Impaired Muscle Performance

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Impaired Muscle Performance

BPHTI: PTH5201 Jul 2015 1


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At the end of this unit the student will be able to:

Explain the consequences associated with sarcopenia in

an aging population and

collate the studies describing ways physical therapistscan counter the associated adverse changes.

Learning outcomes:



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The age-related loss of muscle, coined sarcopenia in

!"!. The loss of s#eletal muscle mass is accompanied by the

loss of muscle strength, rate of force development, and

muscle power.

$arcopenia contributes to deficits in mobility, a decline

in functional capacity, and a reduction in s#eletal

muscle oxidative capacity.

These muscle impairments, in combination with agreater fat mass, contribute to the greater ris# of falling,

frailty, and the development of comorbid conditions

such as insulin resistance or type % diabetes that

adversely impact health.

Consequences of Sarcopenia



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&ecause muscle mass represents the protein reserve of

the body, sarcopenia is associated with a diminished

ability to meet the extra demand of protein synthesis

that is so often necessary with disease and in'ury in oldage.



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Changes in Muscle Structure and

Function Associated with Aging



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A primary mechanism attributed to the development of

sarcopenia in those aged () to (* years and older is a

progressive denervation and reinnervation process

involving the alpha motor neurons.

A *)+ decline in available motor neurons(,%)-%% and a

diminished number and availability of satellite cells

that parallel the age-related temporal changes in muscle

sie and strength have been noted. iber type grouping also characteries aging as

remaining alpha motor neurons enlarge their own

motor unit territory.

Impaired Regeneration of Muscle and the

Progressive enervation !Reinnervation Process"



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hen coupled with the reduction in alpha motor

neurons and motor units, a reduced motor coordination

and strength results, which may underlie age-related

mobility impairments.

/n addition, muscle fiber regeneration is impaired more

in type // fibers than type / in large part due to the

degradation of the myogenic satellite stem cells.

0ompounding these age-related losses are reports ofsubstantially lower basal mixed, myofibrillar, or

mitochondrial muscle protein synthesis rates in older

adults versus younger ones.



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0onsistent with the current interpretation of sarcopenia,

older individuals become wea#er over time.

These strength deficits, however, do not necessarily

match the magnitude of atrophy that has occurred. /n part, this may be explained by the fact that muscle

generally becomes wea#er even if atrophy is avoided,

which suggests that force production, separate from

muscle atrophy, also is impaired with aging. /t appears that the age-related impairment in muscle

force is only partially explained by the loss in muscle

mass.

eficits in A#solute and Specific Force

$eneration"



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The declining force production abilities with aging

occur at a faster rate than the decline in muscle mass1

hence, neural alterations are also thought to contribute

to muscle wea#ness by reducing central drive to the

agonist muscles and by increasing coactivation of the

antagonist muscles.

Muscle Activation eficits"



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A reduction in muscle 2quality3 due to infiltration of

fat and other noncontractile material such as connective

tissue, coupled with changes in muscle metabolism,

also contribute to the deteriorating muscle condition

and advancing frailty with age.

/n addition, oxidative damage accumulated over time is

thought to lead to mitochondrial 45A mutations,

impaired mitochondrial function, muscle proteolysis,and myonuclear apoptosis.

eteriorating Muscle %ualit& and

Meta#olism"



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hole body resting metabolic rate 67879

progressively declines at a rate of + to %+ per decade

after %) years of age.

This change is lin#ed with age-associated decreases inmetabolically active whole-body fat-free mass.

Changes in Meta#olic Function Associated

with Aging



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Altered 'ndocrine Function and Its

Consequences"



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Aging, as well as several chronic medical conditions

6chronic obstructive pulmonary disease 0;a 6T5-a9, interleu#in ( 6/?-(9, 0-reactive

protein 607


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The aging-associated damage to muscle mitochondrial

45A 6mt45A9 may reduce the rate of muscle cell

protein synthesis, adenosine triphosphate 6AT


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Age related loss of myocytes via apoptosis has been

suggested to be a #ey mechanism behind the muscle

loss associated with human aging as well, though this

evidence is preliminary.

7ecent data demonstrate that physical exercise can

mitigate s#eletal muscle apoptosis in aged animals.

These basic science considerations should prompt the

clinician to consider exercise as not only a counter toloss of physical fitness and function, but perhaps also a

mode of slowing down the apoptotic pathways

underlying sarcopenia.

Apoptosis"



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iseases and Conditions Associated with

S(eletal Muscle ecline"



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@enetic epidemiologic studies suggest that between

(+ and (*+ of an individualBs muscle strength and

up to *C+ of their lower extremity performance can be

explained by heredity.

Influence of $enetics"



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7esistance training for individuals age (* years and

older induces predictable increases in muscle strength,

muscle power, and mobility function in community-

dwelling older persons, nursing home inhabitants, and

the hospitalied older adults.

$ignificant improvements in strength and mobility

function have also been reported in individuals ")

years of age and older.

M)SCL' C*)+,'RM'AS)R'S

F*R *L'R I+I-I)ALS



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ithout a doubt, older individuals who participate in at

least ( to % wee#s of resistance training will improve

their strength and mobility function.

$trength improvements range from %*+ to well over

))+.

The effects of age may be influenced by gender,

duration of training, or muscle groups investigated.

Adaptations in Muscle Strength and

Mo#ilit& Levels with Resistance '.ercise"



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7esistance training that specifically targets muscle

power 6D)+ to C)+ 78, 2as fast as possible39 has a

significant impact on physical functioning as well as

muscle power production and muscle strength.

?eg muscle power is especially important when

considering that muscle power declines more sharply

than strength in older individuals.


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The impact of resistance training on muscle

hypertrophy, an expected outcome in the young, is less

predictable in older individuals, especially those older

than age ") years.

;lder women 6mean age "* years9 have also been

reported to have a blunted hypertrophy response at both

the whole muscle and fiber level.

This limited hypertrophic response may or may not beimportant clinically as muscle sie has been reported to

be less influential than muscle power and strength on

functional mobility.

Adaptations in Muscle Si/e and

Composition with Resistance '.ercise"



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There is evidence suggesting that resistance training

that exploits the high-force>producing capabilities of

eccentric muscle activity are both feasible and effective

for older individuals.

&ecause eccentric resistance training can produce high

forces at relatively low energetic costs, eccentrically

biased resistance training programs are especially

useful in an older population.

Resistance '.ercise via +egative0

'ccentricall& Induced 1or("



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/n addition to decreased physical activity, inadequate

protein inta#e may also contribute to sarcopenia.

5utritional inta#e, li#e exercise, is a modifiable

countermeasure that may help to minimie loss of leanmuscle tissue and muscle strength in older adults,

though there is significant controversy as to the

amount, quality, and timing of protein supplementation

in this population.

+utritional Inta(e as a Countermeasure

for Sarcopenia



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0urrently, it is recommended that all meals for olderadults contain a moderate amount6%)+ to *+ energy9

of high-quality protein.


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Andrew A. @uccione, 7ira A. ong, 4ale Avers, %)%@eriatric


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,han( &ou

BPHTI PTH5201 J l 2015 27

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Impaired Muscle Performance