Neuromuscular system and exercise Flashcards
neuromuscular system
interaction between our nervous system and skeletal muscle
muscle contraction
basis for all human movement
proprioceptors are in the
brain
is everything voluntary
no because you have reflexes
4 functions of skeletal muscles
locomotion
body posture
venous return
thermogenesis
4 characteristics of muscle tissue
irritability - ability to receive and respond to stimuli
contractility - ability to respond to stimuli by shortening
extensibility - ability to be lengthened or stretched
elasticity - ability to retrn to resting length after being stretched
how much energy is dissipated as heat?
75%
potential travels along
cell membrane
how many muscles do we have and percent in genders
650
- 40-45% BW in males
- 23 - 25% BW in females
fibres
cylindrical cells that lie parallel to each other
fibres in small vs big muslces
small muscles for precise activities movements may only have 100-300 muscle fibres (Ears and eyes)
large muscles for movement may have 1,000,000 muscles (hamstrings)
fibre length
varies from a few mm in eye muscles to 40 cm in large leg muscles
Eepimysium
upon - surrounds entire muscle and blends into intramuscular tissue shesaths to form tendons
perimysium
around - surrounds a bundle of fibres called a fasciculus
endomysium
within - wraps each muscle fibre
sarcolemma
polarized cell membrane enclosing fiber’s cellular contents
sarcoplasm
contains nuclei that house genes, mitochondria, glycogen and myoglobin
how do you transfer signals
polarized
single multinucleated muscle fibre contains
myofibrils that lie parallel to the fibre’s long axis
t-tubule
continuous with sarcolemma and carries polarization to interior of cell
sarcoplasmic reticulum
stores and releases Ca2
myofibril
composed of myofilaments (actin and myosin)
cross striation patterns
myofibrils -
I band - lighter area
A band - darker area
A band
centre of it is the H zone, M band bisets H zone, consists protein structures that supports arrangement of myosin filaments
Z line
bisects I band and adheres to sarcolemma to provide structural stability
sarcomere
basic repeating unit between two Z lines, comprises the functional unit of muscle fibre
H zone
no overlap
I band
extends across two sarcomeres
how do the thick and thin filaments overlap?
3D space arrangement
3 types of proteins in sarcomere
contractile
regulatory
structural
contractile protein
actin and myosin
regulatory protein
troponin and tropomyosin
structural protein
many diff proteins form the cytoskeleton of the sarcomere
- titin - from z disc to M line, resists sarcomere stretch (as its undergoing eccentric muscle contraction)
Ca binds to
troponin, changes the tropomyosin and moves off and muscle contractin takes place
thick filaments
200-300 myosin molecules
myosin composed of
myosin heavy chain - two globular heads and rod like tail
myosin light chain
myosin heads
2 heads, each has ATPase and actin binding sites
How many heads do they use with mysoin
1 during concentric, not sure what the other one is
what muscle fibres have heavy chain?
type 1, 2A/X
myosin light chain
regulatory - chains looping - loops around myosin molecules
thin filaments
contractile protein actin and regulatory protein
contractile protein actin
- small globular subunits (G actin) combined to form fibrous actin (F actin) - 2 strands of F-actin form an actin filament
regulatory proteins
Tropomyosin and troponin
tropomyosin
blocks the actin binding sites during resting state
troponin
controls the position of the tropomyosin
C- ca binding
I - inhibit binding of actin and myosin
T- binding troponin to tropomyosin
how do muscles shorten
sliding filament theory of andrew and hugh hyxley 0 movemnt of actin filament over the myosin filament
- I band and H zone shorten and may disappear
- A band remains unchanged
axon potential
travel down to the motor end plate
andrew and hugh huxley
published their paper and worked indepen
3 steps of contraction of a muslce fibre
generation of an AP in a motor neuron (ventral root)
transmission of the AP to the muslce fibre (motor end plate of muscle)
excitation - contraction coupling
cell bodies can be found in
spinal cord
dorsal vs ventral root
sensory vs ventral root (cell body)
upper motor neuron will
activate cell body to send a signal down the ventral motor root to alpha motor neuron (lower motor neuron) down to muscle fibers
muscle fibre is wrapped by
endomysium
fascicle is wrapped by
PERIMYSIUM
epimysium AKA
deep fasica
parts of a tendon (7)
paratendon fascicle fascicular membrane fibril subfibril microfibril tropococollagen
in a somatic nervous system, what sends the muscle to release what to stimulate what?
alpha motor neuron releases ACh to target muscle
2 systems in the sutonomic Nervous system and what do they target
sympathetic and parasympathetic
- smooth and cardiac muscles and glands
sympathetic activation
gives Ach in preganglion fibres to release NE
parasympathetic activation
gives ACh in pre ganglion fibres to release ACh
peripheral nervous system is and travels through
skin - somatic sensory fibre
cardio vascular - visceral sensory fibre
central nervous system sends
sympathetic and parasympathetic motor fibres to the heart, motor fiber of somatic nervous system
resting potential
-70mv
depolarization goes up to
30
neuron with a dendrite and a cell body would receive fdbk from
stimuli or other neurons
where does the motor signla come from
ventral horn of spinal cord
what happens when a neuron is excited
permeability changes, voltage gated sodium channels goes to the inside and na is moves in and potassium
how to ensure depolarization
positive charge will excite the axn hillock which sends an AP down the axon
repolarization
voltage gated sodium channels close and potassium rushes out for repolarization
myelinated/shwann cells
saltatory conduction which allows it to move faster down to axon terminal
transmission of AP to muscle fibre
- AP travels the length of axon of motor neuron to axon terminal
at the neuromuscular junction - rush of calcium enters the axon terminal to bind to either ionotropic or nicotinic receptors
-release ACh via exocytosis into the synaptic cleft - synaptic cleft and ACh receptors
- ligand gated cation channels open
more Na than Ca so
it can depolarize
What breaks down Ach
ACh esterase
what inhibits ACh
nerve gas, which stops the regulation of breathing - or botox - stops the release of the contraction - stops the vesicles from releasing ACh
what inhibits ACh
nerve gas, which stops the regulation of breathing - or botox - stops the release of the contraction - stops the vesicles from releasing ACh
what inhibits ACh
nerve gas, which stops the regulation of breathing - or botox - stops the release of the contraction - stops the vesicles from releasing ACh
once the threshold is reached, what does the ap propagate along?
sarcolemma
when does the activation stop
When ach is removed
- diffuse away
- ACH esterase breaks it into acetic acid and choline which is transported back to axon terminal for resynthesis
excitation contraction coupling
sequence of events by which an AP in the sarcolemma initiates the sliding of the myofilaments, resulting in contraction
9 steps of EC coupling
transmission of AP along sarcolemma
depolarization of T tubule
- communication between T-tubule and SR (toilet plunger mechanism) where the voltage gated DHP (Dihydropyridine) receptors cause openings of ryanodine receptors and Ca 2 release to enter the sarcoplasm
ca binds to troponin C
conformational change in the troponin complex
tropomyosin shifts 20 degrees off the actin binding site
attachment of myosin head - cross bridge formation
cross bridge cycling - hydrolysis of ATP
reuptake of Ca by sarcoplasmic reticulum - relaxation (tropomyosin moves back up)
in what direction does EC coupling happen?
every single direction from the motor end plate
muslce triad
two sister cisternae and the T tubule
cross bridging cycle
cyclic events necessary for the generation of force or tension within the myosin heads during muscle contraction
- binding, power stroke, dissociation, activation
during a single muslce twitch myosin binds and detaches from actin _____of times
thousands
binding
cross bridge formation - activated myosin heads binds to actin
ADP and Pi remain bound to myosin
power stroke
myosin head swivels, causing displacement of actin filament
ADP and Pi are released from myosin
dissociation
detachment
- ATP binds to myosin
- actin and myosin dissociate (cross bridges detach)
activation
energy from the hydrolysis of ATP used to activate the myosin head
ADP and PI remain bound to myosin
Rigor mortis
rigor state - dead and you have no ATP so you cant take them off
hang meat - decompose to get more tender - for the bonds to break
motor unit (2)
a motor neuron (alpha 1 or 2) and specific muslce fibres it innervates
- each muscle fibre generally receives input from only 1 motor neuron, a motor neuron may innervate many muscle fibers
all muscle fibers innervated in a motor unit have the same
attributes
- alpha 1 - large diameter neurons innervate type 2 muscle fibers
- alpha 2 - smaller diameter neuron innervates type 1 muscle fibers
smaller cell body/dendrites
graded potential - collecting whole signal for innervation - move faster and less innervation needed - more excitable for slow twitch (why they go first)
skeletal muscle cells can be characterized by their
twitch properties
slow twitch (5)
contract and relax slowly activated by alpha 2 motor neurons only one type - type 1 reply on oxidative metabolism - slow oxidative low excitation threshold
fast twitch (4)
contract and relax quickly
activated by alpha 1 motor neurons
two types - type 2A and 2X
high excitation threshold
2A energy source
2A - rely on glycolytic and oxidative metabolism - FOG - fast oxidative glycolytic
2X
2X - rely on glycolytic metabolism - fast glycolytic
what determines if a muscle fibre is slow twitch or fast twitch
alpha 1 and 2 motor neurons were cross innervated onto slow and fast twitches
- interconverted
- contractile properties of muscle fibres depend on the motor neuron that innervates the muscle fibre
what does increased speed mean for lower
less
P=
fv
2A AKA
FOG
3 things that the SO muslce has the most of
mitochondirial density
capillary density
myoglobin content
4 functional aspects that fast twitch muscles lead in
twitch/contraction time
relaxation time
force production
faitgability
who has the most phosphocreatine stores
FOG and FG
2 functional aspects that FOG leads in
twitch time and relaxation time
Who has the highest glycogen store
FG
who has the highest triglyceride store
SO
who has the highest myosin ATPase activity and glycolytic enzyme activity
FG
who has the highest oxidative enzyme activity
SO
number of muscle fibers /motor neuron relates to
muscles particular movement function
muscles involved in gross movement patterns - ratios
high muslce fibre nerve ration (580 motor neurons for 1,030,000 muslce fibers in gastroc muslce, ratio of 1775
muscle involved in more precise movements - ratios
low fibre to nerve ration (120 motor neurons controlling 41000 muslce fibers in finger
ratio of 342
fiber to nerve ration in eye
1:5
all or none
neural control of muscle contraction - when a motor neuron is stimulated, all the muscle fibers in that motor unit contract to their fullest extent or they do not contract at all
muscle biopsy
assessment of muscle fiber type
- removal and analysis of small portion of whole muscle
- direct measurement of muscle properties
histochemistry
muscle samples can be classified according to
- myosin heavy chain gene expression
- myosin ATPase activity
- glycolytic enzymes
- oxidative enzymes
slow vs fast muscle biopsy
Fast will have a diff pH, diff precipitate
how much NS do you need for force and fast twitch
a lot
immunohistochemistry
classification according myosin heavy chain type antibodies for - MyHC - I - MyHC - IIA - MyHC - IIX hybrid muscle fibres exist in the middle
4 distribution of muslce fiber types
fiber types vary within multi function muslces - quads - 50/50
fiber type varies between diff muscles
- soleus - mainly type 1, gastroc, mainly type 2
fiber types varies according to function of muslces - postural muscles are primarity type 1 because they need to be fatigue resistant for many hours of continuous tension
fiber type can vary between the same muscles of 2 diff people - ind diff in muslc fiber -motor unit ratios contribute to variation in skill performance
is it training or genetics that determine the distribution of the muscle fibre type?
more genetics - you can shift the properties of the muscles but the actual compostion is pre-determined
relationship between fast twitch fibers and performance in strength and power sports
strong linear
- type 2 has an intrinsic speed of shortening and tension development ranging from 3-5 times faster than slow twitch fibers
- activation plays an important role in stop and go or change of pace sports such as baskeball, soccer, tennis etc.
fibre composition and VO2 max in athletes
strong linear relationship between vo2max and slow twitch fibres
- type 1 fibers are fatigue resistnt and ideally suited for prolonged aerobic exercise
is performance solely determined by fiber type?
no
ranking of animals from the highest fast twitch fibres? (7)
cheetah pronghorn ostrich and rhino dog cat and sheep camal, ussain pig
sex difference in fiber type
no diff in the distribution but females have greater type 1 fiber type cross sectional area relative to males
muscle strength
max force generating capacity of a muscle or muslce group, measured as 1RM - dynamic exercise or maximal voluntary contraction - static exercise
- no time constraint
muscle endurance
ability of a muscle or muscle group to repeatedly exert a force against a resistance (performed at a percentage of max strength)
muscle power
max ability to generate force as quickly as possible
measurement of muscular function
electromyography
electromyography (4)
the study of muslce function through the analysis of its electric signal
- sun of AP of active motor units
- EMG voltage - proportional to the force of a muslce contraction
- helps to differentiate which muscles are doing the work
supported vs unsupported feet during sit ups
unsupported will work abdominals more, otherwise rectus femoris
isokinetic dynamometer machines (4)
allows the velocity of the limb movement to be kept constant throughout a contraction
- provides accurate measures of torque (rotational force) and power while the sped of the contraction is kept constant
- can be configured to test the limbs in the upper and lower body
- rate and speed varies at diff angle, eliminate speed by fixing it to see the contraction force (force transducers)
$5000
lab and field methods for musclular function (2)
dynamometers
constant - resistance equipment
- dynamic constant external resistance
- prediction of 1RM
risk with free weights
injury, so you use lower weight to estimate the percentage of 1RM
field tests of muscular function (2)
calisthenic activities - situps, curlups, pushups, pullups, flexed arm hangs
vertical jump/standing broad jump
- more than once for muscle endurance
- jump test for power.
why is it important to measure muscle function (5)
determine muscle weakness or imbalance (delay muscle fatigue) guide rehabilitation exercise prescription selection of exercise research tool
contraction
tension producing process of the contractile elements within a muslce
3 types of muslce fibre contractions
isometric - same measure isotonic - same tone - concentric - shortening - eccentric - lengthening isokinetic - same speed - concentric - shortening - eccentric - lengthening
3 types of whole muscle contractions
static dynamic - - concentric - shortening - eccentric - lengthening isokinematic (dynamic) - concentric - shortening - eccentric - lengthening
isotonic vs isokinetic
essentially the same thing
downhill skiing is eccentric
as youre generating force youre expanding your muscles -
isometric contraction
a muslce fibre contraction that does not results in a length change in muscle fibre - but changes the tone - sarcomere length changes as it goes into elastic components like tendons, it is generating a force but no greater than the external force
static contraction
a whole muscle contraction that produces an increase in muslce tension but does not cause meaningful limb displacement or joint displacement and therefore does not result in movement of the skeleton
isotonic contraction
a mucle fibre contraction in which the tension generated by the muslce fibre is constant through the ROM
- does not actually occur with whole muslce due to changes in joint angles (shortening at a constant velocity)
dynamic contraction
a whole muslce contraction in which the force exerted varies as the muscle shortens to accomodate change in muscle length and/orjoint angle throughout the ROM while moving a constant external load
- concentric - shortening under tension
- eccentric - lengthening of muscle under tension
force produced and joint angle
goes through a ROM, optimal force at some point
isokinetic dynamometer purpose
although the velocity of movement varies with joint angle in an intact human muscle contraction, the velocity of contraction can be held constant with a isokinetic dynamometer
isokinetic contraction
a muslce fibre contraction in which the velocity of the contraction is kept constant - tension and velocity
isokinematic contraction
a whole muscle contraction in which the rate of limb displacement or joint rotation is held constant with the use of specialized equipment - concentric and eccentric
isokinetic/isokinematic function
acceleration or deceleration
isometric/static function
fixation
neural activation - rate coding
(temporal summation)
- increased frequency of motor unit discharge
- repetitive stimuli that reach a muscle before it relaxes
latent period
excitation contraction coupling so Ca can go back to SR for relaxation - more and more Ca will come out
fused tetanus
no relaxation between
where does tentanus not happen
heart
neural activation - number coding
spatial sumation
- increase the number of motor units recruited
- henneman’s size principle - a small motor neuron will fire before a large motor neuron
firing order of 3 diff muscle fibres
SO, FOG, FG
FOG and FG are responsible for the majority of the force production during fast velocity and maximal voluntary contractions (MVC)
- permits orderly recruitment of specific motor units to produce a smoorh muslce action, allows the CNS to fine tune skeletal muscle activity to meet motor task demands
single motor units fires to
produce a relatively smooth and summated contraction - coordinated muscle contractions that overlap
length tension relationship
lab setting - zap and see how much they contract
max tension at resting muscle length due to optimal cross-bridge formation
frank-starling - increases the stretch and decreases the force generation
length tension relationship is defeated under what law
frank starling
when the muscle is shorter, why is it bad for tension production
actin starts to overlap and hides some actin binding sites, myosin hits the z line and no contraction can happen
when the muscle is longer, why is it bad for tension production
because myosin heads no longer interact with the actin filaments
tension angle relationships (3)
muscle tension is influenced by biomechanical aspects of the joint i.e. joint angle
muscle tension will reach a max at some point over the ROM in a joint and the peak tension will vary depending on the joint
due to lever arm mechanics and the angle of pull that a muslce group can exert for that joint movement - greatest force production is not solely based on optimal overlap of myofilaments
tension angle relationship of diff joints
every joint has its own angle
knee - high angle has more force (leg extension - 120 degress for highest)
elbow flexion -in the middle
how to test tension angle relationship
fix the velocity
training implications for tension angle relationships
train at the joint angle required for sport
force velocity relationship
muscle tension varies with the velocity of movement
- velocity is inversely related to force
isometric contractions produce the greatest tnesion
- fast concentric movements produce less tension than slow contractions
why do faster concentric movements produce less tension than slow contractions
faster the muslce movement, less time for optimal MU recruitment
more FT motor units
generate greater torque for a given velocity
why hollow bats
lighter so you can move it faster, but you cant move it as far
muslces can shorten fastest when the load is
the lightest
eccentric contractions are done with
skiers and ultramarathoners so training will increase force -
force velocity relationship
eccentric muscle force increases with an increase in velocity
possible explanations of force velocity relationship
2nd myosin head
decreased rate of cross bridge detachments (increase % of cross bridges remain attached) leading to greater force production
titin protein stiffness increases during eccentric contraction
eccentric muslce force is associated with
delayed onset muscle soreness
power velocity relationship
muslce power increases with an increase in concentric movement velocity then decreases at approximately 50% of max shortening velocity
why does power increase initialy
force reduction drops slower than time
muscle with the greatest percentage of FT/MU
great power/strength output at any given velocity
static
zero power
if force and time are both decreasing
increase in power, initially power is dropping slower than time
peak torque generated by a muscle decreases when
velocities of movements increases regardless of fiber type distribution
elasticity force relationship
a muslce will generate more force if it has been stretched immediately prior to contraction
stretching (eccentric contraction) stores elastic energy in the connective tissue, which is released upon concenric shortening, contributing to greater force production
what kind of contraction provides the greatest force
eccentric dynamic contraction
plyomentric exercise
eccentric conraction is immediately followed by a concentric contraction
eccentic causes
more damage to the muscles and more intensive training
eccentic causes
more damage to the muscles and more intensive training
peak torque is generated by
a muscle decrease in angle with increased velocity of movement regardless of fiber type.
fatigue for FOG
lots of force so it decreases quickly
mechanisms of peripheral fatigue
ions: H, K, Na, Ca, Pi,
Phosphagen depletion
glycogen depletion
reactive oxygen species
central fatigue
pain in brain -
seperation between CNS and PNS
all the way till before the junction, then junction on
muscle pain is sensed by
nociceptors - type of sensory nerve cell and relayed to the sensory cortex
immediate/short term pain
nocicepors are activated by ions (H, K)
stretch due to swelling
subsides relatively quickly during recovery (restoration of pH occurs quite rapidly)
pain receptor center in the brain
thalamus
muslce lactate recovery time
30-60 min
blood lactate recovery time
60 min
muslce H recovery time
12-20 mins
blood H recovery time
30-60 min
what happens when pain signals are received
opioids/endophins 0 encephalins (endogenous) to hyperpolarize so more trigger is needed
what happens when pain signals are received
opioids/endophins 0 encephalins (endogenous) to hyperpolarize so more trigger is needed
central fatigue
neural fatigue
any exercise induced reduction in maximal voluntary contraction forces that is not accompanied by the same reduction in maximal evocable force
how can you measure central fatigue
percentage voluntary muscle activation can be calculated using the super imposed twitch method. this involves applying a supramaximal nerve stimulus to a muscle that is already under maxial voluntary contraction. twitch response is compared to a control, resting twitch
a reduction in voluntary muscle activation indivates CN fatigue
formula for % voluntary activation
1-superimposed twitch/control twitch x100
pre vs post ultramarathon
pre - voluntary muscle activation is close to 100% - super imposed twitch is very small
post - % muslce activaiton is reduced sinificantly after prolonged exercise indicating central fatigue
failure of the superimposed twitch to stimulate maximal force development also indicateds peripheral fatigue
delayed onset muscle soreness
1-4 days - muscle tenderness, prolonged soreness to touch, mechanical stiffness that does not subside after exercise
cause of DOMS
muslce, small blood vessel and connective tissue damge caused by high mechanical stress in muslce, tearing of sarcomeres and muslce tendon - eccentric - tearing myosin off the actin binding sites
DOMS activation of nocireceptors (2)
inflammatory molecules - release of chemical mediators - (prostaglandins, free radicals, histamines, bradykinin, proteolytic enzymes) that continue to stimulate free nerve endings that prolong the sensation of soreness
muscle edema/swellig and spasms/cramps, disruption of Ca - ischemia
is pH/lactic acid a component of DOMS
no because H cleasr quickly
steps of DOMS (6)
structural damage in sarcomere cytoskeleton
intracellular Ca increases
degradation of Z discs and regulatory proteins
change in tissue osmolarity and inflammation which increases WBC
swelling in inflammation (local ischemia) which causes pain
DOMS is most intense with
eccentric form of muscular contraction (heavy weights, plyometrics, downhill running) and unaccustomed forms of exercise
how long does it last
appears after 8 hours, peaking over 24-48 hours and subsides after 4 days
how to measure the extent of muslce membrane damage
indirectly meausred by the release of muslce componenets into the blood stream - creatine, kinase, LDH, myoglobin, troponin
damage to heart muscle
cardiac muscle has blood supply during diastole, during exercise, adenosine increases coronary flow of artery blood, which decreases the Q and HR
demands of heat increases
HR, SV, TPR -> SBP, RPP, VO2
What does chronic endurance training do?
increases VO2 max and a-vo2 diff by increasing eccentric hypertrophy (SV)
increased capillarization
increased blood volume
rhabdomyolosis
breakdown of muslce tissue that leads to the release of muslce fibre contents (i.e. myoglobin) into the bloodstream causing impairment of kidney function
- rare but usually affects ppl who are detrained and perform large volumes of eccentric muslce contractions
- travels to the proximal tubules and form precipitates
how to prevent DOMS with exercise
repeated bout effect - one bout of eccentric exercise can induce adaptations that reduce DOMS with the next bout - adaptation occurs such as fiber size, flexibility hrought the ROM) that helps to reduce DOMS, does not fully eliminate doms
3 potential mechanisms of preventing DOMS with exercise
neural theory - redistribution of contractile stress over a larger number of motor units
connective tissue theory - remodelling of the cytoskeleton and/ot increased intramuscular connective tissue
cellular theory - an increase in the number of sarcomeres connected in the series thus reducing sarcomere stretch/strain during a repeated bout
potential strategies of treating DOMS with meds
leucine - nonsteodal anti inflammatory agents vit I, branched chain AA supplement, and adequate warmup/cool down
is there evidence that compression, massage, stretching, icing, ultrasound, or antioxidants suppress doms?
no
diff in gender on muscle function
differences in absolute strength between males and females arise at puberty- increased muscle mass and larger fiber size (testosterone)
- overall no inherent diff in muscle function between the two
sarcopenia
loss of muscle (fibre) as a natural part of aging process
- still same % of SO, FOG, FG
- SO maintain their ___ better than FOG and FG
cannot be prevented but can be slowed down
