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57 Cards in this Set

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3 recommendations for working with pts with NMD?
Avoid overwork
Avoid Eccentric ex
Avoid stressing a mm <3/5 (No resistance ex!)
How do you avoid overwork?
Submax intensity - pt should be able to perform more reps when they stop the set
Why should pts avoid eccentric ex?
Eccentric induced mm damage that last 2-5 days and is associated with dec strength
You must find a balance with this b/c eccentric mm work is neded in daily life
What is overuse weakness?
Dec strength directly related to activity
What caused all these recommendations for ex with NMD?
Postpolio syndrome coined in 84 - new onset of weakness in mm that were once affected by polio without polio coming back
What is the anecdotal evidence to suggest these recommendations for ex are valid?
Bennet described 3 post-polio pts who aquired weakness due to excessive use of weak muscle
Borg did tisue biopsy and EMG. Found greater proprotion of type 1 fibers and evidence of type 1 hypertrophy. Also, more homogeneous and intermediate frequeny recruitment thresholds for MUs
Dominant hand significantly weaker than non-dominant hand in CMT disease
What is the theory for overuse causing further damage in NMD?
Lost majority of MUs to the deinnervation - reinnervation processs
Remaining neurons sprout to re-innervate the mm fibers (same # of mm fibers innervated by smaller # of axons = large MUs)
Now you are recruiting every single MU and mm fiber and this wears out the nerve or mm fibers
What type of "expression" do MUs tend to adopt with NMD? What does this lead to?
Homogenous expression - don't have large and small MUs, just mid size
The mm fibers start to hypertrophy and the large fibers have difficult getting nutrients they need
This is due to the deinnervation - reinnervation process
Primary complaints of pts with NMD with exercise in general?
Weakness and atrophy/wasting
Pain
Fatigue
Are pts at greater risk for disuse weakness or NMD weakness (overuse)?
Disuse weakness - we must find a place where we are preventing disuse weaknees and overuse weakness
What happens to mm fibers with disuse?
Dec oxidative capacity = fatigue fast
Pt will develop more fast twitch fibers
What does resistance ex do to mm fibers?
Inc oxidative and fatigue resisdent fibers
Type I to Type IIA
Type IIX to Type IIA
Frequency, intensity, duraiton of aerobic ex for NMD in general? Goal?
70% HR max
20-30 mins/day
3-4x/week
GOAL: Dec daily energy cost and/or improve energy efficiency
How will you know if you pushed a pt too far with ex?
Test -- Ex -- Test Right Away -- rest 60 to 120 seconds -- tet again. If strength is less right after ex, they have ex induced fatigue.
Soreness 1-5 days after (DOMS)
Weakness after exercise
Sense of exhaustion that short rest does not recuperate
How do you find 70% of 1RM with this population?
take 50% of 5RM
What do you do to mm that are <3/5 when you are doing ex for a NMD pt?
Need to be supported, braced, or find an alternate way to do the ex, like pool or gravity eliminated position
What is work capacity and how can we use it in treating NMD pts?
Therex X duration
Take breaks! Longer work capacity due to break so you can do more in a day
Breaks don't affect overall work - in fac, less fatigue and greater recovery of strength have been reported
Why do SCI pts need ex?
They are at greater risk for CVD, DM, skin breakdown, respiratory issues
Tend to get age related dx earlier than general population due to being sedentary
Choice for aerobic ex for SCI pts?
Cycle ergometer, UE ergometer, LE with FES, w/c treadmill, swimming, AMB w/ lofstrands
What did the treadmill study with C4-T12 ASIA C's find?
8 years post had inc VO2 max, muscular changes, and healthier blood lipid profiles
What is CO and how can we increase it in SCI pts?
SV x HR
SV = VR x contractility
Inc VR with breathing, vasoconstriction, mm pump
What are C-sp pts at risk for with ex? Interventions?
Ex-induce hypotension b/c VR sucks due to impaired vasoconstriciton and mm pump in LEs
Also, limited HR and contractility inc (100-120 max) due to lack of SNS innervation and PNS response if complete C-sp lesion
Use ted hose, abdominal binders, or ex in supine with feet up
Difference in high paraplegia (T1-T5) heart funciton, VR, and ex
Can inc HR and contractility due to SNS innervation
Improved respiratory support
Still won't have good VR of LEs due to vasoconstriction issues
May have exaggerated HR response
Difference in low paraplegia (T6-down) heart function, VR, and ex
Some capacity to vasoconstrict/mm pump and inc VR
Much better HR and respiratory response
Temp regulation with a high quadriplegic pt?
No shivering or vasodilation due to impaired SNS innervation
Ned fans or insulation clothing
Diseases classified as Ant Horn Cell dx?
Polio
ALS
Diseases classified as Peripheral Neuropathies?
GBS
Charcot-Marie Tooth
Diabetic Polyneuropathy
Diseases classified as myopathies?
Muscular dystrophy
Myositis/polymyositis
Primary, secondary, and tertiary source of weakness in NMD pts?
Primary: Direct affect of dx
Secondary: Disuse atrophy
Tertiary: Overwork weakness
What is the cause of fatigability in NMD?
CNS will work to recruit more MUs to attempt to sustain output to complete the task
May recruit other mm to complete task too
Results in sense of central fatigue
Why is reinnervated mm hypothesized to be at risk for overwork weakness?
All of the remaining MUs are recruited all the time in order to funciton on a daily basis
Normal mm and MUs are never recruited maximally
What could overwork do the disease process?
Create irreversible mm damage
Accelerate disease process or interfere with recovery
What is Agre's advice on frequency, sets, duration for resistance training post-polio syndrome?
Start 50% of 5 RM
Continue with this amt until pt can do 30 non-fatiging reps
Start over with increased weight and go up to 30 again
What did Drory find for ex with ALS vs. not exercising in stages 1-3?
Improved in pain, fatigue, spasticity, strength, functional stastus, and quality of life
Makes a difference in the early stages of dx
What mm are at risk for overuse in ALS?
The ones with LMN symptoms and less than 3/5
How should you strengthen a mm less than 3/5 when recovering from GBS?
Gravity minimized until the mm can move against gravity
General ex recommendations for GBS
Only train eccentrics needed for fxt activity
Submax exercise - max exercise will not speed up the remyelination/regeneration process
2 modes of exercise delivery for SCI pts?
1. Voluntary recruitment (at level and above. Below level f incomplete)
2. Sensory and/or electrical imput for mm below the level of lesion (treadmill combined with FES ie)
2 systems that inc CO and innervations
Heart: T1-T5
Adrenal Gland: T6-T9 (vasoconstrict)
How do complete quadriplegics increase CO?
Only through turning down of PNS b/c no SNS innervation to heart or adrenal glands
How do yo determine maxHR for complete quad?
120 - the max when PNS is taken out of the equation
Why may a T6 and above para have an exaggerated HR response?
Has innervation to heart but not the adrenal glands
In order to inc CO, will try to crank the HR up to make up for impaired VR
High risk for ex induced hypotension
How much is CO compared to the healthy individual?
Para = 1/2
Tetra = 1/2 to 1/3
How should you determine target HR for SCI pt?
take 50-80% max HR
Add resting HR to it
If complete quad, use 120 as max HR for this equation
Recommendation for ex for SCI pts with partial innervation? ie. incomplete or at level of lesion
Moderate intensity ex not to the point of fatigue
Give 3 components of the muscle affected by Disuse & Aging
1. Type 1 fibers
2. Type 2 fibers
3. MHC Contractile protein
With atrophy what specifically happens to the muscle fiber
Loss in
1. cross sectional area
2. muscle mass
3. Contractile protein

Atrophy is most pronounced in Type IIa fibers
What do Type II fibers shift towards
Type IIx fibers--myosin that is fast & fatiguable
What is the result with structural muscle atrophy that occurs at the whole muscle
Total amount of protein for each fiber type will decrease--thus less contractile protein overall
Why do the relative fiber types shift? What fiber types do we shift to with atrophy?
The relative % of contractile protein and fiber types shifts bc certain types are more affected by atrophy than others
-Type IIa myosin content >> than Type 1

-Relative increase in Type IIx myosin
Does the muscle lose type I fiber? Type II fibers?
The muscle loses type I myosin--but does not lose type I fibers

Muscle also loses Type II myosin--and can lose Type II fibers

Type IIa converts to Type IIx
Describe Type I musle fibers
Aerobic, slowly contracting, resistant to fatigue, with small motor units
Type IIa muscle fibers
Moderately fast contracting, fairly fatigue resistant, medium sized motor units, long-term anaerobic (less than 30 min)
Type IIx muscle fibers
Fast contraction, moderately large motor unit, anerobic (less than 5 minutes, not very resistant to fatigue
Describe changing fiber types with aging
With aging large motor axons that innervate type II fibers die

Type I motor axons will innervate the empty muscle fibers--leading to an absolute loss in the # of Type II motor units

We keep the same # of Type I motor units but they innervate more muscle fibers

Therefore, the muscle will have a greater proportion of type I fibers and motor units relative to the type II units--but this is a relative increase as the absolute amount of type I motor units does not increase
Does disuse and aging directly promote the G&D of Type I fibers and Type I myosin protein
No more type I fibers doesnt not mean that small, slow MU thrive in a deceased model

They shrink and lose contractile protein (myosin)

The type II's get killed and die off by disuse and aging and Type I's are shrunk but not killed off--their left behind to reinnervate the muscle
What makes Type I's grow and develop? What makes type II's become Type IIa (Good type II)?
Increased Use

The degree of change depends on the intensity of your exercise stimulus
-Both types will increase their metabolic capacity, fatigue resistance, and their contractile protein mass (hypertrophy)