CHP 11 skeletal muscle physiology

Universal characteristics of muscle

1) Excitability (responsiveness)

2) conductivity ( signals travel along the muscle fibers)

3) Contractility (contracts)

4) extensibility (can be stretched)

5) elasticity (will go back to original position after being stretched)

Characteristics of skeletal muscle

• voluntary

• striated

• usually attached to bones (w tendons)

• cell = muscle fiber

• connective tissue wrappings (endomysium, perimysium, epimysium)

• Collagen somewhat extensible and elastic

Sarcolemma (apart of muscle fiber)

the cell membrane of a muscle fiber

Sarcoplasm (apart of muscle fiber)

cytoplasm of muscle fiber

contains: myofibrils, glycogen, and myoglobin

Myofibrils (apart of muscle fiber)

in the sarcoplasm

long protein chords

Glycogen (apart of muscle fiber)

in the sarcoplasm

stored blood sugar, stored carb energy for exercise

FOR CELLULAR RESPIRATION

Myoglobin (apart of muscle fiber)

in the sarcoplasm

red pigment

provides oxygen needed for muscle activity

FOR CELLULAR RESPIRATION

Myoblasts (apart of muscle fiber nuclei)

stem cells that fused to form each muscle fiber in EARLY development

Satellite cells (apart of muscle fiber nucleus)

unspecialized myoblasts remaining between muscle fiber and endomysium

play a role in regeneration of damaged skeletal muscle tissue

important parts of a muscle fiber

sarcolemma

sarcoplasm

multiple nuclei

mitochondria

sarcoplasmic reticulum

t tubules

triad

Sarcoplasmic Reticulum (apart of muscle fiber)

wraps around each muscle fiber (the net looking part)

releases calcium to activate contraction

Has terminal cisterns on either side (like a little waste pit)

T tubules (apart of sarcolemma in muscle fiber)

tubular infolding of sarcolemma which penetrate through the cell

Triad (apart of T tubule in muscle fiber)

A T Tubule and two terminal cisterns associated with it

Myofilaments

make up myofibril

1) thick filaments: made of several myosin molecules (shaped like golf club)

2) thin filaments: fibrous actin in 2 intertwined strands + tropomyosin molecules (the strands connecting the actin molecules) + troponin molecule (small calcium binding protein on each tropomyosin molecules)

3) Elastic Filaments: made of Titin (huge springy protein), helps thick filaments stay centered between Z discs and M line= stabilize + shock absorber

Contractile Proteins

myosin + actin

they overlap causes contraction

Regulatory proteins

tropomyosin + troponin

allow muscles to relax or contract (it is like an on off switch)

How? by the release of calcium into sarcoplasm, binds to troponin, changes shape, moves tropomyosin off active sits on actin

Dystrophin

SO IMPORTANT PROTEIN

links actin to outermost myofilaments

allows forces of muscle contraction to transfer to connective tissue to the tendon

GENETIC DEFECT = muscle dystrophy

Striations

alternating A bands (dark) and I bands ( light)

A band: has H band (middle of A band) + M line (middle of H band)

I band: Z disc (anchorage for thin filaments, “zigzags”)

Sarcomere (apart of muscle fiber)

segment from Z disc to Z disc

NO ACTUAL SHORTENING OF LENGTH during contraction only OVERLAP changes

Structural hierarchy of muscle

• Muscle- wrapped in epimysium

• Fascicles- wrapped in perimysium

• Muscle Fibers- wrapped in sarcolemma

• Myofibrils- wrapped in endomysium, has striations

  • myofilaments- causes striations from overlap; causes contraction, Thick (myosin), Think (actin)

  • sarcomere- z disc to z disc segment

How does a muscle contract?

It should NEVER contract unless stimulated by a nerve

Denervation atrophy

shrinkage of paralyzed muscle when nerve remains disconnected

Somatic Motor neuron

nerve cells whose bodies are in the brainstem and spinal cord that serve skeletal muscles

• includes somatic motor fibers (their axons lead to the skeletal muscle that then branches out to a number of muscle fibers

• ONLY ONE MUSCLE FIBER TO ONE MOTOR NEURON

Motor Unit

one nerve fiber and all the muscle fibers activated by it

-contract in unison but motor units take turns contracting

-small or large

Small motor unit

-for fine degree of control

-eye and hand muscles

Large motor unit

-for more strength than control

-powerful contractions because they have HUNDRED of fibers

Neuromuscular junction

-one electrically active cell to another

-when target cell is a muscle fiber

-nerve fiber connected to muscle fiber by a synapse

synapse

point where a nerve fiber meets its target cell

Axon terminal

-apart of a neuromuscular junction

-swollen end of a nerve fiber

-contains synaptic vesicles with acetylcholine

Synaptic Cleft

-apart of a neuromuscular junction

-gap between axon terminal and sarcolemma

Schwann cell

-apart of a neuromuscular junction

-envelops and isolates NMJ

The process of the neuromuscular junction

-nerve impulses cause synaptic vesicles to do exocytosis and release ACh into synaptic cleft

-ACh carries signals (neurotransmitters)

-Muscle cell has millions of ACh receptors (proteins incorporated into its membrane)

-lack of these receptors = weakness in skeletal muscles; myasthenia gravis

How muscle cells respond to stimulation (voltage)

-their membranes exhibit voltage changes

-voltage (electrical potential) = a difference in electrical charge from one point to another

-resting membrane potential = about -90 mV which is maintained by the sodium potassium pump

The process of electrically excitable cells

1) REST (-70mv) = more negative ions inside the cell which causes the inside to be negatively charged; potassium ions in the cell, sodium ions outside the cell

-maintained by the sodium potassium pump

2) LOCAL POTENTIAL= chemical stimulant binds to a receptor on a neuron, opens Na+ gates to slowly let Na+ into the cell, but it isn’t anything drastic

3/4) is ABSOLUTE REFRACTORY PERIOD

3)WHEN REACHES CRITICAL VOLTAGE THRESHOLD (-55mv) : SWITCH TO ACTION POTENTIAL: protein channels are now being used to allow the transfer of ions; Sodium gates open up and sodium flows into the cell RAPIDLY NOW = DEPOLARIZATION (inside cell is now positive)

4) ACTION POTENTIAL CONT (+35mv)= sodium gates immediately close and potassium ones open, potassium ions leave the cell =REPOLARIZATION (inside cell is back to negative)

5) RELATIVE REFRACTORY PERIOD: continues until the cell reaches a hyper polarized state (below resting membrane potential) , then potassium gates close

6) Sodium potassium pump plays catch up to get back to resting membrane potential (3 sodiums in, 2 potassiums out)

Resting Membrane Potential vs Action Potential

Resting Membrane Potential= negative intracellular in a waiting cell to be stimulated

Action Potential= causes voltage changes, quick event in a. stimulated cell

• a positive feedback loop that ripples one cell to another is called IMPULSE

Spastic Paralysis

continuous contraction, possible suffocation

Tetanus

(lockjaw)

form of spastic paralysis caused by the toxin Clostridium tetani

how? the toxin blocks glycine release (in spinal chord that normally stops motor neurons from producing unwanted muscle contractions)

Flaccid Paralysis

a state where muscles are limp and cannot contract

How? Curare competes w ACh for receptor sites but does not stimulate the muscles so it being there is a blockage

Botulism

type of food poisoning caused by a neuromuscular toxin in the bacterium clostridium botulinum

how? blocks the release of ACh causing flaccid paralysis

other ways? botox cosmetic injections used for wrinkle removal

How do toxins paralyze muscles?

some things have cholinesterase inhibitors (they bind to acetylcholinesterase and prevent it from degrading ACh; initiating muscle contraction at the neuromuscular junction)

Behaviors of skeletal muscle fibers

1) Excitation= nerve action potentials lead to muscle action potentials

2) excitation-contraction coupling= events that link action potentials on the sarcolemma to activation of the myofilaments, preparing them for contraction

3) contraction= muscle fiber develops tension and may shorten

4) relaxation= stimulation ends and a muscle fiber relaxes and returns to OG length

STEPS FOR MUSCLE CONTRACTION HERE

1) Excitation (review those steps)

2) voltage gradient travels down t-tubule

3) calcium released into the sarcoplasm and binds to troponin

4) tropomyosin pulls away (allowing myosin + actin to interact) = overlapping

5) they STAY stuck together until an ATP molecule attaches

STEPS FOR RELAXATION HERE

1) remove calcium, separate acetylcholine= causes a stop

• diffusion

• acetylcholinesterase breaks it up

2) pulls calcium ions back into the cisterna = pulls away from troponin

3) causes tropomyosin to block the active sites again

Length-Tension Relationship

about of tennis generated by a muscle depends on how much its stretched/shortened before it was stimulated

-optimal resting length = a small overlap to allow for maximum force produced during contraction

Rigor Mortis

= hardening of the muscles + stiffening of the body 3-4 hours after death

• muscles contract (sarcoplasmic reticulum decays releasing calcium into the cytosol and activates the myosin-actin overlapping) but no relax because there is no ATP generated to cause relaxation

• fibers remain contracted until myofilaments decay

• peaks about 12 hours after death then tapers over the next 48-60 hours

Myogram

a chart of the timing and strength of a muscles contraction

Threshold

minimum voltage necessary to generate an action potential in the muscle fiber and produce a contraction

if below threshold = no contraction

Twitch

a quick cycle of contraction/relaxation when stimulus is at a threshold or higher

Latent Period

the delay between stimulus and contraction (the time required for excitation + internall tension)

contraction phase

time when the muscle generates external tension (force can overcome the load = movement)

relaxation phase

time when tension declines to baseline

longer than contraction

SR reabsorbs calcium, myosin and actin detach from each other

the phases of contraction

1) latent period

2) contraction phase

• Isometric phase- tension rises but length no change

• tension overcomes resistance of the load = stops increasing

• isotonic phase - muscle shortens and moves load

3) relaxation phase

What can change contraction strength

• muscles starting length

• fatigue after continual use

• warmer muscles enzymes can speed up process

• hydration levels

• higher voltages = stronger contractions

if a muscle is stimulated by a higher voltage…

there is a stronger contraction due to more nerve fibers being excited = more motor units contracted

Difference between frequencies in contraction strength

• low frequency stimuli = identical twitches

• higher frequency stimuli = temporal (wave) summation creating higher tension as it goes (fluttering)

• unnaturally high frequency stimuli = steady contraction called complete (fused) tetanus

Isometric contraction

apart of contraction phase

= “same length”

• trying to push something you can’t move

• the external resistance causes the muscle to stay the same length

• POSTURE MUSCLES

Isotonic contraction

apart of contraction phase

= “same tension”

• muscles change in length but not in tension

  • Concentric contraction = muscle shortens as it maintains tensions (ex: lifting weight)

  • Eccentric contraction = muscle lengths as it maintains tension (ex: slowly lowering weight)

ATP sources

-ALL muscle contraction depends on ATP

1) Anaerobic fermentation

2) Aerobic respiration

Anaerobic fermentation

atp source for muscle contraction

making ATP and lactate with NO OXYGEN

Aerobic respiration

atp source for muscle contraction

makes WAY MORE ATP
NO lactate made

REQURES OXYGEN

How is energy used in short exercises/sprints? (about 6 seconds worth)

-oxygen briefly supplied by myoglobin but gone FAST

-muscle meets ATP demand by borrowing phosphate groups from other molecules and sending them to ADP, controlled by:

• myokinase = transfers phosphate from one ADP to another, converting latter to ATP

• Creatine Kinase = gets phosphate from phosphate storage molecule creatine phosphate and gives it to the ADP to make ATP

  -Phosphagen system= combining ATP and CP

myokinase

transfers phosphate from one ADP to another to it can be changed to ATP

used for short term sprint energy

creatine kinase

takes phosphate from phosphate storage molecule, creatine phosphate (CP), and gives it to the ADP to turn into ATP
used for short term sprint energy

Phosphagen system

the combination of ATP and creatine phosphate (CP) that provided nearly all the energy needed for short term sprint activities

How is energy used in short term exercise (after phosphagen system is exhausted)? (30-40 seconds of activity)

-shifts to anaerobic fermentation

-muscles take in glucose from blood + stored glycogen to then do glycolysis and get TWO ATP for ONE glucose molecule + turning glucose into lactate (glycogen-lactate system)

-up until anaerobic threshold

Anaerobic threshold

lactate threshold

point when lactate becomes detectable in the blood

glycogen-lactate system

turning glycogen into lactate until it reaches the anaerobic threshold

how is energy used in long term exercise? (after 40 seconds)

-rely on respiratory and cardiovascular systems to deliver oxygen fast enough for aerobic respiration to meet demands

-aerobic respiration = THIRTY ATP for ONE glucose

• after 3-4 minutes: oxygen consumption levels off and aerobic ATP meets demands

• 30 minutes: energy from glucose AND FATTY ACIDS

• after 30 minutes: primarily fatty acids because glucose is gone

Muscle Fatigue

weakness from prolonged use of muscles

cause in high intensity:

• potassium build up in T tubes reducing excitability

• Excess ADP and Potassium inhibits calcium release and decrease force production from myofibrils

cause in low intensity:

• fuel loss

• electrolyte loss (in sweat)

• central fatigue (less motor signals from brain)

both? psychological will to persevere

Central Fatigue

less motor signals coming from the brain

Brian cells inhibited by exercising muscles releasing ammonia

VO2 Max

maximum oxygen uptake

ones ability to maintain high intensity exercise for more than 4-5 minutes

the point at which the rate of oxygen flat lines and doesn’t increase anymore

Excess PostExercise Oxygen Consumption (EPOC)

oxygen debt

difference between elevated rate of oxygen consumption after exercising and the usual resting rate

WHY? needed to replenish ATP, replenish oxygen reserves, get rid of lactate, provide oxygen to the cells

Physiological Classes of Muscle Fibers

1) Slow twitch, slow oxidative (SO), red or type I fibers

2) Fast twitch, fast glycolytic (FG), white or type II fibers

3) Fast twitch, intermediate, type IIA fibers

Slow twitch, slow oxidative (SO), red or type I fibers

-resist fatigue, good for endurance

-use aerobic production

-POSTURE MUSCLES (always contracting muscles)

-lots of mitochondria

-lots of myoglobin = red color

-contain myosin type w slow ATPase + SR that relate calcium SLOW

-for PRECISE movement

-THIN fibers

Fast twitch, fast glycolytic (FG), white or type II fibers

-for quick responses and POWERFUL muscles/movement

-lack of myoglobin = white color

-contain myosin type w fast ATPase and a large SR that releases calcium FAST

-uses glycolysis and anaerobic fermentation for energy

-THICK fibers

Fast twitch, intermediate, type IIA fibers

-fast twitch but fatigue resistant

-RARE in humans

Muscular strength depends on:

• muscle size = bigger muscle = more cross bridges + area

• fascicle arrangement = pennate stronger than parallel, stronger than circular

• size of active motor units = larger motor unit= larger contraction

• multiple motor unit summation = more units together = more tension

• Temporal summation = greater frequency of stimulation = stronger contraction

• length-tension relationship = optimal length is better than over contracted/stretched

• fatigue = more fatigued = weaker contraction

Resistance Training

ex: weightlifting

-contraction of a muscle against a load that resists movement

-stimulates muscle growth + cellular enlargement

Endurance training

ex: aerobic exercises

-improve fatigue resistant muscles

-improves skeletal strength

-enhancing the function of the cardiovascular, respiratory, and nervous systems

Peristalsis

waves of contraction brought by food movement in digestive system

stress-relaxation response

helps hollow organs gradually refill (ex: urinary bladder)

no sloshing around

What muscle contracts forcefully even when greatly stretched?

smooth muscle

why? allows hollow organs like the stomach and bladder to fill and then expel their contents correctly

plasticity

the ability to adjust the tension based on how stretched it is

ex: bladder gets greatly stretched but does not become flabby when empty

Muscular Dystrophy

hereditary diseases where skeletal muscles degenerate and weaken then replaced with fat and scar tissue

Duchenne Muscular Dystrophy

cause: sex linked recessive trait (MALES)

mutation in gene for the muscle protein dystrophin = sarcomere (inside) contracts but not the sarcolemma (outside) = cell death

rarely live past 20 years

Fascioscapulohumeral MD

autosomal dominant trait in both sexes

facial and shoulder muscles dystrophy (upper body)

Limb-girdle dystrophy

combo of several diseases

shoulder, arm, pelvic muscles dystrophy

Senescence of muscular system

-replacement of muscle with fat

-fast-twitch fibers earliest on and most severe atrophy

cause? fibers have less stuff to support them, fewer motor neurons in spinal chord, sympathetic nervous system is less efficient so less efficient blood flow (fatigue and more scar tissue)