Brice Muscle Phys

Excitability - response to stimulus

Contractility - shorten/generate force

Extensibility - passively stretch over wide range

Elasticity - passively stretch, some recoil

Bundle of parallel muscle fibers, length of the entire muscle

multinucleated, under sarcolemma, peripherally located

intracellular fluid

tube like structures filling muscle cells

repeating pattern of striations along each myofibril

Thick filaments - myosin, anchored to z-line by titan

Thin filaments - actin, anchored to z-line

Nebulin

overlapped thin & thick filaments. crossbridge binds to actin-triggers power stoke (thin fil. pulled toward thick fil.) ADP and Pi released, new ATP attaches-crossbridge releases. crossbridge/power stroke occurs asynchronously

tail and 3 heads-cross bridges each crossbridge has 2 actin binding sites and myosin ATPase

G-actin, bunch of G-actin strung together, called actin helix

sequence of events starting with AP in sarcoma and ending in crossbridge activity

synapse of somatic motor neuron on skeletal muscle. ACh always excitatory, at the center of skeletal muscle

portion of the sarcolemma just after the axon terminal, contains N1 receptors with gated cation channels

series of loose connective sacs that surrounds each myofibril, stores calcium when not being stimulated, release Ca++ upon stimulation, reuptake of Ca++ via active transport

voltage gated calcium channel located on SR

internal trigger that allow contraction to occur (any muscle), binds to troponin, pulls tropomyosin out of blocking position, Ca++ stays bound as long as concentration remains elevated

~skeletal muscle - response to 1 AP there is enough Ca++ to saturate all troponins, all cross bridges can participate (not in cardiac/smooth)

-90mV

bacterium releases toxin that blocks release of ACh producing flaccid paralysis

massive release of ACh, spasms and convulsions

autoimmune dz that destroys N1 receptors at MEP, treated with cholinesterase inhibitors

single motor neuron and all muscle fibers it controls, # of muscles are highly variable. activity is all or none, muscles have variety of large and small motor units

generation of tension within a muscle by crossbridge activity

tension exerted by contracting muscle on an object

force exerted by the object on the muscle, after it is stimulated to contract

muscle shortenes

muscle develops tension but does not shorten or lengthen

muscle changes length while the afterload on the muscle remains constant (constant tension)

Muscle shortens

Unsupported load on muscle is greater than tension generated. muscle lengthened inspite of force generated by crossbridging

mechanical response to a single AP

period between excitation and the development of tension. includes time needed to release Ca++ from SR, move tropomyosin, cycle crossbridges, and the influence of series elastic component

not really, each AP results in twitch. Wave summation results in unfused tetanus-slight increase in external tension d/t series elastic component take-up. fused tetanus occurs from rapid APs causing contraction to max or fatigue

transmission of muscle tension to bone. internal tension generated by muscle to load must be transferred through connective tissue. Greatest contribution to latent period

relationship between inital resting length of striated muscle and how much tension it can develop when stimulated at tetanic frequency

resting length of the muscle prior to its stimulation

explained by sliding filament mechanism of contraction, perfect overlap of thin/thick filaments so each crossbridge is in reach of thin filament

velocity of muscle shorting is inversely related to afterload of muscle

~takes longer for internal tension to become greater than external tension

tension of each fiber - AP frequency, fiber length, diameter

Number of active fibers - per motor unit and # of motor units

-phosphorylation of ADP by creatine phosphate

-oxidative phosphorylation of ADP - mitochondria

-phosphorylation of ADP - glycolytic paththway

Creatine phosphate, 1 step chemical rxn, avg. stores last 10-15 sec. 1 CP= 1 ATP, 1 creatine (byproduct)

anaerobic glycolysis, glucose from glycogen converted into pyruvic acid/ATP. 1 Glucose=2 ATP, 1 pyruvic acid-->lactic acid

~60sec until fatigue

Nutrients: Pyruvate (from glycolysis), FFA, AA, glucose - requires O2

32 ATP produced, CO2, H2o byproducts of glucose metabolism

~hours until fatigue

Twitch characteristics

Amount of tension developed related to diameter

Resistance to fatigue
Production of ATP

Fast twitch develop peak tension sooner-related to myosin ATPase activity (ATP can be split faster) as well as calcium kinetics-rate Ca++ can be released from SR

slow fibers - smaller diameter, less sarcomeres

fast fibers - larger diameter, more sarcomeres, pale color, fatigue easier

slow twitch less fatigue, d/t diameter and ATP production

slow oxidative, fast oxidative, fast glycolytic fibers

oxidative phosphorylation: High mitochondria, capillaries, myoglobin content.

Low: glycolytic enzyme activity and glycogen content, myosin ATPase acitivty, contraction velocity. Small fiber diameter, motor unit size

Oxidative phosphorylation. High: mitochondria, capillaries, myoglobin. Intermediate glycolytic enzyme activity and glycogen stores. High myosin ATPase activity, fast contraction, intermediate motor unit size

glycolysis, few mitochondria, capillaries, low myoglobin(white color). high: glycolytic activity/stores, fatigue rate, myosin ATPase activity, contraction velocity. large fiber diameter

Determines respiratory fitness, factors in capacity for ATP production via oxidative phosphorylation, influenced by CV and respiratory systems as well

Genetics

Motor neuron innervating the muscle

synaptic fatigue

Conduction fatigue (K+ buildup)

Lactic acid - H+-->decreased enzyme act.

inhibition of crossbridge cycling -ADP buildup

CNS mechanisms: change in internal environment-feedback info to CNS

Depletion of glycogen- hypoglycemia

hypertrophy - existing cells get larger

hyperplasia - increased # of cells (from satellite cells-undifferentiated myogenic cells)

somatic motor neurons, alpha & gamma

(lower motor neuron) ventral horn of spinal cord and cranial nerve motor nuclei of the brainstem

Always excitatory - EPP-AP-contraction

basic unit of contraction, one motor neuron plus muscle cells it innervates

contain in the descending tracts (corticospinal and extrapyramidal) and synapse on lower motor neuron, can be inhibitory or excitatory

motor neuron cell body groups, a group is composed of multiple neuron cell bodies fro neurons that innervate a specific muscle, extend over several spinal cord segments

Not all are activated in most muscle contractions. Activation is based on size of motor unit, fiber type of motor unit, size of motor neuron, excitability of motor neuron - ease of which it can be pushed to threshold

muscle fibers of a given motor unit are of the same fiber type, slow oxidative are more excitable due to shorter distance to axon hillock, EPSPs have less distance to travel, less chance of decrement. Require a larger stimulus for larger motor units to get activated

thousands of synaptic inputs (EPSP/IPSP) all integrated in the spinal cord

Higher CNS- -excitatory or inhibitory upper motor neurons (motor cortex-corticospinal tracts and extrapyramidal tracts)

Somatosensory afferents - pain, nociceptive

Muscles afferents - spindles, golgi tendons

basic mechanism of skeletal muscle tone present in all skeletal muscle, resistance to a muscle offers to being stretched or lengthened, necessary to maintain posture, counter gravity

Muscle spindle - responsible for monitoring muscle length and rate of change of muscle length

Extrafusal muscle fibers(normal muscle cells) innervated by a-motor neurons

Spindle muscle fibers - parallel-monitor rate of change

-contractile end gamma motor neuron

-primary afferent fiber (grp I) sitmulus is stretch, interprets rate of AP

-secondary afferent fibers (grp I) stimulus is stretch, interprets length

at baseline spindle will fire at a certain frequency and brain interprets this as muscle length

-stretched spindles - fire AP at higher rate

-contract spindles -AP stops firing, only a-stim, no gamma

-2* fibers provide info re: absolute length of fiber

-1* fibers provide info re: rate of change

when muscle shortenens, spindles go slack--> decreased AP firing (but we need feedback)--> intrafusal fibers are also contracted to allow central region to provide info about musc length

Alpha-gamma co-activation

Coordinates agonist/antagonist muscles. excitatory stim to quad muscle, inhibitory stim to hamstrings in patellar tendon reflex

located in tendons (connection of muscle to bone)

monitors tension exerted by the muscle, series arrangement allows monitoring of tension compared to spindles. w/ passive stretch, golgi tendon fire APs-->relax muscle, tension decreases. muscle contraction>stimulus than passive stretch

-deep tendon reflex - golgi reflex

-seen w/ hypertonic limb (SCI)

-myotatic reflex is hyperactive, lots of resistance to passive stretch

-w/ passive stretch-->more tense, golgi activated --> through interneuron muscle inhibited-->relax. (clapsed knife reflex)

-may contribute to smooth onset/termination of contraction needed for walking

-SC mediated, Protective

-stimulus activates pain receptors (1st order aff.) through interneurons activate motor neurons of flexor and inhibit extensors

with pain stimulus in lower extremity, opposite leg extensors must activate/flexors inactivate--keeps body from falling

refex arcs are intact, but higher order inhibition is blocked

virus kills lower motor neurons, produces flaccid paralysis, usually confined to a few motor neuron pools

attacks upper and lower motor neurons controlling skeletal muscles, gradually weaken and atrophy

non-striated, single central nucleus, walls of hollow organs, involuntary (ANS and hormones), often has underlying tone, can be stretched and still generate tension, can replicate(mitosis), underdeveloped SR, no T-tubules, no troponin, tropomyosin present-but no blocking position

Thin filament attached to dense body with thick filament between

Dense bodies - attachment for thin & intermediate filaments(structural component)

thick/thin filament interact - myosin ATPase on crossbridges has low activity

Pi of myosin x-bridge to bind to actin

regulation at level of thick filament

stimulus increases Ca++ conc. (CICR)

Ca++ binds to calmodulin

myosin light-chain kinase binds to Ca++(activation)-->Pi to x-bridge-->binds to thin fil--> power stroke-->ADP/Pi released, new ATP attaches

myosin light-chain phosphatase - cleaves phosphate-x-bridge can no longer interact with thin filament

Enters ECF through voltage regulated channels, chemically gated channels

SR is poorly developed, AP travels down sarcolemma, can trigger release of Ca++ from SR through 2nd messenger

no, graded response to amount of available Ca++

primary active transport pumps in sarcolemma resequester Ca++ to SR

+spontaneous elecitral activity in plasma membrane

+/- NT of ANS

+/- hormones

+/- local factors release d/t changes in chem composition

+ stretch

depolarization - Ca++ entry through volt. gated Ca++ channels

rhythmic changes in membrane potential can result in rhythmic pattern of AP-pacemaker potentials - leaking CA++ and Na+ channels and decreased K+ leaking out of cell

resting membrane potential varies over time

amplitude modulated by enteric nervous system

SNS decreases amplitude

PSNS increases amplitude

found in walls of hollow organs

SM cells contract and relax as single unti d/t they are linked w/ gap junctions

innervated by ANS, hormones, chemical enviornments

found in skin, eyes

Very dependent on ANS, no pacemaker activity

branched single nucleus, striated, woven end to end with intercalated discs

high capillary density, mitochondrial density

Sarcomeres - thin & thick filaments

SR not as well developed as skeletal musc.

T-tubules - larger than skeletal musc

same sliding filament mechanism as skeletal

Heart beat=twitch

no, increased Ca++=incrased contractility - more x-bridge cycling

100x longer than skeletal

phase 4 - resting membrane -90mV (more permeable to K+ than Na+)

Phase 0 - large rapid depol. -->30mV (Na+ gates)

Phase 1 - small repol - Na+ out, K+ in

Phase 2 - plateau - L-type Ca++ channels open

Phase 3 - L-type Ca++ close, volt gated K+ channels open(K+ exits) repolarizing

Ca++ enering from volt gated Ca++ channels in sarcolemma will bind to receptors on SR and cause it to release more Ca++ (1* stimulus for Ca++ release-95%)

Gprotein-activates adenyl cyclase, increased cAMP, incr protein kinase-->phosphorylation of:

-L-type Ca++channels, incr CICR

-phospholambin - incr SR Ca++ pump, increasing reuptake of Ca++ and speed of relaxation(diastole)

-troponin I -- increased removal of Ca++ increased speed of relaxation

Gprotein acts directly on L-type Ca++ channels, incr Ca++influx, incr contractility

inhibit Na/K pump, increase intracellular [Na+] which decreases rate of Na/Ca exchanger (2* active transport Na+ in Ca out) results in more Ca++ intracellular/stored in SR, more CICR

No, mechanical response is as long as the electrical response, nothing left to summate d/t longer AP

In cardiac contraction, all cardiac cells are contracting, however not all x-bridges are contracting at any one time. also # of x-bridges active dependent on [Ca++]