BLINN Ch11 MusclePhysiology Sp2015 New

Ch 11: Muscle Physiology

• Responsiveness / excitability– Stimulated by neurotransmitter, stretch, or electrical change

• Conductivity– Local electrical change moves down the membrane (wave)

• Contractility: Can shorten (e. g. to pull bone)

• Extensibility: can stretch w/o breaking

• Elasticity: Can recoil back to original resting length

Characteristics of Muscle cells

Skeletal Muscle

• Cell called muscle fiber– Because so long– 3 cm, but up to 30 cm– Formed by fusion of several stem cells (myoblasts)

• Striations– Alternating light & dark bands– Dark reflects areas where contractile protein overlap

©Ed Reschke

Musclefiber

Striations

Copyright © McGraw-Hill Education. Permission required for reproduction or display.

Muscle Prefixes: Sarco, myo, mys

• Sarcolemma = muscle cell plasma membrane

• Sarcoplasm (muscle cell cytoplasm) contains:– Bundles of contractile proteins called myofibrils (most abundant)– Glycogen polysaccharide for stored energy– Myoglobin for stored oxygen

• Sarcoplasmic reticulum (SR)– SR wrapped around myofibril

– Stores calcium until needed for muscle contraction

Sarcolemma

Nuclei

Myofibril

sER

Terminal cisternae

Each myofibril contains 2 types of myofilaments

1. Thick filaments• 200-500 myosin molecules• Each myosin is like a

double golf club

• Tail = 2 entwined shafts

• 2 Heads = globular shape– Hundreds of pairs are bundled

together

– Heads extend away from middle bare zone

Myofibril

Each myofibril contains 2 types of myofilaments

Myofibril

2. Thin Filament are 2 intertwined strands of globular actin

• Each globular actin has an active site where the myosin head of the thick filament can bind to start the contraction

6

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• The sarcomere is the functional unit of contraction• Thin and thick filaments alternate

– Areas with only thin filaments( light bands)– Areas the thick filaments (or thick & thin overlap) are dark

Thick & thin filaments are arranged into sarcomeres

Myofibril

Sarcomere

Sarcomere = From Z disc to Z disc

• I band = LIght band (Thin Filaments, where they don’t overlap with Thick Filaments)

• A band = dArk band (Entire length of Thick Filaments)– H-Zone is where there is thick no Thin Filament overlap

Other Proteins Associated with the Sarcomere

• Z disc: Protein complex where Thin Filaments & Titin end– Some proteins are for mechanical stability (alignment)

• M line = proteins @ center of A band; link Thick Filaments

– A huge protein spring

– Anchors thick filaments between Z-disc and M-line

– Prevents over-stretching

– Restores sarcomere to its original length at relaxation

• Elastic filament: made of Titin

Thin FilamentThick Filament Titin

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• Dystrophin (red) is an accessory protein that links outer thin filaments to peripheral proteins (blue) in sarcolemma– Periferal is linked to a transmembrane protein (green)

– Transmembrane protein is linked to an external membrane proteins (dark blue)

– External protein is attach to basal lamina

– Basal lamina is linked to the CT of the endomysium around cell

Connecting the Muscle Cell to the Bone: Layers of CT

Connecting the Muscle Cell to the Bone: Layers of CT

• Endomysium around 1 muscle cell– Sleeve of areolar CT– Contains capillaries & nerves– Keeps extracellular chemicals in

• Perimysium: around bundle of cells– Thicker CT– Carries larger nerves & BV– Has stretch receptors: muscle

spindles

• Epimysium: around ENTIRE muscle– Collagenous fibrous sheath

Endomysium

Perimysim

Epimysium

Skeletal Muscle

• The collagen of the muscle’s connective tissue is continuous with the collagen of the tendon, which is continuous with the collagen of the bone

That’s why contraction of the sarcomere pulls on the

endomysium and contracts the muscle and the muscle moves

the bone

• Z lines move closer together

• Sarcomeres shorten → cell shortens– Cell pulls on Endomysium →

Endomyseum pulls on perimysium → perimysium on epimysium → muscle contracts

– Connective tissue of the epimysium blends into connective tissue of the tendon → pulls on tendon

– Connective tissue of tendon blends into connective tissue of the periosteum of the bone

– Bone is moved

Myofibril contains 2 types of myofilaments

http://images.google.com/imgres?imgurl=http://www.monkeyspirit.org/images/strength/concentric.jpg&imgrefurl=http://www.monkeyspirit.org/en/strength.php&usg=__u_lwsY0Tec6ROg7y5bdxPx6RrXk=&h=246&w=400&sz=24&hl=en&start=7&tbnid=lA-41kbeCthh3M:&tbnh=76&tbnw=124&prev=/images%3Fq%3Dmuscle%2Bshorten%26hl%3Den%26rlz%3D1T4TSHB_en___US339

Muscular Dystrophy: Mutation of Dystrophin

• Defect in dystrophin protein cause sarcolemma to tear when the muscle contracts– Dying muscles replaced with scar tissue

• Duchenne– Most common in children (males 2-6)– Affects arm, legs, spine; death by 20’s

• Becker-similar to Duchenne, but milder • Limb-Girdle-teen to adult

– Hips, shoulder, arms, legs; wheelchair in 20 yrs; death in 40’s

• Oculopharyngeal: Begins in 40’s-70’s– Ears, throat, pelvis, shoulder; slow

• Normal, healthy skeletal muscle does not contract on its own.

– Stimulated by motor neuron (or electrode)

– Denervation (nerve connection is severed) results in paralysis and eventually muscle atrophy

• Somatic motor neurons– Neurons that “serve” skeletal muscles– Their cell bodies are in the brainstem

or spinal cord

Muscle-neuron Partnership

Denervation Atrophy

Muscle Contraction Physiology

Background Information

Neuromuscular Junction (Motor-end Plate)

• Where nerve branch meets its muscle target cell

• Synaptic knob

Somatic motor neuron

Synaptic knob

Synaptic cleft

NT Vessicles

– Swollen end of neuron– Contains vesicles filled with the

neurotransmitter acetylcholine (Ach)

• Schwann cell– Encloses entire junction to

chemically isolates area– Basal Lamina surrounds Schwann

cell & muscle fiber, (including the synaptic cleft)

NMJ: Muscle membrane

• Sarcolemma (plasma membrane) is indented to fit the synaptic knob– Junctional folds = increase surface area of sarcolemma

• Synaptic cleft = fluid filled space between neuron cell membrane and muscle cell membrane

• ACh receptors– Embedded in the

sarcolemma– Bind Ach, a

neurotransmitter

Synaptic cleft

Ach receptors

Junctional folds

20


Stimulus changes charge

• Ligand-activated‐ Opened by chemical

binding to a receptor‐ ACh (previous slide)

• Voltage-activated: ‐ Opened by a change

in charge (the membrane potential)

Two different stimuli can open channels important to muscle contraction

Electrophysiology: Study electrical activity of cells

• Electric potential (or voltage) is a difference in charge between two points

– Na+ ions predominate in the extracellular environment– K+ ions predominate inside the cell, but

• Differences in diffusion and negatively charged anions (proteins, nucleic acids, P) make it slightly more negative on the 2 sides of the sarcolemma

– This is called an electric potential

Na+

K+ -90 V

– When muscle cells are relaxed, they have a Resting Membrane Potential of -90 V

• Sodium-potassium pumps work constantly to maintain the Na+ and K + differences– Na+ tends to diffuse into the cell from high to low concentration– K+ tends to diffuse out of the cell from high to low concentration

• The Na/K Pump constantly fights this “leakage”– Sodium /potassium pump moves 3Na+ out & 2K+ in

Na+

K+

Leakage

Maintaining the resting membrane potential

Maintainance

Muscle Cell Conductivity• Depolarization refers to the

reduction of the negative membrane potential

• Action Potential refers to progression of the membrane depolarization– Initial depolarization occurs when

ligand-gated channels open– Change in charge stimulates the

opening of neighboring voltage-regulated gates

– Causes depolarization of adjacent membrane

– Moves along the ENTIRE membrane

REST

DE

RE

AP

4 phases

1. Excitation: Nerve turns on muscle

2. Excitation–contraction coupling: Change in charge across muscle membrane causes Ca++ release inside cell

3. Contraction: Myosin binds & pulls actin

4. Relaxation: Myosin stops pulling; cell returns to resting length

Excitation

• Action potential in nerve fibers produces an action potential in the muscle fiber

1. Nerve signal @ synaptic knob opens voltage regulated Ca++ gates in neuron

– Calcium enters synaptic knob of the neuron

2. Ca++ triggers ACh exocytosis– Synaptic vesicles release their contents into the

synaptic cleft

4. ACH binding opens fast Na+ channels– Na+ diffuses into cell– Potential goes from rest -90mV

to +75mV– Causes END PLATE potential

(depolarization at the end plate)

– ACh is removed from the synaptic cleft (animation)

3. ACH diffuses across synaptic cleft & binds to receptors on muscle cell sarcolemma– Receptors are ligand-regulated Na+ channels

Excitation

28


5. End Plate Potential Becomes Action Potential

• Na+ has only caused depolarization at the end plate (neuromuscular junction)

• For the muscle fiber to contract, the sarcolemma of the entire muscle cell must depolarize

Na+

• Na+ diffuses away from motor end plate and causes a change in charge @ nearby membrane

5. End Plate Potential Becomes Action Potential

Na+

• Na+ diffuses, depolarizing the next part of the membrane, opening the next Na channels → Action potential– What type of feedback is this, positive or negative?

• Voltage-regulated ion channels are found near the motor end plateT As the Na+ diffuses away

from the end plate, adjacent areas depolarize

T Adjacent voltage-regulated channels open

T Na+ moves in

Repolarization

Na+

• K+ channels open more slowly (as Na+ channels close)– As K+ exits, the membrane

potential returns to negative

– The cell is repolarized

• Terminal cisternae are the enlarged ends of the sER

• T tubules (transverse tubules) are folds of sarcolemma that follow the T cisternae of the SR deep into cell

• Triad = terminal cisterna + T tubule + terminal cisterna

T Tubule

Triad

Terminal cisternae

T tubuleTerminalCisterna of SR

Remember: SR stores calcium until needed for muscle contraction

6. Action potential moves over entire cell membrane and down T tubule

Excitation-Contraction Coupling

7. T tubule charge opens voltage regulated Ca++ channels in terminal cisternae of Sarcoplasmic Reticulum

- Ca++ diffuses from SR into cytosol

• Thin Filament are 2 intertwined strands of globular actin– Each globular actin has an active site where the myosin head

of the thick filament can bind to start the contraction

• Thin filaments are associated with 2 regulatory proteins– Tropomyosin: Blocks actin binding site when muscle is relaxed– Troponin: Keeps tropomyosin “locked” into place

• Binding of calcium “unlocks” the actin binding sites

8. Binding of Calcium to troponin

• Calcium binds to troponin

• Troponin changes shape, moves tropomyosin away from actin binding site

• Myosin is normally already energized by ATP– Just waiting for actin binding site to be uncovered– Step # 10 has already happened

• Energized myosin binds actin and forms a crossbridge– Step #11

9. Troponin changes shape & moves tropomyosin away from actin binding sites

36


Actin is Reactivated12. Powerstroke: Myosin pulls actin

• Myosin head releases ADP + Pi• Flexes to low energy position• Actin to slide past myosin

13. A new ATP is needed for the Recovery Stroke (step #10)• Lets myosin release actin

(breaks crossbridge)• Puts myosin head in high energy

position again• Myosin ready to bind again

As long as Ca+ is available, the cycle will repeat

Relaxation: Tension falls

14. Nerve signal stops @ neuromuscular junction• No more ACH released

15. AChE breaks down acetylcholine• Recycled back into synaptic

vesicles

16. Ca++ pumped back into SR• Calsequestrin protein in SR

binds Ca++

• Pump needs ATP! (ATP needed to relax also)

Relaxation: Tension falls

17. Ca++ falls away from troponin- Concentration in cytosol

decreases

18. Tropomyosin is free to bind actin– Covers actin binding

sites again– Myosin is activated but

has nowhere to bind– Myosin can’t pull,

tension drops

40


11-41

Rigor Mortis

• Rigor mortis: Hardening of muscles and stiffening of body– Beginning 3 to 4 hours after death – Caused when deteriorating SR releases Ca+2

– Results because muscles are already “activated” (no ATP is needed)

– Released Ca+2 initiates muscle contraction

• Contracted muscle cannot relax– Relaxation requires ATP to break the grossbridge– No ATP is produced after death– Fibers remain contracted until myofilaments begin to decay

• Rigor mortis peaks about 12 hours after death, then diminishes over the next 48 to 60 hours

Spastic Paralysis: muscles stay contracted

• Organophosphate pesticides – Contain cholinesterase inhibitors which bind AChE, &

prevent ACh breakdown– Deadly with larynx, respiratory muscles

• Clostridium tetani bacteria causes tetanus disease– Different mechanism– Stops glycine in spinal cord from blocking excess

muscle contractions– Lockjaw = spastic paralysis

Flaccid Paralysis: muscles can’t contract

• Curare competes with ACh for receptor sites– Doesn’t stimulate muscles

– Used in blowgun darts by Amazon natives

– Medically can treat muscles spasms, as during surgery

• Clostridium botulinum: botulism food poisoning– Blocks release of ACh

– Botox cosmetically stops muscle contraction, wrinkles

Myasthenia Gravis: Spastic or Flaccid?

• Most common in women 20-40• Autoimmune disease: antibodies attack NMJ

– Cells less sensitive to ACh– Ptosis (drooping eyelids), double vision, strabismus

(crossed eyes), weakness, respiratory failure

• Bungarotoxin (cobra) assesses # working ACH receptors• Treatment:

– Cholinesterase inhibitors: keep ACH at synapse longer– Immunosuppression– Thymectomy: remove thymus to slow immune system– Plasmaphoresis: remove bad antibodies from blood plasma

11-45

Muscle Contraction

• Threshold: Minimum voltage necessary to generate an action potential in a muscle fiber & produce a twitch– Twitch: A quick cycle of contraction in response to a single

stimulus at threshold or higher– Subthreshold stimulus produces no contraction

11-46

Twitch Cycle: Latent → Contract. → Relax.

• Latent period: 2 ms delay between the onset of stimulus and the onset of twitch response– Time required for

excitation, excitation–contraction coupling, and tensing of elastic components of the muscle

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Contractionphase

Relaxationphase

Time

Latentperiod

Time ofstimulation

Mu

scle

ten

sio

n

• Contraction phase: Phase in which filaments slide and the muscle shortens– Short-lived phase

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• Isometric muscle contraction– Muscle is producing internal tension while an external resistance

causes it to stay the same length or become longer– Can be a prelude to movement when tension is absorbed by elastic

component of muscle– Important for posture muscles and antagonists that stabilize joints


Muscle shortens,tension remainsconstant

Movement

Movement

Muscle developstension but doesnot shorten

No movement

Muscle lengthenswhile maintainingtension

(a) Isometric contraction (b) Isotonic concentric contraction (c) Isotonic eccentric contraction

Isometric and Isotonic Contraction

• Isotonic muscle contraction: Muscle changes in length with no change in tension– Concentric contraction: muscle shortens as it maintains tension– Eccentric contraction: muscle lengthens as it maintains tension

11-48

Muscletension

Musclelength

Isometricphase

Isotonicphase

Time

Len

gth

or

Ten

sio

n

Figure 11.17

• At the beginning of contraction, muscle tension increases

• When tension overcomes resistance of the load, tension levels off & the muscle begins to shorten and move the load

Isometric and Isotonic Contraction

11-49

Threshold, Latent Period, and Twitch


Contractionphase

Relaxationphase

Time

Latentperiod

Time ofstimulation

Mu

scle

ten

sio

n

Figure 11.13

Frog Myogram

• Relaxation phase—SR quickly reabsorbs Ca2+, myosin releases the thin filaments, and tension declines– Muscle returns to resting length – Entire twitch lasts 7 to 100 ms

Factors Affecting Contraction Strength: Variation in the Stimulus

• Although twitch response is all-or nothing, twitches vary in strength for various reasons

− Muscles need to be able to contract with variable strengths for different tasks, and they do…

11-51

Factors Affecting Contraction Strength

1. Concentration of Ca+2 in sarcoplasm (affected by stimulus frequency)

2. Temperature of the muscles—warmed-up muscle contracts more strongly; enzymes work more quickly

3. Lower than normal pH (acidity) of sarcoplasm weakens contraction—fatigue

4. State of hydration of muscle affects overlap of thick and thin filaments

11-52

• With constant stimulus intensity (voltage), strength can vary with the stimulus frequency– Up to 10 stimuli/s =

identical twiches


Twitch

Muscle twitches

Stimuli(a)


(b)

Treppe

Figure 11.15a,b

• 10–20 stimuli/s = treppe– Each twitch more tension than

before– No time for SR to reabsorb all Ca2+ it

released ([Ca2+] in cytosol rises)– Heat from twitches increases muscle

enzymes activity (myosin ATPase)

5. Temporal Summation: Increased frequency of stimulus

11-53

Contraction Strength of Twitches

• 20–40 stimuli per second produces incomplete tetanus– New stimulus before previous

twitch is over– Generating higher tension– Temporal wave summation– Muscel only partly relaxed;

sustained fluttering contraction

Incomplete tetanus

(c)


Complete tetanus

Fatigue

(d)


Figure 11.15c,d

• 40–50 stimuli per second produces complete tetanus– Doesn’t relax between stimuli– One smooth, prolonged

contraction– Four times the tension as 1

twitch– Rarely in the body

11-54

6. Factors Affecting Contraction Strength: Length–Tension Relationship

• Optimum resting length produces greatest force when muscle contracts– Central nervous system continually monitors and

adjusts the length of the resting muscle, and maintains a state of partial contraction called muscle tone

– This maintains muscles at optimum length and makes the them ideally ready for action

11-55

Length–tension relationship: Amount of tension generated by a muscle and force of contraction depends on how stretched

or contracted it was before it was stimulated


0.0

0.5

1.0

Ten

sio

n (

g)

gen

erat

ed u

po

n s

tim

ula

tio

n

1.0 2.0 3.0 4.0

Overly contractedOverly stretched

Optimum resting length(2.0–2.25µm)

z z

z

z z

z

Sarcomere length (µm) before stimulation

Figure 11.12

• If too stretched before stimulated, a weak contraction results– Little overlap

of thin and thick does not allow for very many cross-bridges to form

• If overly contracted at rest, a weak contraction results– Thick

filaments too close to Z discs and cannot slide

56


11-57

7. Factors Affecting Contraction Strength: Multiple Motor-unit Summation (MMS):


1 2 3 4 5 6 7 8 9

1 2 3 4 5 6 7 8 9

Threshold

Sti

mu

lus

volt

age

Stimuli to nerve

Ten

sio

n

Proportion of nerve fibers excited

Responses of muscle

Maximum contraction

Figure 11.14• Occurs as stimulus increases in intensity (voltage)– Low intensity – only muscle fibers

with low thresholds fire off– Higher intensity, more muscle

fibers are stimulated to contract– Produces stronger contractions– Used by CNS to produce force

adequate for the specific need

Motor Unit = One motor neuron and all the muscle fibers it controls

• Each motor neuron branches out to several muscle fibers– One nerve branch synapses with

1 muscle fiber (1 muscle cell)– Neural branches are dispersed

throughout the muscle– When 1 neuron “fires off”, each

of its branches stimulates the muscle fiber to which it is linked

• If more neurons “fire off”, more muscle fibers contract– Produces a stronger contraction

Motor unit size varies

• Average motor unit ~ 200 muscle fibers

• Small motor units = fine control– In the eye, 1 neuron controls 3-6 cells– Low strength, BUT fine control

• Large motor unit = strength– In gastrocnemius, 1 neuron can control

1000 cells– Less fine control; more strength

• Several motor neurons per muscle– Nervous system reflexes alternate which

motor units are turned on– Delays fatigue

gastrocnemius

11-60Figure 11.18Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

• Two main pathways of ATP synthesis– Aerobic respiration: More ATP & less toxic biproducts, but

requires a continual supply of O2

– Anaerobic fermentation: Necessary when O2 is not available

• ATP production depends on supply of: Oxygen, energy sources (glucose, glycogen, and fatty acids)

All muscle contraction depends on ATP

11-61


Aerobic respiration using oxygen from myoglobin

Glycogen–lactic acid system (anaerobic fermentation)

Phosphagensystem

Duration of exercise

0 10 seconds 40 seconds

Aerobic respirationsupported by cardiopulmonary function

Repayment ofoxygen debt

Mode of ATP synthesis

Short, intense exercise (100 m dash)

– Pi is transferred to ADP from other creatine phosphate (creatine kinase) or other ADPs (myokinase) to make ATP

– O2 is briefly supplied by myoglobin; rapidly depleted

Figure 11.18

11-62

Immediate Energy:• Phosphagen system—

ATP and CP collectively– Fast-acting system that

helps maintain the ATP level while other ATP-generating mechanisms are being activated

– Provides nearly all energy used for short bursts of intense activity• 1 minute of brisk walking; 6

seconds of sprinting• Important in activities

requiring brief but maximum effort (football, baseball, and weightlifting)

11-62

Creatinephosphate

Creatine

Creatinekinase

Myokinase

Pi

ATP

ATP

ADP ADP

ADP

AMP

Pi

Figure 11.19

11-63


Aerobic respiration using oxygen from myoglobin

Glycogen–lactic acid system (anaerobic fermentation)

Phosphagensystem

Duration of exercise

0 10 seconds 40 seconds

Aerobic respirationsupported by cardiopulmonary function

Repayment ofoxygen debt

Mode of ATP synthesis

Short, intense exercise (100 m dash)

Figure 11.18

• Shift to this when Phosphagen system is exhausted

• Use blood glucose & glycogen

• Net gain of 2 ATP/glucose• Lactic acid waste product• ATP for 30-40 s max

activity

• After 40 seconds or so, the respiratory and cardiovascular systems “catch up” and deliver O2 fast enough for aerobic respiration to meet most of the ATP demands

11-64

Long-Term Energy

• Aerobic respiration produces 36 ATP per glucose– Efficient way to meet ATP demands of prolonged exercise

– Oxygen consumption rises for 3 to 4 minutes and levels off to where aerobic ATP production keeps pace with demand

– Not much lactic acid accumulation

– Depletion of glycogen and blood glucose, together with the loss of fluid and electrolytes through sweating, set limits on endurance and performance even when lactic acid does not

11-65

Muscle fatigue: Progressive weakness and loss of contractility from prolonged use of the muscles

• Proposed mechanism for fatigue:– Glycogen runs low → ATP declines → Na+–K+ pumps need ATP

• Resting membrane potential can’t be maintained• K+ accumulates outside the cell• Hyperpolarizes the cell and makes the muscle fiber less excitable

– Lactic acid lowers pH of sarcoplasm enzymes of muscle function– Motor nerve fibers use up their ACh

• Less capable of stimulating muscle fibers—junctional fatigue– Central nervous system, where all motor commands originate,

fatigues by unknown processes, so there is less signal output to the skeletal muscles

11-66

Endurance: The ability to maintain high-intensity exercise for more than 4 to 5 minutes

• Determined largely by maximum oxygen uptake (VO2max)

• VO2 max = Point at which O2 consumption rate plateaus & does not increase with an added workload– Proportional to body size– Peaks at around age 20– Usually greater in males than females– Can be twice as great in trained endurance athletes

11-67

Beating Fatigue

• Taking creatine orally– Increases CP in muscle tissue so ATP is regenerated more quickly– Useful in burst-type exercises: weightlifting– Possible risks: muscle cramps, electrolyte imbalances,

dehydration, water retention, stroke, kidney disease

• Carbohydrate loading– Packs extra glycogen into muscle cells, – But also gain 2.7 g water for every gram of glycogen

• Sense of heaviness may outweigh benefits of extra available glycogen

11-68

Oxygen Debt

• Excess post-exercise oxygen consumption: Difference between resting & post-exercise O2 consumption rate

• About 11 extra liters are needed after strenuous exercise

• Used to:– Replace O2 reserves depleted in the 1st minute of exercise

– Make ATP to replenish the phosphagen system• Donate phosphate groups back to creatine & restore resting levels

– Oxidize lactic acid back to pyruvic acid (in kidneys, heart & liver)• Liver converts most pyruvic acid back to glucose, then glycogen

– Maintain elevated metabolic rate resulting from higher body temp

11-69

Physiological Classes of Muscle Fibers

1. Slow-twitch, red fibers (Also slow oxidative or type I)– Abundant mitochondria, myoglobin, capillaries– Deep red color– Good at aerobic respiration and fatigue resistance (long twich)– Examples: Soleus of calf and postural muscles of the back

2. Fast twitch, white fibers (Also fast glycolytic or type II)– Good for quick responses (7.5 ms/twich)

• Fast myosin ATPase, SR releases and resorbs Ca++ quickly

– Fatigue more easily• Fewer mitochondria, myoglobin, & capillaries (pale), so more anaerobic• More anaerobic fermentation (phosphagen & glycogen-lactic acid syst)

– Ex: Extrinsic eye muscles, gastrocnemius, and biceps brachii

Physiological Classes of Muscle Fibers

• All muscles have both red (SO) & white (FG) muscle fibers

• Ratios vary in different muscles– Gastrocnemius contains more FG

for quick movements (jumping)– Soleus has mostly red fibers, used

for endurance (jogging)

11-70

Figure 11.20

FG

SO


Dr. Gladden Willis/Visuals Unlimited, Inc.

• Ratio in the same muscle vary in people with different activity levels

• There may be a genetic predisposition to higher amounts of one or the other– Born for sprinting -vs- born for cross country

11-71

Muscular Strength and Conditioning

• Muscles can generate more tension than the bones and tendons can withstand; has to be tempered.

• Muscular strength depends on:1. Muscle size (3 or 4 kg tension/cm2 of cross-sectional area)

2. Fascicle arrangement (Pennate > parallel > circular)

3. Size of motor units (Larger motor unit = stronger the contraction)

4. Multiple motor unit summation: recruitment• For a stronger contraction nervous system activates more motor units

11-72

Muscular Strength and Conditioning

• Resistance training (weightlifting)– Contraction of a muscle against a load that resists movement– A few minutes, a few times a week can stimulate muscle growth– Growth is from cellular enlargement– Synthesizes more myofilaments and myofibrils and grow thicker

• Endurance training (aerobic exercise)– Slow twitch fibers gain mitochondria, glycogen, and capillaries– Increases the RBC count and O2 transport capacity of the blood

– Enhances cardiovascular, respiratory, and nervous systems– Improves fatigue-resistant muscles– Improves skeletal strength

11-73

Cardiac muscle cells (cardiocytes)

• Striated

• Shorter and thicker

• All muscle cells of each chamber must contract in unison– Myocytes are joined to mechanically

• Mechanical junctions; intercalated discs appear as dark lines

– Myocytes are joined electrically • Electrical gap junctions allow myocyte to directly stimulate its neighbors

• Contractions must last long enough to expel (pump) blood– Very slow twitches (No quick twitches like skeletal muscle)– Maintains tension for about 200 to 250 ms– Gives the heart time to expel blood

11-74

Cardiac Muscle

• Contracts without nervous stimulation (autorhythmic)– Pacemaker sets off waves of electrical excitation, rhythmically– Wave travels through heart & triggers contraction of chambers– Able to contract rhythmically and independently– Auto nervous syst can change heart rate & contraction strength

• Must work always (asleep, awake, conscious or not)– Must be highly resistant to fatigue– Uses aerobic respiration almost exclusively

• Rich in myoglobin and glycogen• Has especially large mitochondria (25% of cell volume)

11-75

Smooth Muscle

• Smooth muscle myocytes have a fusiform shape– No visible striations (why it’s called “smooth muscle”)– Thick and thin filaments are present, but not aligned

• Smooth muscle is capable of mitosis and hyperplasia– Injured smooth muscle regenerates well

• Smooth muscle is involuntary and can contract without nervous stimulation or by stimulation from ANS– Can contract in response to chemical stimuli (Hormones, carbon

dioxide, low pH)– Can contract in response to stretch– Can be innervated by the autonomic nervous system

• Exhibit plasticity: Can stretch a lot, & adjust its tension to the degree of stretch it’s not flabby when recoiled

11-76

Types of Smooth Muscle

• Multiunit smooth muscle

– Occurs in some of the largest arteries and pulmonary air passages, in piloerector muscles of hair follicle, and in the iris of the eye

– Autonomic innervation similar to skeletal muscle

• Terminal branches of a nerve fiber synapse with individual myocytes and form a motor unit

• Each motor unit contracts independently of the others


Synapses

Autonomicnerve fibers

(a) Multiunit smooth muscle

Figure 11.23a

11-77

Single-unit smooth muscle

• Up to 20,000 varicosities– Each contains synaptic vesicles – Nerve fiber passes amid several

myocytes and stimulates all of them at by releasing neurotransmitter

• No motor end plates; receptors scattered – Myocytes are electrically coupled to each

other by gap junctions– Directly stimulate each other and a large

number of cells contract as a single unit– In the digestive, respiratory, urinary,

reproductive tracts, & most BV• 2 layers: inner circular & outer longitudinal

Figure 11.23bCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Varicosities

Gap junctions

Autonomicnerve fibers

(b) Single-unit smooth muscle

Circular layer

Longitudinallayer

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• Contraction and relaxation very slow in comparison to skeletal muscle– Latent period in skeletal 2 ms, smooth muscle 50 to 100 ms– Tension peaks at about 500 ms (0.5 sec)– Declines over a period of 1 to 2 seconds– Slows myosin ATPase enzyme and pumps that remove Ca2+

– Ca2+ binds to calmodulin instead of troponin• Activates kinases and ATPases that hydrolyze ATP

• Latch-bridge mechanism is resistant to fatigue– Heads of myosin molecules do not detach from actin

immediately; maintains smooth muscle tone

Contraction and Relaxation

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• Response to Stretch: Unlike skeletal muscle, smooth muscle contracts forcefully even when greatly stretched

• Can open mechanically gated Ca++ channels in the sarcolemma causing contraction– Peristalsis: waves of contraction brought about by food

distention of the esophagus or feces distention of the colon• Propels contents along the organ

• Stress–relaxation response (Receptive Relaxation)—Helps hollow organs gradually fill (urinary bladder)– When stretched, tissue briefly contracts then relaxes– Helps prevent emptying while filling

Documents

BLINN Ch11 MusclePhysiology Sp2015 New