Physiology chapter 9

3 types of muscle

• skeletal

• cardiac

• smooth

skeletal muscle attachment and appearance

• attached to bone (supports and moves the skeleton)

• long, striated and multinucleated muscle fibers

voluntary movement of skeletal muscle

• contractions initiated by somatic motor neurons

• quick contration

• tires easily

• develop variable amounts of power

What is something every skeletal muscle fiber must have in order to be contractile

one neuromuscular junction

cardiac muscle attachment and appearance

• in the heart, contracts to propel blood through the circulatory system

• short, striated, uniculeated, branched cells connected by gap junctions

Regulation and movement of cardiac muscles

• shows automatism and is regulated by the autonomic nervous system, hormones, and other signals

• involuntary movement

smooth muscle location and appearance

• in the walls of hollow organs and tubes → contraction supports internal movements

• fusiform cells with no striations, some of them connected by gap junctions

regulation and movement of smooth muscle

• shows automatism and is regulated by the autonomic nervous system, hormones, and other signals

• involuntary movement

name a few organs in which we would see smooth muscle

• uterus

• intestines

• stomach

• blood vessels

• urinary tract

organization of skeletal muscle fibers (4)

• organized in bundles bound together by sheets of connective tissue

• reinforce and hold together the tissue

• transmission of energy

• continuous with tendons

3 components of skeletal muscle fibers (4)

• many nuclei

  • result of embryonic fusion of myoblasts

• abundant mitochondria, lipid droplets and glycogen granules

  • needed for energy production

• sarcoplasm (cytoplasm)

  • packed with long protein bundles → myofibrils

sarcolemma

• structure of skeletal muscle fiber

• plasma membrane of the muscle cell

  • express abundant voltage gates Na+ channels (same as hillock + axon)

sarcoplasmic reticulum

• structure of skeletal muscle fibers

• form networks around each myofibril

• Ca2+ reservoir (ryanodine receptors coupled to voltage sensitive dihydropyridine receptors in T tubule)

• dilated terminal cisterns that express ryanodine receptors

transverse (t) tubules

• structure of skeletal muscle fibers

• sarcolemma invaginations that penetrate the cell and run between two terminal cisterns (triads)

• lumen of t tubules is an extension of the extracellular space

• express voltage gated Na+ channels

• express dihydropyridine receptors (DHP), voltage gates Ca2+ channels

• mechanically coupled to RyR in the SR

• upon depolarization, induces Ca2+ release from SR cisterns → initiates contraction

What are myofibrils composed of

sarcomeres

sarcomeres

• skeletal and cardiac muscle contractile unit

• bundled back to back through interconnecting proteins at the Z line

• responsible for the striated pattern in the skeletal and cardiac msucles

• formed by an arrangement of myofibrils

  • thick filaments

  • thin filaments

what are myofibrils composed of

myofilaments

Thick myofilaments

• made up of myosin

  • two heavy chains → intertwined, form a tail along the axis of the thick filament

  • two light chains (form globular head) → directed outwards towards the surrounding thin myofilaments

    • two binding sites

      • one for actin

      • one for the ATP with ATPase activity

titin

• elastic protein

• connects the thick filament to the z line

• responsible for most of the passive elastic properties of relaxes muscle fibers

thin myofilaments

• twisted double strand of bound actin monomers

  • each monomer of actin has a myosin binding site

  • stabilized by nebulin

• tropomyosin

  • rod like protein, in relaxed muscle it partially blocks myosin-binding sites preventing the actin/myosin interaction

• troponin

  • anchor between actin and tropomysoin

    • tropmyosin binding subunit

    • actin-binding subunit

    • Ca2+ binding subunit

Sliding filament model of contraction

• no change in the size of the myofilaments (only size of sarcomere decreases)

• myosin heads pull thin filaments making them slide over the thick myofilaments

• contraction implies a decreases in the length of the myofibrils in the muscle fiber because of an increase in the overlap of the actin and myosin myofilaments on it

When the muscle is contracted, explain what happens the the zones and bands

• I bands = shorten

• Z band = distance between the two shortens

• H zone = disappears

• As the phenomenon happens at the same time in all the sarcomeres, the total length of the myocyte decreases

How do myofilaments know they must start sliding against each other to contract the muscle and develop force?

• skeletal muscle is voluntary, we need to give the order, otherwise the muscle does not contract

• action potential is generated by a neuron in the primary motor cortex of the brain

• it travels through the axon in tracts along the brainstem and spinal cord

• makes a decussation and a snaps with one or several alpha motor neurons in the ventral horn of the spinal cord, triggering an action potential

• axon of the alpha neuron comes out of the spinal cord and travels through a spinal nerve carrying the action potential

• the action potential reaches the axon terminal and activates a discrete number of muscle fibers within the target muscle (triggering action potentials)

motor unit

• all the muscle fibers that are innervated by a single motor neuron

• motor units have different numbers of muscle fibers per neuron

• muscle fibers stimulated by a motor neuron are scattered across the. muscle

• muscle fibers in a motor unit can have different sizes and develop different amounts of power

• a single motor neuron innervates many muscle fibers, but each muscle fiber is controlled by a branch from only one motor neuron

When the muscle fiber is stimulated by the motor neuron, what happens?

all of the muscle fibers trigger action potentials and contract simultaneously

How do motor neurons activate the muscle fiber?

• an electrical nerve impulse is converted into a chemical signal

Anatomy of the neuromuscular junction

• axon terminal

  • acetylcholine vesicles

  • voltage gated Ca2+ channels

• synaptic cleft

  • 50-80 nM

• motor end plate in sarcolemma

  • juntional folds

  • ACh receptors (nicotinic, inotropic, Na+ channels)

Behavior of neuromuscular junction

• very similar to the behavior in other neural synapses

• action potential reaches the axon terminal

• depolarization opens voltage gated Ca2+ channels

• rise in Ca2+ causes ACh exocytosis

• ACh binds nicotinic receptors in the junctional plate

• Na+ crosses the plasmalemma and depolarize the junctional plate

• depolarization trigger an action potential that spreads along the sarcolemma

The behavior of a neuromuscular junction is very similar to that of a synapsis between an axon terminal and a dendrite. How is it that we generate action potentials instead of graded potentials? Where are these action potentials generated if there’s no hillock?

How does muscle stimulation end?

Acetylholinesterase degrades acetylcholine into choline and acetate

• ionotropic ACh receptors close

• Voltage-gated and leaked K+ channels, Na+/K+ pump repolarize the membrane

How do pesticides affect muscle stimulation?

• organophosphates bind to receptors and cannot be degraded by acetylcholinesterase so they are locked in position

• ACh accumulates since there is nowhere for it to bind

  • the muscle can not repolarize

  • the muscle becomes desenitized

• Muscle spasms occur and then paralysis

How does botulinum toxin affect muscle stimulation?

• blocks ACh release by blocking the fusion of the synaptic vesicles

• No ACh is available to depolarize the muscle

• Muscle paralysis occurs

How do non-depolarizing neuromuscular blockers affect muscle stimulation?

• Bind ACH receptors with high affinity but do not activate them

• There is no ACH binding so AChR cannot be activated

• No muscle depolarization

• Muscle paralysis occurs

What is excitation-contraction coupling?

Mechanism linking plasma membrane stimulation with cross-bridge force generation in muscle fibers

What happens to the T-tubules once depolarized

• Dihydropyridine receptors change conformation and open ryanodine receptors in the sarcoplasmic reticulum

• Ca2+ leaks out of the reticulum

Once Ca2+ leaks out of the sarcoplasmic reticulum, explains what happens next

• Ca2+ binds troponin causing a conformational change in the protein

What happens once Ca2+ is bound to troponin

• Tropomyosin is pulled away from the myosin binding sites on actin

When tropomyosin undergoes conformation with the calcium bound, what occurs next?

• The myosin head binds actin and the cross-bridge cycle takes place

Once the myosin head is bound to the actin filament, what is attached?

• ADP and Pi, but Pi leaves shortly after

What is the significance of the release of Pi once the myosin head is bound to actin?

It allows for the released of stored ATP energy

Power stroke

• Occurs after Pi is released from the myosin head

• The myosin head bends and pills the actin filament towards the sarcomere’s M line

When ADP is released from the myosin head, what is going on?

• The myosin head remains attached to actin but shortly after, a new ATP molecule binds the myosin head

What happens when a new ATP molecule binds the myosin head? (2)

• The myosin head is released from actin

• the myosin hydrolyzes the ATP into ADP + Pi and the cycle restarts

If there is no ATP present in muscle contraction, what will happen?

• Myosin will never be released from actin

Do all myosin heads in the sarcomere bind actin simultaneously?

• No, some of the myosin heads are attached or pulling

• Other ger detached and reenergized

How does muscle contraction end? List the 5 steps

• Ca2+ gets pumped back into the sarcoplasmic reticulum through the SERCA pump

• As intracellular Ca2+ decreases, troponin changes conformation

• Tropomyosin covers the myosin binding sites on actin

• Myosin is no longer able to bind Actin

• Muscle relaxes

What is a muscle twitch?

Single muscle contraction produced by a single action potential

How do we measure a single muscle twitch?

• isometric system

  • the face developed by a muscle is recorded after stimulation without letting the muscle fiber shorten

Why do muscle twitches last way longer than the action potential?

3 phases of a muscle twitch

• latent period

• contraction period

• relaxation period

latent period of a muscle twitch

• few milliseconds

• excitation-conctraction coupling occurs actin/myosin interactions start

Contraction period

• from the onset to the peak of tension

• active cross bridges

• fast twitch fibers ~ 10ms

• slow twitch fibers ~ 100 ms

Relaxation period

• Ca2+ sequestration in SR

• decrease in cross bridges

• decrease in tension

• variable duration

Why is the muscle fiber designed to develop long lasting twitches that outlast the action potential?

Why do muscles require ATP (3 reasons)

• detachment of action from myosin bridges

• pump Ca2+ back into the SR (relaxation)

• reestablish the Na+/K+ gradient

Where does ATP come from in the cell?

• direction phosphorylation of ADP by creatine phosphate

• oxidative phosphorylation

• glycolysis

muscle fatigue

what is it

what are the 2 variables that cause muscle fatigue

• decline in muscle tension because of previous contractile activity

• physiological and psychological variables

  • decrease in ATP concentration

  • increase in concentrations of ADP, Pi, Mg2+, H+

  • Decrease in central drive

Slow fibers

• type 1 fibers

• myosin with low ATPase activity → low rate of cross bridge cycling

Fast fibers

• type 2 fibers

• myosin with high ATPase activity → fast rate of cross bridge cycling

Small fiber diameter

• less and thin myofibrils → less possible cross bridges → less tension developed

large fiber diameter

• more and thicker myofibrils → more possible cross bridges → more tension developed

slow-oxidative fibers

• low myosin-ATPase activity → slow contraction

• small fiber diameter → small amounts of tension

• high oxidative capacity

• high resistance to fatigue

Fast-oxidative-glycolytic fibers

• Type 2A

• Intermediate myosin-ATPase activity → fast contraction

• large fiber diameter → large amounts of tension

• high oxidative capacity and intermediate glycolytic capcity

• intermediate resistance to fatigue

fast-glycolytic fibers

• high myosin-ATPase activity → fastest contraction

• large fiber diameter → large amounts of tension

• high glycolic capacity

• low resistance to fatigue

what activates slow-oxidative motor units

• small motor neurons

• require a small stimulus to active

what activates fast-oxidative-glycolytic motor units

• medium-size motor neurons

• require an intermediate stimulus to activate

what activates fast-glycolytic motor units

• large motor neurons

• require a large stimulus to activate

Recruitment sequence

• slow oxidative muscle fibers → fast oxidative-glycolytic muscle fibers → fast glycolytic muscle fibers

postural muscles in the back

• mostly slow oxidative motor units

large muscles in the thigh

• balanced combination of the three types of motor units

muscles in the arm

• mostly fast glycolytic motor units

two types of muscle contraction

• isometric contraction

• isotonic contraction

isometric contraction

• the load exceeds the force produced by the muscle

• the muscle contracts and produces force but do not shorten

• the load does not move

• ex. trying to pick up a car

isotonic contraction

• 2 types

  • concentric

  • eccentric

• the face produced by the muscle exceeds the load

• the muscle shortens and moves the load

• the tension remains relatively constant during the movement

• also, muscle length increases while developing

• ex. lifting a dumbell

Concentric contraction

• the muscle develop force while it shortens

eccentric contraction

• the muscle generates force as it lengthens

Latency and shorting of a muscle when lifting a light load

• lower latency

• faster and greater shorting sustained by longer time

intermediate load

intermediate response

Latency and shorting of a muscle when lifting a heavy load

• highest latency

• slowest, lower shortening sustained by lesser time

As the load increases in weight:

• more myosin heads must be attached to generate force

• it will take longer to each power stroke to be completed