Sarcopenia Flashcards

1
Q

aging in Canada

A
  1. Canada’s aging population is increasing at a high rate with adults over 75 growing the fastest
  2. Canada is a car centric country, older adults more likely sedentary leading to institutionalization
  3. current aging pop outnumber working pop, gov must decide how to allocate spending to senior care since we need to spend more in the future with less people paying taxes
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2
Q

sarcopenia definition
1. overview
2. criteria in the literature
3. clinical def

A
  1. progressive loss of muscle mass and function that reduces mobility and QoL by making it harder to do every day tasks independently, and lead to higher fall risk and insitiutionalization
  2. higher inconsitency of diagnositic criteria and indicators for measuring sarcopenia makes it challenging to determine cut off points for sarcopenia tests and thus changes in sarcopenia in the literature, reducing power in meta analysis
  3. loss of muscle mass/strength (1% decrease mass and 3% decrease strength per year starting in late 30s-early 40s), function (gait speed decrease greatly after 50), and size (reduced size and number esp in type II) with age; faster decrease in strength than size due to loss of neurological adaptations, SM replaced by adipose tissue in old muscle therefore thigh circumference and BMI stays the same
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3
Q

declining muscle mass with age

A
  1. muscle mass and function start to decline greatly after late 30s or early 40s
  2. in healthy individual, decline does not reach disability threshold (unable to do ADLs independently) until 80 but poor life choices can accelerate this decline pushing people past disability threshold and into institutionalization and leading to early mortality (dying before 80)
  3. sarcopenic slope is accelerated with inj or illness causing individual to age faster in the period of illness or inj; while young adults may exp wasting from short-term disuse they usually make a complete recovery and can even exp hypertrophy with RT; poor life choices, rapid muscle wasting disorders, chronic muscle wasting disorders, or incomplete recovery in older individuals increase sarcopenic slope and likelihood of crossing disability threshold faster
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4
Q

sarcopenia and disuse

A
  1. Sig disuse loss 10% but in young people resuming habitial activity and training return to healthy normal, older adults have less drop but never return to initial vol
  2. when this cycle repeats, accumulated muscle loss
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5
Q

root causes of sarcopenia
1. risk factors
2. protein synthesis and breakdown
3. hallmarks of aging

A
  1. many risk factors such as MU pool, capillarization and CV health, protein absorption and uptake, thus sarcopenia impairs many different parts of the body, all factors that influence sarcopenic is called anabolic res
  2. SM has a balance between muscle PRO synthesis and breakdown, must consume AA from diet to synthesize PRO, older SM has more impaired PRO synthesis comp young SM, age has no impact on PRO breakdown
  3. all hallmarks of normal aging related to sarcopenia, aggravation of hallmarks accelerates aging and amelioration slows aging process and increases lifespan
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6
Q

satellite cells

A
  1. normally quiescent SM stem cell (denoted by marker Pax7, upon activation (denoted by myoD) by stimulus such as exercise proliferate to replenish stem cell pool and differentiate into satellite cell by fusing to myofibre and donating nucleus to provide new myonuclei (denoted by DAPI) with various cytokines influencing the process
  2. myonucleus reg muscle activity thru transcription to create PRO for SM maintence, repair, and growth
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7
Q

capillaries and satellite cells relationship in muscle repair

A
  1. attraction exists between endothelial and satellite cells, capillaries provide muscle with O2, nutrients, and growth factors from systemic environment and influence function for muscle repair
  2. cell to cell communication using cytokine exchange
  3. with aging decrease SM CSA, number and function (don’t respond to exercise unlike youg people) of type II satellite cells, capillaries per fibre, and index of blood perfusion exclusively in type II due to greater distance between capillaries and type II satellite cells for decreased muscle repair
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8
Q

capillarization and CV health in aging

A
  1. sedentary adults in 60s experience 20% decrease in CO and VO2max declines from peak capcaity by 35-40% in sedentary men and 65% in women
  2. END trained individuals have higher capilliarazation and lean mass which allow them to maintain a certain level of aerobic capacity, thus decrease in capilirazation in decreases lean mass which decreases aerobic capacity
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9
Q

anabolic resistance on proteostasis
1. MPS at baseline and exercise
2. MPB at baseline and exercise

A
  1. no differences between MPS at rest between young and old; both increase MPS in response to exercise but MPS response x2 greater in young comp old esp at higher intensity, since MPS rate is affected by anabolic res; however when old trains x2 the amount as young able to stim same level of MPS as young
  2. no difference in MPB between young and old at baseline or following exercise thus ages does not have an effect on MPB
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10
Q

RT on sarcopenia
1. strength and size
2. satellite cell content
3. capillarization

A
  1. strength increases greatly in frail old adults due to neurological adaptations; all people increase in size, able to hypertrophy at any age but rate of growth in size has a large variability, but might not see results if shorter training period since older adults req more vol to increase muscle CSA
  2. SC number linked to capillary density, RT increases satellite cell content in type II muscle
  3. greater type II hypertrophy after RT for those who had higher muscle capillarization at baseline comp those with low capillarization; pre-RT no change in type II SC content or response after acute exercise but increase capillarization post-RT increase type II SC number and response better to exercise
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11
Q

END on sarcopenia

A
  1. increases fibre CSA, number of SC, VO2peak, mitochondrial enzymes, and capitalization
  2. even small stimulus can stim hypertrophy by recovering degraded muscle rather than making new muscle
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