed, it was already well known that skeletal muscle regenerates after injury, but the cellular origin of new adult myofibers was still obscure
Part 2: Central Nervous System Control of Muscle in Exercise a. the motor unit: Single spinal (1 A) motor neuron innervates and activates a group of muscle fiber. Brain can activate more motor units (**) or each motor unit more frequently (##) to enhance muscle contraction ## **
Skeletal muscle fiber/motor unit types; predominance after exercise training *
b. Spinal Circuitry and Spinal Reflexes (i) stretch of limb -> withdrawal = stereotypic limb movements. Ex. patellar ligament -> knee jerk) 1 A sensory fiber a (i) Reflex arc: stretch of muscle -> activation of stretch receptor fibers in muscle -> activation of 1 A afferent sensory nerve to spinal cord -> synaptic transmission (pre-synaptic release and post-synaptic reception of glutamate) -> activation of a motor neuron to muscle -> conduction of AP down motor neuron and release of Ach at neuromuscular junction -> muscle contraction to restore length (ii) Voluntary contraction: Impulse generated in cerebral cortex of brain travels down upper motor neuron to activate a motor neuron synapsing on muscle
c. Supraspinal activation of motor units: Upper motor neurons beginning in the cerebral cortex or brain stem synapse on, and activate, alpha motor neurons in ventral horn of spinal cord and shape voluntary contraction of motor units.
d. Complex CNS control of voluntary movement: Recruitment and modulation of activation of motor units
Neurology Lab Standard Neurological exam • Mental status (date, time, place, memory, facts) • Cranial nerves (long nerves of head to eyes, ears, face sensation, face muscles) • Motor exam (moving extremities) • Reflexes • Station (able to stand); Coordination (moving limbs together) and Gait (walking) • Sensory exam (light touch, pressure) Directed Neurological Exam • Passive properties of muscle = rigid or plastic • Spinal reflexes • Tests of cerebellar (smoothness of action) and basal ganglion (tremor) function
Motor System and Deep Tendon Reflexes • Muscle strength, graded on scale 0 to 5 (i. e. , Paralysis to Nl Power). • Muscle tone and signs of rigidity (cogwheeling; gegenhalten: increasing resistance to passive movement) or spasticity • Deep tendon reflexes (ankle, knee, elbow) • Posture – Normal – decerebrate – decorticate – hemiparetic • Tremor: none, at rest, on action • Gait: walking and stopping; shuffling • Abnormal movements – seizures – fasiculations (twitching)
a. Adaptation of skeletal muscle function
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