Chapter 5: Muscle Physiology - Powerpoint

how does skeletal muscle contract?

1. somatic motor neuron activation (neuromuscular junction activity)
2. excited contraction coupling (myofiber action potential, and cell signaling via Ca2+ messenger)
3. cross-bridge cycling (development of tension)
4. relaxation (release of tension)

what type of neuron does the skeletal muscle use?

one efferent neuron (alpha LOWER motor neuron)

cell body is in the brain or ventral horn of spinal cord

neuroeffector junction utilizes ACh that acts on nAChR

how are somatic neurons activated?

1. axon terminal may synapse with multiple cells
2. action potential opens voltage gated Ca2+ channels
3. Ca2+ channels activate SNARE proteins that initiate neurotransmitter exocytosis
4. neurotransmitters released in the synaptic cleft
5. motor endplate (postsynaptic neuron) consists of nAChR that produce end-plate potential (EPP; EPSP)
6. acetylcholinesterase (AChE) breaks down ACh in the cleft

what is excitation-contraction coupling

1. end-plate potential (EPSPs only)
2. action potentials in myofiber sarcolemma spread bidirectionally


1. voltage gated ion channels depolarize and K+ repolarizes
3. action potential in t-tubules


1. dihydropyrodine receptors (DHP) uses L-type voltage gated Ca2+ channels
4. ryanodine receptors stop Ca2+ influx
5. Ca2+ binds to troponin causing a tropomyosin shift
6. actin-myosin cross-bridges form

how does cross-bridge cycling development of force or tension?

1. ATPase activity
2. cross-bridge formation
3. power strokes and Pi and ADP release
4. ATP binds to release myosin head

force and tension continues as long as _________________

tropomyosin is shifted away and if ATP is available

what is rigor mortis?

stiffening of joints and muscles in a dead body because blood circulation ceases and the skeletal muscles no longer receive the nutrients and O2 required to maintain cell life

how does a skeletal muscle relax?

1. stop somatic motor neuron stimulation via voltage gated DHP channels and ryanodine channels which stops Ca2+ release
2. Ca2+-ATPase pumps in sarcoplasmic reticulum remove calcium from the cytoplasm
3. Ca2+ is released from troponin which stops cross-bridge cycling
4. elastic elements return sarcomere to relaxed position

what is a single contraction?

1 alpha motor neuron action potential → one myofiber action potential → one myofiber twitch

what are the phases of myofiber contraction?

latent period (excitation-contraction)

contraction phase

relaxation phase

what is summation?

a more powerful muscle contraction occurs with wave summation as stimulation continues and the muscle is never allowed to relax completely; tension will then rise and peak

what is tetanic contraction?

a sustained muscle contraction caused by a motor neuron firing action potentials at a very high rate

what is incomplete/unfused tetanus?

the muscle fibers only partially relax before the next stimulus because they are being stimulated at a high frequency

what is complete/fused tetanus?

occurs with a *very* high rate of stimulation, and relaxation is not apparent in the tension measurements

what is passive tension?

passive stretch of the muscle that contains elastic components (connective tissue in sarcomeres, myofibers, and muscle)

what is active tension?

utilizing sarcomeres and myofibers that take part in cross-bridge cycling with actin and myosin

true/false: anytime you are using cross-bridge cycling, you are using active tension

true

one action potential → ___________________

one twitch in all innervated myofibers

true/false: all myofibers in a motor unit have different types of fibers

false

\
all myofibers in a motor unit are the SAME fiber type

what are fast twitch motor units?

fatigue-resistant fibers are recruited when the input onto motor neurons is large enough to recruit intermediate-sized motor neurons

generate more force than slow-twitch fibers, but they are not able to maintain the force as long as the slow-twitch fibers

how do fast twitch fibers work?

uses myosin with high ATPase activity (cross-bridge cycling is 2-3 times faster)

high Ca2+ ATPase activity (return Ca2+ to SR faster)

what are slow twitch motor units?

fatigue resistant, and focused on sustained, smaller movements and postural control

contain more mitochondria and myoglobin, and are aerobic in nature compared to fast-twitch fibers

how do slow twitch fibers work?

uses myosin but with lower ATPase activity

lower Ca2+ ATPase activity (slower to return Ca2+ to SR)

small motor units = ____________ and ____________ develop less force

small alpha motor neuron axon diameter; small diameter myofibers

large motor units = ____________ and ____________ develop more force

large alpha motor neuron axon diameter; large diameter myofibers

which size motor unit is recruited first?

small

how does our muscles reduce fatigue?

recruit motor units asynchronously (consistently switching between motor units)

what is resting myofiber length?

moderate level of overlap (80-120% of the resting length) of the actin and myosin

what is optimal myofiber length?

the greatest amount of tension within a fiber occurs (L_o)

myofiber length and active tension

how is ATP used in myofiber action?

1. return Na+ and K+ after myofiber action potential via Na+/K+ ATPase
2. cross-bridge cycling energizes myosin head and releases it after a power stroke


1. relaxation occurs via Ca2+ ATPase

what are the ATP sources?

phosphocreatine and cellular respiration

how does phosphocreatine used for ATP?

at rest: creatine + ATP → phosphocreatine + ADP

at work: phosphocreatine → creatine + ATP

where is phosphocreatine stored?

myofibers

how long does phosphocreatine contribute to exercise?

10-15 seconds of maximal exercise

what is creatine kinase?

enzyme catalyst for both reactions (at work and rest)

is released into bloodstream after muscle damage

two isozymes are used to identify type of muscle damage (skeletal and cardiac)

what are the two types of cellular respiration?

anaerobic and aerobic

what is anaerobic cellular respiration?

no oxygen is required

fast process, but lower ATP yield per glucose (2 ATP) and lasts for less than one minute

uses glucose and glycogen stores

lactic acid is produced

what is aerobic cellular respiration?

oxygen is required

slower process, but higher ATP yield per glucose (32 ATP), but lasts for hours

uses glucose, glycogen stores, *and* fatty acids

what type of ATP source is used during short and intense exercises?

phosphocreatine and anaerobic glycolysis

i.e., HIIT, sprinting for a bus

what type of ATP source is used during prolonged exercise?

aerobic pathway

i.e., endurance, long-distance running

what is muscle fatigue?

loss of ability to develop or maintain tension

faster fatigue in subsequent contractions (i.e., explains why the third set of an exercise is harder than the first)

what is central fatigue?

in the CNS, neuronal control, may be psychological

what is peripheral fatigue?

* in the PNS


* when myofiber action potential increases, the overall loss of K+ to extracellular reduces ability of myofiber to repolarize causing voltage gated channels to remain open or inactive resulting in no additional myofiber action potentals
* lack of Ca2+ available to bind to troponin reduces the probability of excitation-contraction coupling
* high levels of cytoplasmic ADP and Pi may inhibit the release of ADP from myosin decreases cross-bridge cycling to occur

what are other factors that cause muscle fatigue?

dehydration, low blood sugar, low glycogen stores

what is the muscle recovery period?

replenish oxygen, pH, glycogen, and creatine phosphates

removal of wastes via the cori cycle

what is the cori cycle?

lactate is converted back to glucose

myofiber → blood → liver → blood → myofiber

lactate → glucose → glycogen

what is delayed onset muscle soreness (DOMS)?

feelings of soreness is not felt until 24-72 hours after exercise

small muscle tears, connective tissue damage, local inflammation

origin of muscle is to ____________; insertion of muscle is to ____________

proximal; distal

agonist is to _____________; synergist is to _______________

prime mover; antagonist

what is reciprocal inhibition?

the antagonist muscle is relaxed while the agonist muscle is stimulated to create movement

it begins when the central nervous system sends a stimulating message to the agonist muscle to contract; simultaneously, it inhibits activation of the antagonist muscle thus ensuring its relaxation

concentric is to ____________; eccentric is to _____________; isometric is to ____________

contraction (actual movement: curling up in a bicep curl

relaxation (returning back to starting position: movement back down in a bicep curl)

holding (continual contraction at a specific point in the movement)

what is isometric?

force is less than the load/resistance

build force because force has not been met

true/false: sarcomere shortens, muscle does not in isometric contractions

true

\
sarcomere shortens due to cross-bridge cycling and elastic components of stretch

what is resting muscle tone?

posture/position

constant tension on tendons

stabilize joints

what is isotonic?

force is equal to load

muscle and sarcomere shorten to maintain force development

what is the relationship between load and latent period?

as load increases, latent period increases

what is the relationship between load and shortening velocity?

as load increases, shortening velocity decreases

what are the two pathways off ATP production and rates of fatigu?

oxidative fibers and glycolytic fibers

what are oxidative fibers?

small fiber diameter = fewer myofilaments = less force

increased myoglobin, blood supply and miitochondria

“red fibers”

what are glycolytic fibers?

large diameter fiber = more myofilaments = more force

decreased myoglobin, blood supply and mitochondriia

“white fibers”

what are slow-oxidative fibers?

slower contraction, resist fatigue, decreased size = decreased tension

what are oxidative-glycolytic fibers?

faster contraction, intermediate fatigue rate, increased size = increased tension

what are fast twitch glycolytic fibers?

fastest connection, fatigue quickly, increased size = increased maximal tension

what happens when there is hyperexcitability and excessive stimulation (tetanus)

muscles with contract more readily

can be due to hypocalcemia: low ECF \[Ca2+\] and increased Na+ permeability

what happens when there is a hypoexcitablity and reduced stimulation (muscle weakness)?

muscles will not contract more readily

can be due to hypercalcemia: high ECF \[Ca2+\] and decreased Na+ permeability which makes it harder for an action potential to reach threshold and contract

what happens when muscle use is increased or overused?

building muscle tissue (hypertrophy) can cause soreness, fatigue, and tears

increased metabolic activity

true/false: you can make more muscle fibers

false

\
cannot make more fibers, but can increase size

what happens when muscles are not used or denerved?

atrophy (use it or lose it)

what is denervation?

any loss of nerve supply regardless of the cause

what is poliomyelitis?

neural damage to alpha motor neurons causing a lack of stimulation (PNS neurons cannot function anymore) and flaccid paralysis

what is muscular dystrophy?

lack of dystrophin which is a protein that anchor sarcomeres in place and there is a degradation of muscle cells

duchenne (early childhood onset, survival into late 20s)

becker (adolescent/adult onset, less severe, survival into mid-late adulthood)

what is mcardle’s disease?

muscle cells lack myophosphorylase which cannot covert glycogen to glucose 6-phosphate

what is myasthenia gravis?

autoimmune disease where antagonistic antibodies mimic ACh

decreased sensitivity to ACh causes reduced end-plate potential (EPSPs)

what is the location and control of smooth muscles?

integumentary, cardiovascular, gastrointestinal, urinary, respiratory, reproductive and ocular

**autonomic nervous system (ANS)**, both para and sympathatic

what are phasic smooth muscles?

alternating between relaxation ad contraction

what are tonic smooth muscles?

always someone contracted, may increase or decrease level of contraction

how do electrical signals innervate smooth muscles?

* **single unit (visceral) smooth muscle** uses electrical synapses/gap junctions and is a functional unit
* **multi-unit smooth muscles** uses individual chemical synapses with varicosities
* there is a **combination** of both !

are smooth muscles capable of contracting over a wide range of lengths?

yes, smooth muscles have a wider rage for optimal length and force generation

ex: stomach becomes full, but it is still capable of contraction in order to digest food

do organs generally have multiple layers of smooth muscle?

yes, contraction of organs can go in multiple directions

is contraction and relaxation of smooth muscle slow?

yes, myosin ATPase activity is slow and actions are coordinated with other functions

is there less energy required for maintenance of tension in smooth muscle?

yes, it allows for prolonged contraction

can contractions be maintained without fatigue?

yes !

are smooth muscle contractions initiated by a variety of stimuli?

yes, electromechanical coupling, pharmacomechanical coupling, myogenic stimulation or contraction

what is electromechanical coupling?

changes in membrane potential due to electrical signals

what is pharmacomechanical coupling?

minimal changes in membrane potential due to chemical signals

what is myogenic stimulation or contraction?

originates in smooth muscle cell where mechanical signals produce muscle cell stretch and pressure

does the autonomic system control smooth muscle?

yes, parasympathetic (sphincter muscle of iris) and sympathetic divisions (radial muscle of iris)

what is the structure of myofilaments in smooth muscle?

* actin surrounds myosin
* longer myosin filaments, fully covered by myosin heads
* no troponin and tropomyosin regulation
* no sarcomeres
* actin is anchored to dense bodies throughout the cells, dense bodies anchored to cell membrane, individual cells anchored together

what is the structure of the sarcoplasmic reticulum in smooth muscle?

less developed

what is the caveolae in smooth muscle?

invaginations on the plasma membrane that perform a number of cellular functions involved in cell-cell communication

close association with the SR

how is smooth muscle stimulated?

1. depolarization opens voltage gated Ca2+ channels (extra cellular calcium and calcium from SR enter cytosol)
2. Ca2+ binds to calmodulin
3. calmodulin activates myosin light chain kinase (**MLCK**)
4. MLCK become phosphorylated and myosin ATPase activity is enhanced
5. cross-bridges form
6. cross bridge cycling is the same in skeletal muscles

how do smooth muscles relax?

1. myosin light chain phosphatase (**MLCP**) dephosphorylates myosin
2. myosin ATPase activity is reduced


1. cross-bridges *may* be released (latch state)

what is the latch state in smooth muscles?

dephosphorylated myosin heads don’t always release from actin which maintains a level of tension without cross bridge cycling

conserves energy

how is Ca2+ returned to the ECF or SR?

1. Ca2+ ATPase pumps are primary active transports (SR and sarcolemma)
2. Ca2+/Na+ antiport are secondary active transport (sarcolemma)

true/false: MLCP is always someone active

true

when MLCK is more active than MLCP, ________________

smooth muscle contracts

when MLCP is more active than MLCK, _______________

smooth muscle relaxes

what are the two sources of calcium for contraction in smooth muscles?

extracellular fluid and sarcoplasmic reticulum (SR)

how do voltage gated Ca2+ channels stimulate smooth muscle?

electromechanical coupling

graded potentials

Ca2+ enterring results in rapid depolarization