Exam Review Flashcards
For fine motor movements (fiber type and #/MU)
type I fibers
Few fibers per motor unit
Motoneuron soma size (largest to smallest)
IIX-IIA-I
Fiber size-CSA (diameter) (Largest to smallest-males)
IIA-IIX-I
Type I muscle fibers characteristics
-slow ATP breakdown
-Smaller (diameter)
-More mitochondria
-Better blood supply
-Fatigue resistant
-AKA Slow Oxidative
Type IIA Muscle fiber characteristics
-Fast ATP breakdown (fast myosin ATPase)
-Larger than type I
-less mitochondria
-less blood supply
-less aerobic capacity
-AKA fast oxidative-glycolytic
Type IIX muscle fiber characteristics
-larger than type I (but smaller than type IIA)
-fewest mitochondria
-least blood supply
-lowest aerobic capacity
-fatigable
-AKA Fast glycolytic (FG)
Determinants of fatigue resistance
-mitochondrial size and number
-myoglobin concentration
-muscle fiber diameter (diffusion distance)
-capillarization
Main differences between onion skin and after hyperpolarization models
onionskin: lower threshold MU recruited first (size principle) and firing rate increases significantly to increase force- higher threshold MU are recruited but the firing rate is not increase significantly- this is reserved for extreme circumstances- more indicative of voluntary contraction humans
AHP: lower threshold recruited and FR increases slightly, then higher threshold MU recruited- it is these fibers increased FR that result in a great increase in force production
During an Eccentric contraction of the same absolute force as Concentric there are
more force/ CB
less CBs needed
less muscle fibers needed
less motor units needed
less motor units activated (Seen on EMG)
For the same relative force, eccentric and concentric contraction have:
same number of CBs active
Same number of muscle fibers active
same number of motor units active
same motor unit activation
*** this relation tappers off at very high relative force
Why is there a lower max EMG activation during high velocity Eccentric contraction
fear of max eccentric actions
unfamiliar with max eccentric contractions
reflex inhibition- Golgi tendon organs?
- throw voluntary limitation may be present throw baseball as had as can vs pulling arm stretched as much as possible
Firing rate impact on rate of force development
higher firing rate
more frequent MAPs
faster rate of Ca2+ release from SR
More rapid onset of CB cycling
Greater rate of force development
Factors impacting EMG magnitude
-Number of fiber active (MUs recruited)
-motor action potentials per fiber (firing rate)
-size of fiber
-Amplitude= action potentials on top of each other
-muscle specific differences exist- different distribution of MU in muscles (eye vs quads)
MU recordings overlap force production with MU potentials- take home
integrated signals give us better insight, combining both
What happens to Motor unit number estimates with ageing 2 take homes
-MUNE (motor unit number estimation?) decreases with ageing in human skeletal muscle
-this is likely due to alpha motor neuron loss in the spinal cord- Motoneuron number decreases
** can somewhat avoid with use it or lose it principle
What happens to relative recruitment threshold after training- take homes (3)
-can decreases relative recruitment threshold (gets easier to recruit) after training
-while relationship between recruitment and training (lower threshold) is driven by fibers recruited at higher MVC there is still an overall effect (all fibers easier to recruit with training)
-recruitment threshold gets lower, and also our discharge rate gets faster (recruit and fire faster)
Fatigue: Isometric contractions
reduced force
reduced rate of force development (RFD)
reduced rate of force relaxation (RFR)
Fatigue: concentric contractions
reduced force
reduced velocity
overall reduced power
Fatigue: eccentric contractions
-reduced force- reduced force at given velocity
-reduced velocity? - may or may not- control velocity determined by external load
-mor likely to cause damage
How is exercise intensity expressed
Isometric
weightlifting
isokinetic
aerobic exercise
% MVC
% 1RM
Maximal contractions
% V02Max (can go over 100%)
Bottom line on fatigue
fatiguing exercise–> various causes/sites of fatigue–> decreases CB function
Effect of fatigue on force-velocity and power-velocity relationships
Reduced Isomax (lower force)- reduced number of CBs
Reduced Vmax (lower max velocity)- Reduced rate of CB cycling
lower force at a given velocity (each)
see overall decreased relation and leftward shift
*** major impact on Power- why power athletes need more rest
-Larger impact on CON contraction- can’t rely on positive braking
Sites of fatigue: brain
failure of volitional “drive” to motor cortex
decreased excitation of motoneurons
MU dropout and decreased MU firing rates
Sites of fatigue: Spinal cord
decreases excitability of motoneurons
reflex inhibition
MU drop out and decreased MU firing rate
Sites of fatigue: NMJ
NMJ failure
Muscle fiber drop out
Sites of fatigue: excitation contraction coupling
decreased excitability of endplate- decreased MAP size
impaired T-tubule-SR function - No Ca2+ release
excitation contraction coupling failure
Sites of fatigue: muscle fibre
direct effect on CB function- eg Lactic acid, H ion, metabolic in nature
Central fatigue
decreased MU activation
Peripheral fatigue
Neurotransmitter depletion
Reduced membrane excitability- ion exchange (Na, K)
Fuel depletion- ATP, PCr, Glycogen
Metabolic by-products- Pi, H+, heat
Fatigue: MU activation
Mu dropout
less active fibers
less active CBs
less force/ power generating capacity
also
decreased FR
less summation/fiber
less active CB/fiber
less force/power generating capacity
Sustained submax contraction activation fatigue
fatigue (decreased # active CB and decreased force/CB)
increase Mu recruitment and increase MU FR (increase # active CB)
Compensates of fatigue- fatigue progresses and process continues until no more MU can be recruited and firing rate can’t increase further- failure (can no longer maintain force)
Possible causes for fatigue- 400m race
lack of will, neurotransmitter depletion, increased metabolites, decreased membrane excitability, reflex inhibition (caused by increased metabolites)
Possible causes for fatigue- 42km race
lack of will, neurotransmitter depletion, hypoglycemia, decreased membrane excitability
NMJ failure
Ach depletion - firing too quickly for too long
reduced endplate excitability- firing too quickly- can’t reestablish resting potential
result: no MAP- fiber dropout
Fuel depletion: ATP
decreased ATP:
-decreased sensitivity of Ca2+ channels
-Decreased CA2+ release through SR release channels
-Decrease # active CBs
Fuel depletion: glycogen
Decreased glycogen:
-decreased sensitivity of Ca2+ channels
-decreased Ca2+ release
-Decreased # of active CBs
Accumulation of metabolites: Pi
Increased Pi:
-decreased Ca2+ release
-decrease sensitivity of Ca2+ channels
(Main metabolite contributing to fatigue)
Accumulation of metabolites: H+
Increased H+:
-interference of Ca2+ binding to troponin
-Decreased rate of CB activation
-decreased # active CBs
-decreased PH can also inhibit Ca2+ release channels
-Not sure if H+ of lactic acid caused issues
Direct effector of CB function: decreased number of active CBs
-from decreased ATP- with greater contractile intensity ATP need is increased
Direct effector of CB function: Force/ CB
-force comes from actin myosin pulling
-increased Pi= decreased bond strength, increased likelihood of detachment
-increased Pi= decreased Ca2+/troponin interaction therefore Ca2+ requirement increased (more for the same force)
Direct effector of CB function: H+
role is still debated- slows ADP release during the CB cycle- decreases cycling speed- contraction probability decreases, force decreases and number of active CB decreases
Major sources of depletion
Fuel:
glucose, glycogen, Pcr, ATP
Major accumulations
metabolites: lactate (and H+), Pi, occurs in both central and peripheral (muscle and brain)
Fuel depletion- flow chart
decreased Pcr and/ or decreased glycogen
decreased rate of ATP resynthesis
decreased ATP (small initial store)
decrease # active CBs
Metabolite accumulation- flow chart
Pi:
- decreased force/CB
-impaired E-C coupling–> decreased # active CBs
H+:
-decreased rate of glycolysis–> decreased rate of ATP resynthesis–> decreased ATP stores–> decreased # active CB
-muscle afferents-pain, inhibition
-impaired E-C coupling???–> decreased # active CBs
-Decreased force/CB???
High intensity isometric (30s)
-limited O2
-decreased ATP
-decreased PCr
-increased Pi
-increased H+
High intensity (4-5 mins)
-limited O2
-decreased ATP
-decreased Pcr
-increased Pi
-increased H+
-likely some decrease glycogen
Low intensity (2hrs)
-O2 ok
-significant glycogen depletion
-hypoglycemia (C and P)
-dehydration
-hypothermia (C and P)
Muscle vs blood lactic acid exercise intensity and duration
muscle lactic acid (H+)- increased with sprint time and distance)
blood lactic acid at finish- decreased with running distance in KM
Fatigue: rate of force development- flow chart
type IIx MU drop out, decreased MU firing rate
-decreased force and rate of force development–> both caused decreased speed/ velocity performance
also
decrease rate of Ca2+ release/ Ca2+ sensitivity, decreased rate of CB cycling–> decreased rate of force development and decreased Vmax –> both decrease speed/velocity performance
Fatigue rate of force relaxation
Ca2+ reuptake is active process0- requires ATP – slower Ca2+ reuptake from SR
- decreased Ca2+ ATPase activity; SERCA pump- may be caused by interference from metabolite accumulation
Fuel and metabolite clearing/resynthesis
-ATP very fast
-PCr fast
-Pi fast
-H+ takes much longer
-glycogen resyntheses take long time
Type II- greater metabolic power- fuel/metabolites chart
greater decrease in ATP, PCr, glycogen (but also greater storage of ATP and PCR- but slower recover than type II since less mitochondria)
Greater increase in: Pi and H+
compared to type I and average
Female muscles: why have greater relative endurance
smaller fiber diameter
smaller II/I area ratio
grater capillary density
more elastic tissue (???)
higher % type I fiber
more Fat metabolism (glycogen sparing)
enzymes for oxidative metabolism also more efficient
Effects of training on fatigue
-greater cardiac output- increased VO2 max- greater absolute and relative endurance
-increased muscle oxidative capacity: increased: mitochondrial density, myoglobin, capillarization–> increased VO2 max, increased relative endurance
Also see overall increased ability to sustain a given % VO2 max
Absolute strength directly related to
CSA- highly correlated to mass, but CSA is inversely related to Strength/mass
Strength/CSA is unrelated to muscle CSA
Mass and area- square cube law
Mass is directly related to volume
Area is related to force
Type II fiber have a greater
specific force and Vmax
Ageing: up to age 20
increase muscle size (increase fiber size)
Ageing: 25-60
decrease: CSA, fiber CSA, fiber # (greater loss of type II)
Ageing: 60+
Decrease: muscle CSA, fiber CSA, fiber #, # motoneurons, # of fibers (greater loss of type II)
Neuromuscular compensation results in
greater number of fibers per motoneuron
Females Vs Males
-lower absolute strength- lower CSA
-Greater body fat %- less strength/BM
-Less muscle mass per lean body mass (remove fat)- less strength/LBM
-Lower upper body: lower body muscle mass ratio: bigger difference versus males in upper body strength
-Small difference in strength/CSA- due to males having slightly more type II fibers than females
Strength training hypertrophy
No addtion of fibers (hyperplasia)
increased number of myofibrils (splitting)
increased number of myofilaments (no change in size)
Parallel loss/ growth
adding muscle size (add on top or bottom)
Series loss/growth
-greater optimal zone (stretched-add more)
add left and right
Fibers with the same CSA, longer fibers will (more sarcomeres in series)
-greater range of motion
increased absolute range of length-tension curve
-greater force at given velocity
2 fibers same length, greater CSA (more sarcomeres in parallel)
shifts length tension curve higher- retains shape
Unipennate, bipennate, fusiform/multipennate
unipennate: all force in same direction- greatest force
bipennate: force in 2 directions- slightly less force, but over a greater length
fusiform/multipennate: force in many directions, least force but over the greatest length
PCSA
muscle volume/ fiber length- better indication of force than ACSA
Training neural adaptation
what you see first when start training (before hypertrophy), allows increased FR- allows greater FRD, also less co contraction
Faster development during training means it is
faster to be lost… but maintainemce is easier than development (1x/ week)
