module 1 Flashcards
what is the skeletal neuromuscular system key for
- facilitation of energy to action
- fine to gross motor movement
- high plasticity
what is the structure of the muscle unit
- skeletal muscle
- muscle fascicle
- muscle fiber
- myofibril
- myofilaments
what is the smallest functional unit of muscle structure
sarcomere
what is the band with only thin filaments
I band
what is the center of H zone also known as
M line
what holds the M disc of thick filament to the Z disc
titan
what is the connection between thick and thin filaments called
cross bridge cycle
define satellite cells
located within the sarcolemma (between plasma and basement membrane)
- helps regenerative cell growth
what occurs with age for satellite cells
proliferation declines with aging
what happens when you stress muscle and role of satellite cells
- proliferation (mitosis)
- some cells activate to differentiate and become part of muscle
- important when you have atrophy because they help rehabi
explain the myogenic pathway
- mitosis into additional satellite cells
2.formation of myotube - translocation of myotube across sarcolemma
- fusion of myotube with existing myofibrill
what are the contractile properties of muscle
- thick filaments
-6 subunit myosin protein
-2 heavy chains
-2 light chains - thin filaments
-2 twisted strings of spherical actin molecules
-tropomyosin on actin
-troponin
explain the contractile contractile mechanism for thick filament
- before binding to actin, myosin must be activated by hydrolysis of ATP
- ATP hydrolysis –> myosin head 45 deg -> 90 deg
- aftering binding to actin, Pi+energy released from myosin -ATP binding site=> myosin head rotate swing back (bound to actin)
4, ADP then released from myosin head binding site - myosin stays attached until another ATP binds
explain the contractile mechanism for thin filaments
- at rest, tropomyosin provides steric block on actin-binding sites
- to initiate contraction:
i)Ca2+ released from SR, binds to troponin C sites
ii) troponin makes conformational change, move tropomyosin from actin binding
iii) allows myosin-actin cross-bridging to occur
explain how calcium is released from SR (contraction)
- t-tubules progate electrical depolarization resulting from AP from motor neurons
- DHP and RyR convert to chemical signals to terminal cisternae
what does speed of relaxation depend on
muscle tissue ans fibre type
how is calcium handled during relaxation
- decrease Ca2+ requires ATP
- SERCA responsible for reuptake Ca2+
-ability to release ans resequester Ca2+ MAY CONTRIBUTE TO EXERCISE INDUCED FATIGUE
what are the 3 charateritisc of nerve action potentials
-large axons
-myelinated
-inside resting neuron is approx -70mV (membrane ATPase pump works to keep gradient
what are the two factors that influence neural speed
-axon size (thicker = faster)
-myelinated (causes faster speed conduction through insulated properties)
name 4 piece of protein that create the muscle architecture
- desmin: connects z-discs of sarcomeres from 2 myofibrils
- nebulin: binds actin, nonelastic
- titin: connects m-line to z-discs. a molecular spring
- a-acinin: forms z-discs
what are the 5 steps of nerve action potential
1.membrane is completely polarized
2. AP is initiated, region of membrane depolarizes, resulting in adjacent regions becoming depolarized.
3. when an adjacent region is depolarized to its threshold, AP starts there
4. repolarization occurs due to K+ outflow. The depolarization spreads forward, triggering AP
5. depolarization spreads forward, repeating the process
why is the refractory period important in a-motor neurons and heart cells.
-a-alpha MN=shorter because of fast contractions
-heart cells=ventricles need time to fill with blood
what happens at the neuromuscular junction
- AP arrives at an axon terminal (sends electric signal along surface)
- voltage gated calcium channels open and calcium enters the motor neuron
- calcium entry causes a release of ACh into synaptic cleft (vesicles undergo exocytosis)
- release neurotransmitters across synaptic cleft
- neurotransmitters bind to receptors on postsynaptic neuron
- acetylcholinesterase degrades ACh where reuptake by the presynaptic neuron and diffusion occurs (closing channels)
what happens when AChE is removed
channel stays open, CA2+ keeps coming in and causing depolarization resulting in symptoms such as spasm
how does a cell stay at rest
thru hyperpolziation
- excitatory postsynaptic potentials
-inhibitory postsynaptic potentials
(determine whether nerve reaches “all or nothing” threshold
how does botulism affect Ach
prevents release of ACh into the NMJ. Causes paralysis (extreme)
-no Ca2+ gets released from SR
-Gates close stopping AP
what are nicotinic receptors
ligand gated ions channels
describe a muscle AP
transmission of nerve impulse by neurotransmitte across synaptic cleft to postsynaptic motor end plate
–opens voltage gate Na2+ channels = MAP
fine movement
low ratio
-ie. 1 muscle fibre/motor neuron (occulur movement)
gross movement
high ratio
-ie. 100 fibres. motorneuron (quads)
what is a limiting factor in generating muscle power
energy producing capacity of the muscle protein filaments
how do smaller animals have a bigger advantage in physical activities
endurance (mito: smaller > larger)
-speed and power (smaller > larger)
ie. running uphil
what percent of slow twitch fibres do athletes carry
45-55%
twitch
contractile response of a muscle fibre to a single MAP
define response to meural firing
the brief contrcation of all muscles fibres in a MU in response to a single action potential
what are the four periods during an Action potential
- latent period: delay between arrival of AP and initiation of contraction
- contraction period: when ca2+ binds to troponin and the actin-myosin cross bridges are formed
- relaxation period: when Ca2+ is actively pumped back into the SR, myosin heads detach from actin and muscle tension decreases
- refractory period: the period when the muscle tissue is unable to respond to a subsequent AP
define summation
when a second AP trigger muscle contration before the first contraction has finished result: stronger contraction
tetanus
very frequent wave summations
what are the 2 types of wave summation and define
unfused (incomplete) tetanus: - occurs when muscle fibers are stimulated at a rate where it is an incomplete relax between stimuli
fused (complete) tetanus
- occurs when muscle fibers are stimulated at a rate where there is no relax between stimuli
what is hennemans size principle
smaller (fatigue resistent) to larger - slow twitch fibers are activated first
why is the size principle important
- allows for smooth movement
- we do not always need maximal force
-save energy(type 1 MF have more mitochondria to resist fatigue)
what is the definition of fatigue and the two types
fatigue: inability to meet force/energy demand
-peripheral fatigue: brain send a signal but the muscle is not responding
-central fatigue: brain cannot send signal
motor unit rotation
-some MU’s deactivate and others become active, maintaining contraction strength
-occurs in postural muscle groups and others
basically rotation the muscle fibres so you can sustain the demand for longer
what are proprioceptors and how do they send information
- proprioceptors: send info to CNS about changes in length, tension ans joint angles
1. muscle spindle: detect change in length
2. GTO: resong th force and tension ans inhibit agonist muscles
explain muscle length and passive tension
as muscle hit critical length, they “load” passive components of sarcomere
- titin/tendon will load up like a spring creating tension
- as we extend we load potential force which creates tension
describe passive force (length tension relationship)
force produced by contractile mechanism
describe active force (LT)
force produced by contractile mechanism
describe optimum length
maximum active force
- optimal overlap of actin - mysion XB produce greatest tension develop
during a length tension relationship why doesn’t the muscle show a plateau
none of the bare zone are happening at the same time
-helps make movement smooth
why might concentric force decrease the more velocity is given
- it takes time to create CB to attach and detach
-atp needed to hydrolyze with myosin atpase
-myosin head cant detatch fast enough, therefore, drag effect is created causing decrease in force
why does force increase during fast eccentric contraction
the greater the strain placed on myosin heads, facilitates the attachment of the second myosin heads more frequently
- z disc more away from each other we generate less force than demanded - we mechanical pull apart the myosin heads which myosin heads bind back creating a mini power stroke which needs less ATP
how can improvements in max power output be caused
through increasing max force we can more/and increasing our movement velocity
what is the force velocity and power velocity relationship dependent on?
the number of attached cross bridges
-force production decreases as the velocity of the contraction increases
what are 2 main factors that the force and power velocity relationship are affected by
muscle fibre type
- typeIa and IIx generated 2-4x the peak power (compared to type I)
-type IIx have fastest velocities (5.6 fiber length/s)
- type IIa have 3.5 fibers
- type I contract at 0.8fib/s
describe the characteristics of resistance training
- train close to current force generating capacity
- overload (beyond current capacity)
-dynamic and static (iso) training to increase strength - all ages if safe practices followed
describe the difference between isokinetic and isometric
-isometric: help isolate angles of strength, remove pain points
-isokinetics: maximize force through ROM
what are the benefits of understanding where peak force occurs
- inform rehabiiation, strengthing and performance
what are benefits of graphs showing abnormal strength
-detect injuries, efficiency concerns and return to play
-injury site, pain, compensations
what are factors affecting fatiguability
-F-V & P-V relationships (ECC exhibits greater absolute but less relative decrease in force)
-fibre-type distribution (type I less fatigue)
-training (delay fatigue, increase absolute intensities and relative intensities)
what are some mechanisms for neuromuscular fatigue
decrease in XB formation/function
-# of cycling XB
-force per XB
-rate of activation & deactivation of XB
-rate of XB cycling
what decreases during fatigue in the brain
-decrease in excitation and firing rates of MN
-failure of volitional drive to motor cortex
what decreases during fatigue in the spine
decrease in excitability of MN, spindles support, reflex inhibition, MU firing rates
what decreases during fatigue in the NMJ
neuromuscular junction failure– muscle fibers drop out
what decreases during fatigue in the muscle
- decrease excitability of sarcolemma (decrease in MAP size)
-impaired t tubules SR function - ECC failure
summarize the 4 neural mechanisms of fatigue failure
- decrease activation from higher centres (motor cortex signals)
- altered reflex inputs to MN (reflex inhibition, muscle spindles)
- decrease MN excitability
- failure neuromuscular transmission (decrease in neurotransmitter release, sarcolemma propagation)
name the 9 steps in Excitation contraction coupling (ECC)
- MAP along sarcolemma
- MAP down t-t
- MAP excites voltage-sensing protein in t-t
- voltage sensing protein excites SR Ca2+ release channels to open
- Ca2+ release from SR
- Ca2+ binds to troponin on actin filament
- CB cycling
- SR Ca2+ reuptake
- CB cycling stops
name the two main muscle mechanisms to fatigue
1.impaired ECC
-decrease in Ca2+ released per MAP
-increase K+ intracellular = repeated MAPs would decrease amplitude of MAP along sarcolemma
-Ca2+ uptake by SERCA pumps
2. metabolic factors
-decrease ATP and PCr in hi-intensites exercise (decrease # of XB’s)
-increase ADO leads to decrease Vmax
-increase Pi leads to decrease in Ca2+ sensitivity of myofibers
