Sci - Ex Pres For Nmd

Front 1

3 recommendations for working with pts with NMD?

Back 1

Avoid overwork
Avoid Eccentric ex
Avoid stressing a mm <3/5 (No resistance ex!)

Front 2

How do you avoid overwork?

Back 2

Submax intensity - pt should be able to perform more reps when they stop the set

Front 3

Why should pts avoid eccentric ex?

Back 3

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

Front 4

What is overuse weakness?

Back 4

Dec strength directly related to activity

Front 5

What caused all these recommendations for ex with NMD?

Back 5

Postpolio syndrome coined in 84 - new onset of weakness in mm that were once affected by polio without polio coming back

Front 6

What is the anecdotal evidence to suggest these recommendations for ex are valid?

Back 6

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

Front 7

What is the theory for overuse causing further damage in NMD?

Back 7

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

Front 8

What type of "expression" do MUs tend to adopt with NMD? What does this lead to?

Back 8

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

Front 9

Primary complaints of pts with NMD with exercise in general?

Back 9

Weakness and atrophy/wasting
Pain
Fatigue

Front 10

Are pts at greater risk for disuse weakness or NMD weakness (overuse)?

Back 10

Disuse weakness - we must find a place where we are preventing disuse weaknees and overuse weakness

Front 11

What happens to mm fibers with disuse?

Back 11

Dec oxidative capacity = fatigue fast
Pt will develop more fast twitch fibers

Front 12

What does resistance ex do to mm fibers?

Back 12

Inc oxidative and fatigue resisdent fibers
Type I to Type IIA
Type IIX to Type IIA

Front 13

Frequency, intensity, duraiton of aerobic ex for NMD in general? Goal?

Back 13

70% HR max
20-30 mins/day
3-4x/week
GOAL: Dec daily energy cost and/or improve energy efficiency

Front 14

How will you know if you pushed a pt too far with ex?

Back 14

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

Front 15

How do you find 70% of 1RM with this population?

Back 15

take 50% of 5RM

Front 16

What do you do to mm that are <3/5 when you are doing ex for a NMD pt?

Back 16

Need to be supported, braced, or find an alternate way to do the ex, like pool or gravity eliminated position

Front 17

What is work capacity and how can we use it in treating NMD pts?

Back 17

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

Front 18

Why do SCI pts need ex?

Back 18

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

Front 19

Choice for aerobic ex for SCI pts?

Back 19

Cycle ergometer, UE ergometer, LE with FES, w/c treadmill, swimming, AMB w/ lofstrands

Front 20

What did the treadmill study with C4-T12 ASIA C's find?

Back 20

8 years post had inc VO2 max, muscular changes, and healthier blood lipid profiles

Front 21

What is CO and how can we increase it in SCI pts?

Back 21

SV x HR
SV = VR x contractility
Inc VR with breathing, vasoconstriction, mm pump

Front 22

What are C-sp pts at risk for with ex? Interventions?

Back 22

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

Front 23

Difference in high paraplegia (T1-T5) heart funciton, VR, and ex

Back 23

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

Front 24

Difference in low paraplegia (T6-down) heart function, VR, and ex

Back 24

Some capacity to vasoconstrict/mm pump and inc VR
Much better HR and respiratory response

Front 25

Temp regulation with a high quadriplegic pt?

Back 25

No shivering or vasodilation due to impaired SNS innervation
Ned fans or insulation clothing

Front 26

Diseases classified as Ant Horn Cell dx?

Back 26

Polio
ALS

Front 27

Diseases classified as Peripheral Neuropathies?

Back 27

GBS
Charcot-Marie Tooth
Diabetic Polyneuropathy

Front 28

Diseases classified as myopathies?

Back 28

Muscular dystrophy
Myositis/polymyositis

Front 29

Primary, secondary, and tertiary source of weakness in NMD pts?

Back 29

Primary: Direct affect of dx
Secondary: Disuse atrophy
Tertiary: Overwork weakness

Front 30

What is the cause of fatigability in NMD?

Back 30

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

Front 31

Why is reinnervated mm hypothesized to be at risk for overwork weakness?

Back 31

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

Front 32

What could overwork do the disease process?

Back 32

Create irreversible mm damage
Accelerate disease process or interfere with recovery

Front 33

What is Agre's advice on frequency, sets, duration for resistance training post-polio syndrome?

Back 33

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

Front 34

What did Drory find for ex with ALS vs. not exercising in stages 1-3?

Back 34

Improved in pain, fatigue, spasticity, strength, functional stastus, and quality of life
Makes a difference in the early stages of dx

Front 35

What mm are at risk for overuse in ALS?

Back 35

The ones with LMN symptoms and less than 3/5

Front 36

How should you strengthen a mm less than 3/5 when recovering from GBS?

Back 36

Gravity minimized until the mm can move against gravity

Front 37

General ex recommendations for GBS

Back 37

Only train eccentrics needed for fxt activity
Submax exercise - max exercise will not speed up the remyelination/regeneration process

Front 38

2 modes of exercise delivery for SCI pts?

Back 38

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)

Front 39

2 systems that inc CO and innervations

Back 39

Heart: T1-T5
Adrenal Gland: T6-T9 (vasoconstrict)

Front 40

How do complete quadriplegics increase CO?

Back 40

Only through turning down of PNS b/c no SNS innervation to heart or adrenal glands

Front 41

How do yo determine maxHR for complete quad?

Back 41

120 - the max when PNS is taken out of the equation

Front 42

Why may a T6 and above para have an exaggerated HR response?

Back 42

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

Front 43

How much is CO compared to the healthy individual?

Back 43

Para = 1/2
Tetra = 1/2 to 1/3

Front 44

How should you determine target HR for SCI pt?

Back 44

take 50-80% max HR
Add resting HR to it
If complete quad, use 120 as max HR for this equation

Front 45

Recommendation for ex for SCI pts with partial innervation? ie. incomplete or at level of lesion

Back 45

Moderate intensity ex not to the point of fatigue

Front 46

Give 3 components of the muscle affected by Disuse & Aging

Back 46

1. Type 1 fibers
2. Type 2 fibers
3. MHC Contractile protein

Front 47

With atrophy what specifically happens to the muscle fiber

Back 47

Loss in
1. cross sectional area
2. muscle mass
3. Contractile protein

Atrophy is most pronounced in Type IIa fibers

Front 48

What do Type II fibers shift towards

Back 48

Type IIx fibers--myosin that is fast & fatiguable

Front 49

What is the result with structural muscle atrophy that occurs at the whole muscle

Back 49

Total amount of protein for each fiber type will decrease--thus less contractile protein overall

Front 50

Why do the relative fiber types shift? What fiber types do we shift to with atrophy?

Back 50

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

Front 51

Does the muscle lose type I fiber? Type II fibers?

Back 51

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

Front 52

Describe Type I musle fibers

Back 52

Aerobic, slowly contracting, resistant to fatigue, with small motor units

Front 53

Type IIa muscle fibers

Back 53

Moderately fast contracting, fairly fatigue resistant, medium sized motor units, long-term anaerobic (less than 30 min)

Front 54

Type IIx muscle fibers

Back 54

Fast contraction, moderately large motor unit, anerobic (less than 5 minutes, not very resistant to fatigue

Front 55

Describe changing fiber types with aging

Back 55

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

Front 56

Does disuse and aging directly promote the G&D of Type I fibers and Type I myosin protein

Back 56

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

Front 57

What makes Type I's grow and develop? What makes type II's become Type IIa (Good type II)?

Back 57

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)