Term
| know spinothalamic tract, pain and temp crosses over immediately, coritcospinal tract |
|
Definition
|
|
Term
| what types of things can change with increased use? |
|
Definition
-architecture
fiber type distribution
tendon length
fiber diameter
Myosin HeavyChain profile
mitochondrial distribution
capillary density
fiber length |
|
|
Term
| what happens when you stimulate a muscle 8-24 hours a day for 8 weeks maximally at 10 hz? |
|
Definition
SR begins to swell after 3 h of stimulation B. mitochondria volume increases
C. increase in capillary density and SDH (dark stain).
E. decrease amount and activity of Ca
2+ ATPase (becoming slow twitch!)
F. myosin profile altered
G. decrease muscle mass and fiber area (less distance for O2 to diffuse, so we can get oxygen faster) |
|
|
Term
Comparison of unfused tetani between stimulated (left
panel) and control leg (right panel). what does this slide tell us? |
|
Definition
| after stim, you get a slower contraction, so you get a bit more tentanus or summation of forces |
|
|
Term
| what does the F1, S1, S1F2, F2 experiment tell us? |
|
Definition
| you can't get all of the changes in metabolic capacity. you will either get more fast twitching, or more slow twitching |
|
|
Term
| what happens if you cut the gastroc and soleus off a rat? |
|
Definition
| the plantaris muscle will gain size and strength, but it changes its fiber type from type II to type I. |
|
|
Term
| what are the principles of strength training? |
|
Definition
specificity gradual progressive overload variation
appropriate recovery |
|
|
Term
| what is the definition of strength? |
|
Definition
Ability of muscle/muscle group to produce tension during a
maximal effort, either dynamically or statically
• Measured as force or torque (or estimates of it – one
repetitation maximum – 1 RM) |
|
|
Term
| what is the power vs work? |
|
Definition
Work - total amount of force exerted over time (force X
distance)
• Power - rate of performing work (force X velocity) |
|
|
Term
| what is the definition of endurance? |
|
Definition
Also fatigue resistance
• Ability to perform sustained or repetitive contractions over
time |
|
|
Term
|
Definition
| it is the concept that Gains in performance are specific to task practice. |
|
|
Term
| what is the speed/force trade off? |
|
Definition
Training at high forces/low speeds (low
reps), gains in high force performance
• Training at low forces/high speeds (high
reps) results in improved velocity of tasks
• Greatest increase in strength at or near
velocity of training exercise (Caiozzo et al.,
1981) |
|
|
Term
| at what speed do you get the greatest increase in strength? |
|
Definition
Greatest increase in strength
is at or near velocity of training
exercise. |
|
|
Term
| what is the reps vs force tradeoff? |
|
Definition
| the more reps you do in a set, the less force you can produce, whereas the less reps you do in a set, the more force you can produce. |
|
|
Term
| what did early research in the 1950's conclude about strength gains? |
|
Definition
10 reps at 40-50% of MVC gives greatest gains according to hettinger muller in the 1950's.
duration - Duration-1-2 s – needed 100% effort,
4-6 s – only 66% percent |
|
|
Term
| what are the ACSM guidelines for intial strength training |
|
Definition
-12 RM, 2-3 days/wk, small initial increases in volumes
• Progression: Wider loading range (1-12 RM) 4-5 days/wk |
|
|
Term
| What are the ACSM guidelines for intermediate to advanced lifters? |
|
Definition
Wider loading range, 1-12 RM inperiodized fashion
• Eventual emphasis on heavy loading (1-6 RM) with 3 min rest
• Moderate contraction velocity, 2-10% load increase with > 4 reps
• Potential gains
•40% in untrained personnel, 20% in moderately trained
•16% in “trained”, 2% in elite |
|
|
Term
| how does training train with different goals like hypertrophy, power training, or endurance training>? |
|
Definition
Hypertrophy –
• Loading 1-12 RM, moderate velocity, 1-2 min rest
• Higher volume, multiple set programs
Power training
• 1) strength training (describe above)
• 2) light loads (30-60% 1RM at fast velocity with 2-3 min rest
• 3) multijoint exercises
Muscle endurance training
• Light to moderate loads (40-60% 1RM)
• High repetitions (15-20 reps)
• Short rest (< 90 s) |
|
|
Term
|
Definition
High initial training volume (reps x sets, 8-15 RM) and low
intensity (load or power)
Gradually progress to low volume (reps), high loads (1-6 RM) –
Undulating cycle
Available data
• superiority of periodization models vs other general weight training
regimens, although not conclusively
• No data that periodization is worse than general “workouts" |
|
|
Term
how do you overload?
is their a dose response relationship with overload? |
|
Definition
Strength Training
• Increased resistance/load – guidelines
Endurance Training
• Increased contraction time
• Increased repetitions
YES! optimal dose of therapeutic exercise
which will provide the greatest adaptations
• Too much: over-stress injury
• Too little: failure to achieve desired results |
|
|
Term
Variability
• Eccentric > concentric training
(Jones and Rutherford 1997),
Both better (Aagaard et al. 2003)
• Free weights vs isometric tasks
• Other examples
•Altering velocities, speeds
•Cross- training (different
tasks) |
|
Definition
| variability (allowing the joint to move through its range of motion will allow greater gains in isometric strength, even if you are testing for isometric strength) |
|
|
Term
| how does rest time between sets alter a workout>? |
|
Definition
Training with short vs long
rest between sets alters
metabolic demands, alters
adaptations |
|
|
Term
| what is hypertrophy vs hyperplasia? |
|
Definition
Increase in muscle fiber
cross-sectional area –
splitting of myofibrils
increased size and number of
actin/myosin, additions of
sarcomeres (Mac Dougall et
al., 1979; Goldspink, 1992)
Decreased degradation
Not all muscle fibers undergo
the same amount of
enlargement (II > I)
response depends on the
stress applied to the muscle |
|
|
Term
| what are some chronic adaptations to resistance training? |
|
Definition
hypertrophy primary cause of increased muscle size,
particularly in Type II fibers
visible after 4-8 weeks of training, adaptation plateaus after ~1
year
little or no change in [ATP] and [CP]
Some change in mitochondrial number – little change in
oxidative enzymes
SR and t-tubules changes |
|
|
Term
| with adaptation, are you getting an increase in force from each muscle fiber? |
|
Definition
| you are not getting more or less strength from each muscle fiber, the muscle itself is just getting larger or smaller. |
|
|
Term
| what is the bidriectional shift of resistance training with bodybuilder type training? |
|
Definition
30 to 55% increase in Type IIA fibers with resistance training
Decrease from 24 to 3% in IIB or IIX fibers
With resistance training, Type I fibers can “adapt” towards properties of Type IIA fibers |
|
|
Term
| what are some adaptations to sprint training? |
|
Definition
Increase in anaerobic
enzymes
Increased phosphorylase
Increase (sometimes) in
muscle glycogen stores
Increased muscle/blood
buffering capacity
Potential shift to higher IIX/IIB proportions with sprint or
plyometric training
• Higher proportion of hybrid fibers (IIX – mix of IIB and IIA) |
|
|
Term
| what are the effects of endurance training? |
|
Definition
decreased CS(CSA of fibers and fibrils)
•Decreased fatigability (mitochondrial enzymes, angiogenesis)
•Increased % of Type I, IIA and Intermediate (IIx) Fibers
• increase storage, use of intramuscular triglycerides
• increase muscle glycogen synthase and storage, little effect on glycolytic
enzymes
IIB--->IIX--->IIA--->I |
|
|
Term
| Why is the muscle able to produce more force after very few training sessions, when there are no signs of muscle hypertrophy until the 4-6 week mark? |
|
Definition
| its all neural drive effects |
|
|
Term
| what are the Contributions of neural and muscular adaptations to resistance training? |
|
Definition
| know what these two graphs mean |
|
|
Term
| what are some neural adaptations to strength training |
|
Definition
increased agonist activity, reduced antagonist activity.
more rapid motor unit recruitment
higher initial and sustained motorneuron firing rate |
|
|
Term
| if you ask somone (old or young) to do 10%, 50%, and 100% of MVIC, what happens? |
|
Definition
| at 10% and 50% you dont get any increase in firing rates, but at 100% you have a large increase in the first 8 days, but in young people it plateu's. old people continue to improve for a longer time. |
|
|
Term
| how can we tell if the changes are neural or muscular? |
|
Definition
through motor evoked potentials with transcranial magnetic stimulation
for a neural change, you would see an increase in the EMG, as well as force. For a muscular change, you would see an increase in force but NO increase in EMG or neural activation |
|
|
Term
| WHat are some changes in TMS-evoked MEPs with resistance training? |
|
Definition
Maximum MEP amplitude
increased with strength
training
• Increase in strength by 18%
• Increase in MEP by 32%
• No change in M-wave (this tells us that the change are in the brain and spinal cord)
Jensen et al 2005 – no
evidence of cortical
changes (only during skill
acquisition) this tells us that some people think its more spinal cord mediated |
|
|
Term
| what are the adaptations with MENTAL training? |
|
Definition
- 22% increase with mental training
- 30% with physical training
- 3.7% in control group
- contralateral increases only in physical training group (increased activation of association areas)
- Contradictory data (Herbert et al. 1998) –
laboratory of Simon Gandevia)
- 6% changes in elbow flexion MVC
in both imagined and control groups
- 18% with physical training |
|
|
Term
| what are some more neural adaptions to mental training? |
|
Definition
12 weeks, 15 min/day, 5 days/wk
• With mental practice
• 35% increase with hypothenar
• 14% with biceps training
• Physical training (ABD) – 53%
• Munn et al. 2005 – 7% changes
over 4 weeks with at least 3 sets
Cross-education
• opposite limb can increase force
production which means possibly that some pathway from the cortex is going to both sides
• Specificity of training to crosseducation effects
Augmented feedback (afferent)
• Decreased GTO feedback
• Augmented stretch responses? |
|
|
Term
| with aging, does the muscle get less fatigue resistant or more fatigue resistant |
|
Definition
| more fatigue resistant! as you get older maybe you dont use your type II muscle fibers as much and they convert to type I's. young people can drive the muscle harder, but are more fatigued |
|
|
Term
| to see muscle changes you would need to do twitch torques. what does this mean>? |
|
Definition
| early changes would see increase in meps but no increase in twitch torques, late changes you would see the same increase in meps, but an increase in twitch torques. |
|
|
Term
what are some Adaptations to Forced
Immobilization |
|
Definition
Type I atrophy more than Type II
•Extensors (anti-gravity) atrophy more than Flexors
•Occurs rapidly - reduction of 1/3 muscle mass in only 1
month
Fiber type transformation
•Decreased number of Type I
•Increased number of Type IIa/IIb
No loss of fiber number |
|
|
Term
| in the chronically paralyzed group, their twitches aren't summating. why? |
|
Definition
| their type I muscle fibers have converted to type II's |
|
|
Term
| in forced immobilization, your type I's are atrophying and changing to type II's, whereas in aging what happens? |
|
Definition
| the type II's are changing to type I's |
|
|
Term
what is a caveat to Immobilization:
Adaptation to chronic stretch |
|
Definition
Immobilization in stretched position yielded no atrophy, but rather hypertrophy
Sarcomeres added to fiber length - allowed length to
return to “normal”
• Younger animals increased length by increasing muscletendon length
• Older animals increased length only by increasing
muscle length
Immobilization in shortened position causes atrophy
and shortening (sacromeres deleted) |
|
|
Term
| what are the mechanisms of strength loss? |
|
Definition
Muscular
•First 3 days: Decreased myofibrillar synthesis
•Afterwards: Increased degradation rate of myofibers
Neural
•Decrease MU firing rate, decreased cortical/
descending drive, inability to sustain firing
•Can recover neural adaptations rapidly (similar to
strength training) |
|
|
Term
| what are mechanisms of strength loss due to aging? |
|
Definition
Sarcopenia
• Muscle atrophy
• Muscle fiber loss (apoptosis)
Alterations in neural patterns
of activity
• Decreased extent and speed of
activation
• Motoneuron death – changes in
innervation of remaining units
• NMJ changes
Mechanisms – altered use
• Loss of Fast MU primarily – hardly
ever utilize these units
• Loss of strength for same
%MVC, no decrease in fatigue |
|
|
Term
| what are the general symptoms of nerve injury? |
|
Definition
lossof voluntary movement and conscious sensation
• autonomic functions (blood pressure and flow, respiration)
• Bladder/ bowel control, sexual function
• reflexes (PNS vs. CNS)
• TO REPAIR THESE PATHWAYS,
• AXONS must REGROW and/or SYNAPTIC CIRCUITS MUST RE‐ESTABLISHED
• Mechanisms of injury – similar between PNS and CNS
• Mechanisms of recovery –extremely different |
|
|
Term
1.If the cell body is damaged, what happens to the neuron?
2. what happens if the axon is
severed close to the cell body, . . .
3. are the post- and presynaptic
neurons also affected? |
|
Definition
1.it is lost!
2.there is a chance that the axon will
regenerate, this is less likely in CNS.
3. yes, they may degenerate. |
|
|
Term
| if the axon is damaged, what are the chances the cell regenerates in the PNS vs the CNS |
|
Definition
In the PNS there is a relatively good chance of regeneration.
• CNS neurons have the capacity to regenerate, it is just less likely. |
|
|
Term
| do you know what oligodendrocytes, schwann cells, astrocytes, and microglial cells do? |
|
Definition
|
|
Term
| 1st thing that happens with nerve injury is synaptic terminal degeneration. how does this happen? wallerian degeneration |
|
Definition
Immediately following injury
• Synaptic transmission cut off
• Cut ends pull apart and seal up, and swell
• Terminal degeneration (1) within hours
• accumulation of neurofilaments, vesicles
• Astroglia interpose between terminal and target;
cause terminal to pull away from postsynaptic cell |
|
|
Term
| what happens after wallerian degeneration in neural injury? |
|
Definition
Myelin breakdown, debris (3)
• Phagocyte infiltration (4)
Chromatolysis (5) |
|
|
Term
| what are the two potential outcomes of nerve cell injury? |
|
Definition
If regeneration of synaptic contacts, chromatolysis reversed
• If no synaptic contact, cell apoptosis |
|
|
Term
| what is anterograde and retrograde transneuronal degeneration? |
|
Definition
Anterograde – the damaged cell axon TARGET (downstream) degenerates
• Retrograde ‐ inputs to cell degenerate
• Synaptic terminal withdrawal
• Synaptic stripping ‐ ensheathment by glial cells –depress
potential recover
both are caused by astrocytes |
|
|
Term
| what are the two interrelated factors that cause transneuronal degeneration?? |
|
Definition
| activity and growth factors |
|
|
Term
| what is the role of growth factors in synapse function? |
|
Definition
Activity promotes generation
of diffusible signals from
neurons to neurons
• Growth factors from:
• Neuronal cells
• glial cells
• endocrine organs
• inflammatory mediators
• Transport to nucleus ‐ protein
synthesis
• Promotes growth and/or
maintenance
• Absence causes loss of cell
function or death!!
activity helps promote growth factors |
|
|
Term
if you cut off a limb bud, you can see that the alpha motor neurons in the spinal cord die (this means there is obviously some communication)
if you give an extra limb, you see a large increase in alpha motor neurons in that side. |
|
Definition
| some growth factor in the muscle TISSUE was signalling growth |
|
|
Term
Neurons begin with simple dendritic trees, which become progressively more
complex with age
• The number of synapses made by the presynaptic terminals of axons also
increase in number
What happens with injury? |
|
Definition
| retraction of dendritic arborizations (loss of activity or trophic inputs) |
|
|
Term
Why is transneuronal degeneration
important? |
|
Definition
| there are two interrelated factors that affect transneuronal: activity and growth factors. |
|
|
Term
What happens to the muscle with …
1.• motoneuron injury (peripheral nerve damage)? -
2.• corticospinal injury (stroke, spinal cord injury)? - less atrophy, still have reflexes, multiple cortical pathways, and other interneuronal pathways that can still activate it |
|
Definition
1.MASSIVE ATROPHY, dennervation atrophy
2.less atrophy, still have reflexes, multiple cortical pathways, and other interneuronal pathways that can still activate it |
|
|
Term
What type of transneuronal degradation happens to the motor cortex with
1. motoneuron injury?
2. corticospinal injury?
3. sensory cortex injury? |
|
Definition
motorneuron injury - retrograde degeneration of the cortex
corticospinal injury - retrograde degeneration
sensory cortex - anterograde
spinal cord is retrograde or anterograde? |
|
|
Term
| what is regeneration post-axonopathy |
|
Definition
Peripheral nervous system
‐strong likelihood of regeneration if target is
available and in proximity
‐if no reconnection
1) search for another target or
2) die of |
|
|
Term
| how does regeneration work in the PNS? |
|
Definition
Degeneration of the distal stump, with retention
ensheathing connective tissue
•Macrophages clean debris, release mitogens to
activate Schwann cells
•Previous and newly‐activated Schwann cells form
tubes, conducive environment for growth
• Mechanical guidance cues
• Chemical guidance cues (laminin, growth factors) |
|
|
Term
| how do macrophages eventually stimulate axon growth? |
|
Definition
Macrophages activate Schwann Cells →
→release Nerve Growth Factor →
→NGF stimulates axon growth |
|
|
Term
| how does pathfinding work to the old target? |
|
Definition
Neuron has to re-establish
specific contact
• Developmental conditions –
polyneuronal innervation (normally one muscle fiber is innervated by 1 motor nueron, but in regeneration you can have them innervated by more than 1 motor neuron)
– Competition between cells
– Activity and growth factors
• With regeneration, same
process occurs (eventually the competition makes it so the best axon makes the connection, and the others withdrawal)
– Multiple target innervations
– Synaptic retraction/elimination |
|
|
Term
Basal lamina differentiated
at synaptic contact
• Synaptic terminal is well
differentiated
• Acetylcholine receptors
aggregated under synaptic
terminals |
|
Definition
| synaptic basal lamina is well differentiated and VERY important |
|
|
Term
in muscle regeneration, the acetylcholine receptors line up exactly where they should be
in rennervation, the nerve terminal goes exactly where it should be.
why is this the case? |
|
Definition
| there is bidirectional communication through the synaptic basal lamina giving chemical signals for where to grow/regrow |
|
|
Term
What happens if nerve doesn’t get to
muscle? |
|
Definition
• Opposite of what occurs in embryonic development of
neuromuscular junction
• During development . . .
• Acetylcholine receptors expressed all over sarcolemma
• With growth cone contact – organization of receptors under presynaptic terminal
With injury
• Acetylcholine receptors scatter throughout sarcolemma
• Change in receptor conductance (isoform)
• By re‐contact by same or another terminal, re‐organization of receptors
under terminal, back to original excitability |
|
|
Term
| what is Synapse Organization and Reorganization? |
|
Definition
•Synaptic interactions facilitate development of mature synapses (activity and growth factor
dependent)
•Both muscle and nerve can reassemble synaptic
organization following injury secondary to
trophic support
•Organization disintegrates if no reconnection or
re‐weights itself to other synapses |
|
|
Term
| what are fasciculations and fibrilations? |
|
Definition
Fibrillations –sharp depolarization
associated with increased Ach
receptors opening (only on EMG; can't see these)
• Fasciculations ‐ small
spontaneous
depolarization of
nerve/muscle
• Smaller associated with
muscle injury
• Larger twitches
associated with post‐
workout sensitivity (you can see fasciuclations)
both are due to acetylcholine sensitivity |
|
|
Term
| What is the rate of PNS regrowth following Axonopathy. |
|
Definition
Rate of PNS axon growth is approximately 1
mm/day (1 in per month) |
|
|
Term
•Prognosis for reinnervation of tibialis anterior
following. |
|
Definition
peroneal nerve injury - pretty good chance
• L4‐L5 disc herniation. - poor chance
Prognosis for sensory reinnervation
• slow recovery of cutaneous sensation
• minimal recovery of proprioceptive afferents |
|
|
Term
|
Definition
damage to Schwann cells
• Slowed/blocked of nerve conduction
• Schwann cells usually survive, and remyelination
usually follows
• Small changes in skeletal muscle (possibly disuse
atrophy |
|
|
Term
|
Definition
cell body damage
• Highly selective involvement of specific neuronal areas
• Similar clinical features as axonopathy |
|
|
Term
| what are the stages of classification of PNS nerve injury>? |
|
Definition
Class I ‐neurapraxia
• transient ischemia or myelin damage, axon is preserved
• “conduction block” e.g Saturday night palsy
• recovery is complete with remyelination
• Class II ‐ axonotmesis
• crush injury ; injured axon, maintained Schwann cells intact
• Axonal regeneration may be incomplete
• Class III ‐neurotmesis
• total nerve severance; damage to axons and connective tissue
• limited regeneration if excessive scarring |
|
|
Term
| Neurons in the PNS can regenerate. can neurons in the CNS? |
|
Definition
| they have a limited capacity to regenerate |
|
|
Term
Regeneration of CNS axons
what are the 4 basic mechanisms of why CNS doesnt recover? |
|
Definition
1) Peripheral nerves have favorable environment
‐ CNS axons can grow through Schwann cells (laminin
and CAMs)
‐ Peripheral distal stumps upregulate neurotrophic
factors
2) Inhibitory factors prevent regeneration of axons
in CNS
‐ Myelin associated proteins (myelin associated
glycoprotein –MAG, Neurite Inhibitor of 35kDA (NI‐
35); Nogo)
‐ CSPGs (chondroitin sulfate proteoglycans)
3) Central axons not as capable for regeneration
• pathfinding even in peripheral nerve tracts (Schwann
cells) not as good as peripheral axons
• Growth associated protein of 43 kDA (GAP‐43)
• High in maturity, increased in PNS post‐injury
• Low in CNS axons
4) Astroglia scar formation inhibits growth – difficult to
bridge over scar |
|
|
Term
In the absence of CNS regeneration .
. .
• Recovery of function could be due to parallel
pathways to activate motoneurons
• In PNS –only one motoneuron contacts a single muscle fibers
• In CNS ‐ motoneurons receive inputs from multiple afferent
pathways, interneuronal circuits and descending inputs
• Continued work on regenerative therapies
• Antibodies, knockout experiments to block inhibitory proteins
• Growth factor application
• Bridging over injury site
• Limit initial injury |
|
Definition
|
|
