week 3 - nerve, muscle and movement Flashcards
how to increase the force of a muscle movement
more complete activation of one muscle
more activation of agonist muscles
more inactivation of antagonist muscles
muscle fascicle
bundle of cells (fibres) surrounded by connective tissue
motor unit
single motor neurone and all the muscle fibres it innervates
what is the number of motor units dependent on
muscle size and the muscle function
what is the number of muscle fibres in a motor unit dependent on
muscle function
small motor units give good force control eg. hands
can a muscle contain motor units with different properties
yes some muscles contain slow and fast motor units
describe the connective tissue in a muscle
epimysium - dense irregular collagenous connective tissue surrounding the entire muscle
perimysium - surrounds fascicles and is derived from epimysium
endomysium - surrounds muscle cells
types of muscle fibres
red fibres (type I) white fibres (IIa and IIb)
difference between muscle fibre types
red fibres - thin, abundant mitochondria, contract weakly and slowly but for long period
white fibres - larger, fewer mitochondria, brief but powerful contractions
difference between type IIa and type IIb muscle fibres
IIb use glycolysis almost exclusively to fuel contractions and fatigues rapidly
IIa uses a combination of oxidative metabolism and glycolysis - fatigues at intermediate rates
types of motor unit
slow (s or type 1) fast fatigue resistant (FFR, 2a) fast fatiguing (FF, 2b, 2x)
properties of the different motor units
type 2x has a larger force/twitch, not many high force contractions and faster fatigue
type 1 has a smaller twitch, slower rise, slower fatigue
effects of strength training
early changes - better motor unit activation, less antagonist activation, improved glycolytic metabolism
after 6 weeks - FF fibre hypertrophy
effects of endurance training
enhanced oxidative metabolic profile, more mitochondria, improved O2 supply, more myoglobin, S and FFR fibre hypertrophy
which fibre type is associated with good endurance
type I fibres
which fibre type is associated with strength training (high force output)
type II fibres
what is fatigue
inability to maintain power output, reversible by rest
reduces force and power
causes of peripheral fatigue
failure of excitation-contraction coupling, t tubule action potential, SR activation, Ca++ release
failure of force generation at cross bridges
failure of ATP generation by depletion of energy stores
causes of central fatigue
loss of excitability of motor cortex - probable reflex inputs from metabo-receptors in muscle
can also include failure of transmission in peripheral nerve and NMJs
what is a nociceptor
pain receptor - sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals to the spinal cord and the brain
what is a mechanoreceptor
receptor that relays extracellular stimulus to intracellular signal transduction through mechanically gated ion channels. The external stimuli are usually in the form of touch, pressure, stretching, sound waves, and motion
what is an ergoreceptor
Any of the sensory receptors in muscle that detect chemical by-products of skeletal muscle contraction and relaxation - tells you how hard the muscle is working
main tasks for cardiovascular system during exercise
to provide adequate oxygen to fulfil metabolic demand of exercising muscles and to guarantee metabolic end-products washout
to regulate arterial blood pressure in order to maintain adequate perfusion of the vital organs without excessive pressure variations
Describe the excitation failure in t-tubules during fatigue
high AP firing rate leads to extracellular accumulation of K+
this makes some t-tubules inexcitable and impair excitation contraction coupling
recovery from this type of fatigue will be rapid as K+ concentrations are restored by ion pumping and diffusion
what happens to muscle if ATP runs out
muscle goes into rigor not fatigue
rigor muscles do not move - rigid
changes to ADP, Pi and H+ conc in fatigue
all increase - this impairs calcium fluxes and impairs force delivery at cross bridges
impairment of calcium fluxes in fatigue
ADP, Pi and H+ all inhibit Ca++ release and uptake into SR
this affects force and speed of shortening and relaxation
H+ also competes with Ca++ for troponin binding
describe lipid recruitment in exercise
during long duration exercise, lipid metabolism starts after ~90% or the initial glycogen has been used
lipids come from adipocytes and intramuscular stores
very long duration activities utilise lipids almost entirely
describe the different motor unit use in different types of exercise
long duration exercise - low power, uses type 1 (slow fatiguing)
moderate duration exercise - higher power, uses type 1 and type 2 (slow and FFR)
short duration exercise - higher power, all units active
describe metabolism differences in different exercise durations
long duration - aerobic, good at carbohydrate and lipid metabolism
moderate duration - aerobic, fuel mix uses more carbohydrate
short duration - includes aerobic and anaerobic metabolism, carbohydrate metabolism, inefficient glycolytic metabolism
changes to fibres in endurance training
type 1 fibres may enlarge
reduced number of type 2x
type 2a response varies
(selective hypertrophy of S and FFR fibres)
changes to fibres in strength training
type 2x, 2b and 2a fibres enlarge
describe the phases of strength gain
neural - first 4-6 weeks - activation of motor units improves
hypertrophic - development of new contractile proteins which are added laterally to existing myofibrils, later there is fibril splitting where the most enlarged fibrils divide longitudinally - large motor units grow
connective tissues also strengthen
improvements due to endurance training
improved cardiovascular performance - improves O2 delivery: cardiac output, better regional flow, higher capillary density, blood volume
improved metabolic performance - improved enzyme concentrations, improved mitochondrial density, better substrate storage and mobilisation
structure of a neuron
cell body has the nucleus
axon relays info from cell body to axon terminals
axon terminals released NTs to activate target of the nerve cell
direction of sensory neurons
afferents - towards CNS
direction of motor neurons
efferents - to muscle
two types of axons in a peripheral nerve
myelinated axons and unmyelinated axons
describe myelinated axons
they have a series of schwann cells lined up along the axon, each having a wrapped coating of myelin insulating the axon
describe unmyelinated axons
encased by schwann cell cytoplasm but there is no wrapped coating of myelin surrounding the axons
differences between myelinated and unmyelinated axons
M - larger diameter, faster AP conduction - touch, vibration, motor
UM - pain, thermal (hot and cold)f
connective tissue in a peripheral nerve
epineurium - connective tissue surrounding the peripheral nerve
perineurium - connective tissue surrounding fasicle
describe a pseudounipolar neuron
sensory afferents
axon from cell body splits into 2 - one branch to periphery and a branch to the CNS
what do mechanoreceptors respond to
mechanical deflection, touch
what do thermoreceptors respond to
hot/cold
what do nociceptors respond to
noxious (pain)
what does the dorsal horn contain
cell bodies of sensory neurons
what does the ventral horn contain
cell bodies of motor neurons
organisation of spinal cord segments
C1-8 T1-12 L1-5 S1-5 C1
how many spinal nerves does each spinal segment give rise to
each segment gives rise to a pair of spinal nerves
cervical plexus
C1-5
innervates neck
brachial plexus
C5-T1
upper limb innervation
lumbrosacral plexus
T12-S5
lower limb innervation
nerves of the brachial plexus
axillary musculocutaneous radial ulnar median
spinal segments and the muscle they innervate
C3, 4, 5 - diaphragm C5 - deltoid C5, 6 - biceps brachii, brachialis C6, 7 - extensor carpi radialis, longus and brevis C7, 8 - triceps brachii C8 - flexor digitorum, superficialis and profundus C8, T1 - interossi L2, 3 - adductor longus and brevis L3, 4 - quadriceps L4, 5 - tibialis anterior L5, S1 - extensor hallucis longus S1, 2 - gastrocnemius and soleus S2, 3, 4 - sphincter ani extemus
how is the extent and level of a spinal injury evaluated
ASIA scale - clinicians consider voluntary movement, reflex movement, sensory responses and awareness of body parts
pathway for voluntary movement
upper motor neuron to lower motor neuron
upper recruits lower
difference in the pathway for reflex movements and voluntary movements
no upper motor neuron component in reflex
inducing spinal reflexes
relax limb - tap on tendon - stretches the muscle
biceps, triceps, ankle and rectus abdominis all have jerk reflexes
disruption of the motor pathway in paralysis
disruption in lower motor neuron component means muscle wont contract - no reflexes and no voluntary movement
disruption in upper motor neuron means no voluntary movements below the level of the lesion but reflexes persist
causes of upper and lower motor neuron damage
upper - stroke, lesion of axons eg. SCI
lower - motor neuron disease, lesion of motor axon
what is gastrulation
process of cell division and migration resulting in the formation of the 3 germ layers
regions of the mesoderm layer
notochord paraxial mesoderm intermediate mesoderm lateral plate mesoderm extraembryonic mesoderm
role of the paraxial mesoderm
forms from cells moving bilaterally and cranially from the primitive streak
lies adjacent to notochord and neural tube
forms the somites in the embryo
role of the intermediate mesoderm
forms genitourinary system
describe the lateral plate mesoderm
split by a cavity (intraembryonic coelom) into 2 layers:
somatic or parietal layer
splanchnic or visceral layer
notochord function
signalling centre - controls specification of surrounding cells
important in sending signals to ectoderm and in development of NS
influences somite formation
what are the oropharyngeal and cloacal membranes
only regions in the embryo with no mesoderm
oropharyngeal membrane breaks down to form mouth
clocal membrane breaks down to form anal canal
origin of each muscle type
skeletal - paraxial mesoderm
smooth - visceral layer, lateral plate mesoderm around gut tube
smooth - ectoderm or splanchnic mesoderm
cardiac - visceral layer, lateral plate mesoderm around heart tube
somitogenesis
paraxial mesoderm gets organised into segments called somites
form alongside the developing neural tube in a craniocaudal sequence over time from day 20
appear at approx 3 pairs a day until the end of week 5
controlled by a number of genes
regulation of somitogenesis
FGF family, Wnt and notch - tell cells to switch between a permissive and non permissive state in a constantly timed fashion
a wave of factors then sweeps along the embryo and interacts with cells that are permissive (switched on) at the right time in the right area
notch needs to be on for somite formation - then switches off
FGF8 travels in opposite direction and controls somite formation when it gets to cells expressing notch
role of somitogenesis
42-44 pairs at the end of week 5 - forms axial skeleton
what is a somite
a block of paraxial mesoderm that gives rise to skeletal muscles
describe somite differentiation
cells in ventral and medial area undergo an epithelial mesenchymal transition - becomes the sclerotome - forms vertebrae and ribs
cells in dorsal half form the dermomyotome
what does the dermomyotome form
splits into dermatome (forms the dermis of the back) and the myotome (forms muscles)
what do the lateral plate mesoderm layers form
parietal - body wall, CT and bones
visceral - wall of gut tube, serous membranes
what are myocytes
mature muscle cells
made from myoblasts which are muscle cell precursors
differentiation of myoblasts
myoblasts align into chains and fuse, cell membranes disappear creating multinucleated myotubes
myogenin mediates this differentiation
when growth factors are depleted:
myoblasts stop dividing
myoblasts then secrete fibronectin onto ECM, bind to it via an integrin-crucial step
function of MYOD and MYF5 in muscle development
transcription factors that activate muscle-specific genes
enable the differentiation of myogenic precursor cells in the dermomyotome into myoblasts
can convert non-muscle cells to cells expressing all the muscle proteins = muscle cell
MYF5 required for myoblast formation
how are MYOD AND MYF5 activated
WNT proteins and BMP combine to activate MYOD in the dermomoytome - creates a group of muscle cell precursors which express MYF5
inducing sclerotome formation
sonic hedgehog and nogin induce it
function of wnt family
signalling molecules
in development they control - body axis patterning, cell fate specification, cell proliferation and migration
function of BMPs
GF/cytokine family
control tissue “architecture” throughout body
induce formation of bone/cartilage in development and dysregulated BMP signalling leads to many pathological processes including cancer
sonic hedgehog function
belongs to hedgehog signalling pathway family
acts as a morphogen (molecule that diffuses to form a conc gradient and has different effects depending on its conc.)
function of notch
family of transmembrane proteins that control cell fate decisions
FGFs function
family of cell signalling GFs which activate cell surface receptors
often act as mitogens
in development - often stimulate Wnt signalling
play an important role in mesoderm induction and limb development
regulation of smooth muscle cell differentiation
serum response factor is responsible for smooth muscle differentiation
SRF upregulated by kinase phosphorylation pathways
myocardin/ myocardin related transcription factors enhance SRF activity
skeletal muscle formation
myoblasts fuse to form long multinucleated fibres - myotubes
under control of a number of gene sets including MYOD, MYF5 and myogenin
tendons are derived from the sclerotome under control of the transcription factor scleraxis
cardiac muscle formation
originates from splanchnic mesoderm surrounding the developing heart tube
myoblasts adhere to each oter via intercalated discs
myoD not involved in early cardiac muscle development
