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Kinesiology > 4434 Midterm > Flashcards

4434 Midterm Flashcards

1
Q

Most common types of disability

A
  1. Pain related
  2. Mobility
  3. Flexibility
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2
Q

Aging is the accumulation of what?

A

Physiological, psychological and social changes

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3
Q

Senescence

A

Decline of biological function

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4
Q

Chronological age

A

Exact age from birth - Can’t be modified

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5
Q

Biological age

A

Age determined by physiology - can be modified

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6
Q

Functional age

A

Age in terms of functional performance - can be modified

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7
Q

Programmed Longevity Theory

A

Aging is genetically programmed
- Biological clock turning specific genes on/off
- Pre-programmed cell death

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8
Q

Hayflick’s Limit

A

Telomeres are caps on the end of chromosomes - once no cap damage to chromosomal DNA which leads to a stop in function/division so can’t make more healthy cells

Telomeres shorten with each division

Limit to the # of times cell can divide before it dies

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9
Q

Telomerase

A

Enzyme that helps to replace DNA and replenish the lost telomere.
- Does not exist in most adult cells
- Don’t make more telomerase as an adult

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10
Q

Immunological Theory

A

Left with some uncontrolled inflammation which can lead to cell death that is thought to lead to the process of aging

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11
Q

Immune System Breakdown

A

Have non-specific - e.g., skin barrier and phagocytes (made in bone marrow)

Have specific - B cells and T cells which respond if it’s not taken care of by phagocytes

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12
Q

B cells

A

Attacks invaders OUTSIDE the cells

Made in bone marrow

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13
Q

T cells

A

Attacks infected cells - respond to pathogens inside a cell

Made in thymus

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14
Q

Immune system with aging

A

Weakened barriers

Phagocyte dysfunction

Decrease in bone marrow so lowered B-cells

Decrease in thymus mass so lowered t-cells

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15
Q

Immune system and cell division

A

Phagocytes - do NOT divide

Bone marrow - DOES divide

T-cells DO divide

B-cells - do NOT divide

Thymus - does NOT divide

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16
Q

Immune system flow chart

A

Reduction in barriers, phagocyte function, b-cells & t-cells –> decrease in immune system function –> increased inflammation

also have increase in ROS pointing to increased inflammation

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17
Q

How can we prevent this low level chronic inflammation?

A

Exercise & Nutrition
- Nutrition can help reduce the amount of inflammation that acts through ROS
- Exercise can reduce the amount of inflammation, can improve immune system function and ROS
- Can use anti-inflammatories

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18
Q

Describe the relationship between the programmed longevity theory and the immunological theory of aging

A
  • Both are systemic and affect multiple systems
  • Hayflick’s is specific to cells that continues to divide throughout life. Bone marrow continues to divide. If telomere length lessens every time they divide you can explain the reduction in bone marrow cells by Hayflick’s limit
  • If you decrease number of cells in bone marrow (we do because we see decrease in mass) so our ability to produce b-cells and phagocytes lowers. They themselves (b and phagocytes) are not susceptible to Hayflick’s limit but the tissue that makes them is susceptible
  • Eventually would lose t-cells because they do divide and this impacts immune system function
  • Things not subjected to Hayflick’s limit are subjected to the biological clock
  • The dysfunction in the immune system could lead to (genetic) changes or cell death that isn’t related to Hayflick’s limit.
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19
Q

Hypothalamus

A
  • Portion of the brain
  • One function: connect the nervous system with endocrine system through pituitary gland
  • Stimulates or inhibits functions to maintain homeostasis
  • Reduction of cells in hypothalamus with age
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20
Q

Hypothalamus Pathway

A
  • Hypothalamus sends output to pituitary and through that gland we communicate with many different endocrine organs to either inhibit or increase production of hormones
  • In some cases we have direct contact from the pituitary to the target tissues
  • In other cases (mostly cardiovascular system) it’s a multi-step process in this example through the adrenal cortex
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21
Q

Endocrine organs with age

A
  • The endocrine organs change. See an increase in calcification. There is more calcium deposits and this means that the endocrine organs are less able to function appropriately
  • The calcified tissue is non-functional so have less functional and more non-functional tissue in that organ as calcium can’t release hormones
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22
Q

How could you test the importance of hypothalamus cell # on aging?

A

The most direct way is to increase/decrease number of cells in the hypothalamus and then observe the impact on some function that has to do with aging or endocrine function

  • Looked at coordination which had to do with hitting a lever to get food. There is a sig drop in function for those that had a decrease in hypothalamus cells
  • Same is true when they looked at treadmill running. How much work they could put out before giving up. Impacted by metabolism. Again no diff between control and increase but decrease fewer cells
  • Same thing in cognitive. Novel object. The reduction in number of hypothalamus cells was important
  • Reduction in number of cells significantly impacts their ability to socialize
  • We have enough cells in our control system (in our hypothalamus) to produce the functions we need to. So increasing them doesn’t give us any increase in performance.
  • If you’re older and have lost cells then adding cells was beneficial in those mice

This is direct evidence that the loss of hypothalamus cells we expect with age has an impact on our hormones and all the functions associated with that endocrine system.

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23
Q

List one similarity between the immunological theory and the endocrine theory of aging.

A
  • Both involve a decrease in mass of an organ that affects the system
    Not the direct cells themselves
  • In immunological see decrease in thymus and decrease in hypothalamus in endocrine
  • The calcification in the endocrine organs can contribute to the inflammation.
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24
Q

Describe the relationship among the programmed longevity theory, the immunological theory and the endocrine theory of aging.

A
  • All 3 involve some sort of damage to cells that results in a loss of function (whether it’s loss of hormones being produced, t-cell,b-cells)
  • Biological clock could be involved in all 3

As things stop working you put more stress on the system.
- Endocrine system isn’t functioning and so we have things being thrown out of homeostasis and that lack of homeostasis or calcification of those endocrine organs can increase inflammation which means further taxing on the immune system and then the function then continues to decline

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25
Q

Wear and Tear Theory

A

Progressive damage to cells and tissues due to use over time

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26
Q

Free Radicals

A
  • Atoms with an uneven number of electrons (unpaired electron)
  • Unstable
  • Easily react with other (healthy) molecules

The atom which is necessary to the healthy tissue then becomes unstable so it leads to a disruption of function in that tissue

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27
Q

Reactive Oxygen Species

A

Free radicals that contain oxygen

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28
Q

How and why do we get ROS?

A
  • Produced through metabolism
  • ETC in mitochondria
  • Functions: cell signalling –> cell differentiation, autophagy, immune system
  • Highly regulated
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29
Q

Autophagy

A

ROS - when cells should be killed or consumed they help to signal that

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30
Q

ROS and inflammation

A

ROS are a signal to the immune system to come deal with that damaged tissue. Damaged tissue produces ROS and the more ROS the more inflammation. This is fine in a healthy system.

Antioxidants help by donating an electron so they get rid of ROS

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31
Q

Oxidative stress

A

When we don’t have enough antioxidants to neutralize the ROS.
- can get damage to DNA in cells
- See DNA fragmentation, mitochondrial DNA damage, telomere attirition

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32
Q

Other causes of ROS

A
  • UV rays
  • Air pollution
  • Chronic inflammation
  • Smoking
  • Obesity
  • Radiation
  • Metabolism
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33
Q

Reducing ROS

A

Diet and Exercise
- Caloric restriction (describe the study in mice)

Thinking originally was that if you restrict amount of calories that a person/animal are taking in that will reduce the resting metabolic rate. And if that is reduced you’ll reduce amount of ROS being produced naturally through metabolism. Some convincing evidence in animals that it works well.
- The survival rate stays elevated longer the more restriction there is. Max lifespan increases the more caloric restriction there is.
- When we exercise, we increase metabolism so short term increase in ROS but long-term increase in our ability to deal with them and increase our natural antioxidants

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34
Q

There is a reduction in muscle mass with advanced age. How would this reduction be explained by each of (i) the programmed longevity theory, (ii) the immunological theory, (iii) the endocrine theory, and (iv) the wear and tear theory?

A

Programmed longevity – muscle cells programmed to die after a certain period of time (have a code that is preprogrammed)

Immunological – as we use our muscles, they produce waste products through generation of ATP primarily and if they accumulate that leads to inflammation. Immune system isn’t as good at dealing with it so end up with chronic inflammation which leads to cell death
- Waste product can lead to inflammation – body can’t keep up with inflammation b/c with age you have a weakened immune system (have fewer cells like phagocytes, b cells or t cells that can respond to the inflammation, so it doesn’t get taken care of). Have this low level of chronic inflammation which will disrupt cell function and will lead to cell death.

Endocrine – decreased cells in hypothalamus, effects system producing growth hormone (hypothalamus controls output to endocrine organs). Reduced input and reduced function b/c of calcification so those organs are less able to produce correct amount of hormone. Could be something like growth hormone (which is affected) which helps maintain healthy function in muscle.
- When muscle cells die, they get replaced by fat cells which will affect endocrine function

Wear and tear – as we age produce more ROS, which we do produce naturally through metabolism but have more accumulation as we age (less able to deal with it so out of balance between antioxidants and ROS). When elevated level of ROS present in and around cells that elevate level will eventually disrupt cell function as it damages all types of DNA and leads to cell death which is a loss of muscle mass.

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35
Q

Components of CV system

A
  1. Heart
  2. Blood vessels
  3. Nervous system
  4. Blood
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36
Q

Functions of CV system

A
  1. Transport of nutrients, gases, waste products
  2. Maintain body temp
  3. Protect from infection
  4. Distribute hormones
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37
Q

3 main changes in the heart as we age

A

Decrease valve function

Death of pacemaker cells

Thickening and decreased elasticity of LV wall

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38
Q

Decrease valve function

A

Cell loss & dysfunction
- Repeated mechanical stress (and hypertension)
- Infection/inflammation
- Genetic

39
Q

Death of pacemaker cells

A

Cell loss & dysfunction
- ROS
- Infection/inflammation
- Genetic

40
Q

Thickening & decreased elasticity of LV wall

A

Myocyte death/hypertrophy, increased fibrosis
- Repeated mechanical stress (and hypertension)
- ROS
- Infection/inflammation
- Genetic
- Hormones

41
Q

Overall changes in heart with age

A
  • Decrease contractile force
  • Decrease CO
  • Decrease blood flow
  • Increase BP
  • Increase arrhythmia
42
Q

Describe three changes in the heart with advanced age, including the impact on CV function. Explain one of the three changes based on each of the programmed longevity theory, the immunological theory, the endocrine theory, and the wear and tear theory of aging.

A
  • Decrease valve function
  • Death of pacemaker cells
  • Thickening & decreased elasticity of LV wall
  • These are the 3^ Increased fibrosis of LV wall can lead to increased BP especially in BP as the stiffness means the blood is hitting the wall harder every time. Decrease in valve function can contribute to reduction on blood flow. Death of pacemaker cells can lead to arrythmias.
  • Death of pacemaker cells may be preprogrammed to die – not Hayflick’s limit b/c neural cells don’t contribute to divide throughout life but it’s possible that there is some genetic code that tells the pace maker cells when to die.
  • Reduction in function of the valves – reduction in hypothalamus, reduction in release of hormones and that reduction in hormones could effect HR (and would effect it). So if you have increase in HR due to hormonal imbalance means there is more wear and tear on the valves. This is an indirect explanation of how endocrine function can affect valves. More direct is wear and tear – degradation over time of the valve cells.
  • Endocrine theory can also play a role in LV mass. Loss of hypothalamus cells so lowered output of hormones. Can affect myocytes of the heart. May affect fibrosis process. Also see a reduction in things like growth factors that help maintain those muscle cells.
  • Immunological theory – for fibrosis the chronic inflammation leads to weakened immune system which increases rate myocytes die at.
43
Q

Atherosclerosis

A
  • Narrowing of the artery due to plaque build-up
  • Lipids, cholesterol, Ca2+

Why?
- Decrease immune system function
- Increase inflammation
- Increase ROS
- Decrease decalcification

44
Q

Arteriosclerosis

A

Thickening/stiffening/hardening of artery wall

Why?
- Repeated mechanical stress (increase hypertension)
- ROS
- Genetic
- Infection/inflammation
- Hormones

45
Q

Blood vessel damage causes

A
  • Increase in inflammation and increase in ROS leads to disruption of typical decalcification processes. Typically, these deposits form and we have decalcification processes that get rid of them fairly quickly. But with the 2 things above (inflammation and ROS) our ability to get rid of the calcium deposits is lower.
  • Hypertension can make this worse – will increase mechanical stresses. Also see some loss of cells b/c of the other things on the slide (ROS, genetic, inflammation, poor hormone control). See loss of smooth muscle cells that are replaced with fibrous tissues that are less elastic.
46
Q

List one similarity and one difference between atherosclerosis and arteriosclerosis.

A
  • Both are narrowing of the arteries. Increased BP so down the line might get more wear/tear on the arteries in both cases. Both result in reduction of blood flow (less space available).
  • ROS is a possible contributing factor in both cases.
  • The reason we have the reduction in blood flow is different. Risk of death from athero is greater.
  • Wear and tear is more directly involved in arteriosclerosis. Less likely to explain the buildup of those plaques.
47
Q

Impact on heart and BV

A

↓ Contractile force
↓ Cardiac output
↓ Blood flow -
↑ Blood pressure -
↑ Arrythmia
↓ Responsiveness of Baroreceptors -

ones with dash have further contributions from changes in blood vessels

48
Q

Baroreceptors

A

Mechanical receptors
- Detect changes in blood pressure/volume
- Maintain appropriate blood pressure

Detect changes in stretch of these tissues. Neural receptors (as in they are attached to the nervous system)

Increase in BP –> increase stretch –> decrease HR
Reduction in BP –> reduction in stretch –> increase HR

49
Q

Where are the baroreceptors?

A

Carotid sinus receptors and aortic arch

50
Q

Baroreceptors with age

A
  • The receptors stay intact but the tissue it’s in becomes stiffer so end up with reduction of responsiveness of baroreceptors.
  • Need a bigger change in BP for the baroreceptors will respond in either direction which means it’s more challenging to maintain BP.

↑ Orthostatic hypotension
↓ Responsiveness to onset/offset of exercise (longer to increase and return to baseline)

51
Q

What is Orthostatic hypotension?

A

When you change positions e.g., from sitting to standing – your BP drops rapidly. Typically, this is compensated for by baroreceptors. BP drops rapidly from sitting to standing typically baroreceptors notice this almost immediately and increase your HR to compensate. Common cause of falls in older adults.
- In older adults, b/c there is a lag (need a bigger change in BP before it’s detected by baroreceptors) much more frequently have the feeling of dizziness when standing. Don’t get that increase in HR so aren’t circulating oxygen enough.
- Because of these changes in the arteries the mechanical receptors responding to stretch need more input before they became activated.
- Orthostatic hypotension –BP drops rapidly when we change posture – that feeling of dizziness accompanied with that.
Takes longer to increase that cardiovascular response and it takes longer for it to return to baseline after you have stopped exercising

52
Q

CV short term response to exercise

A
  • Increase HR
  • Increase SV
  • Increase BP
53
Q

Pressor response

A
  • Chemo/mechanoreceptors
  • CV Control centers
  • Increase SNS and decrease PSNS
  • Increase HR, BP, SV
54
Q

Changes to pressor response with age

A

Start with decreased function and response - decreased sensitivity
- Increase stiffness, decrease muscle mass
- Decreased feedback to CV centers
- Decreased SNS response

  • One change is change in the muscle itself. Muscle becomes stiffer. So with less mass have fewer sensory receptors in the muscle. Increased stiffness means mechanoreceptors are not as responsive. Need a bigger mechanical change to stimulate a response. Have a reduced sensitivity of the sensors (don’t function as well). Takes bigger metabolic change (chemicals in muscle) before the chemoreceptors become activated.
  • This means decreased feedback so less feedback to cardiovascular control centers of the brain. Sensory neurons also translate info more slowly, so less info and slower to get to the brain. So less of a sympathetic response from the SNS.
55
Q

Based on the pressor response, explain why warming up before exercise is particularly important for older adults.

A
  • The warmup allows the CV system to slowly build up its output to supply enough blood to the working muscles to support the movement. Allowing the receptors the time to respond.
  • If you start with high intensity of exercise the muscles really need a lot of blood flow to support that activity. Because the receptors are taking longer to respond it takes longer for the SNS to respond in older adults. In that case with high intensity exercise you are putting a huge amount of stress on the heart to try to get that blood flow to the working muscles in a compromised system already.
  • When you provide a warmup you are giving enough time for the receptors to respond to the changes in the muscle. Need more buildup of those metabolic byproducts for the chemoreceptors and more mechanical build up for the mechanoreceptors before the sensory neurons become activated.
56
Q

Longterm CV responses to exercise

A
  • Decreased resting HR
  • Increase SV
  • Decrease BP
  • Increase exercise capacity

functionally:
- Increased longevity
- Increased function
- Decreased cholesterol
- Decreased risk of diabetes

57
Q

Ontario Exercise Heart Trial

A

Some of the first work in this area (exercise being safe in older adults) at western.
- Did this first trial. Developed an exercise protocol specifically for older adults who were cardiac rehab patients. At the time this was unheard of. Did this in late 70’s early 80’s
- They knew the benefits of exercise were so vast and if you didn’t exercise thought cardiovascular functions would continue to decline
- They then founded the Canadian Centre for Activity and Aging – tested exercise protocols on diff populations of older adults.

58
Q

Skeletal System Function (5)

A
  1. Support structure
  2. Allows movement
  3. Makes blood cells
  4. Protection for organs
  5. Stores minerals
59
Q

Skeletal system and age (4)

A
  1. Decreased bone density
  2. Decrease in concentration of minerals (Ca2+ and phosphate)
  3. Decrease in collagen
  4. Decrease in bone marrow

Bones become less flexible and more brittle - see less bone mass and poorer quality

60
Q

Osteoblasts

A

Cells that form new bone
- produced in bone marrow

61
Q

Osteoclasts

A

Cells that dissolve bone (resorption)
- see more osteoclast activity with age (not number but function)

62
Q

Osteocytes

A

Mechanosensors that help signal bone remodelling
- Respond to loading on the bone. When there is excessive stress and maybe damage the osteocytes signal the osteoclasts to come in and dissolve the weakened portion of the bone and signal the blasts to come in and replace that bone that is resorbed.

63
Q

What leads to the imbalance of osteoclasts and osteoblasts with age?

A

Decreased osteoblasts in marrow
- Increase in fat deposits (produce ROS)
- Increase ROS (contributes to further marrow loss)

Increase Inflammation
- Decrease bone healing

Decrease Ca2+, Vitamin D
- Decreased absorption of Ca+
- Calcium is needed to form bone and calcium needs vitamin D

Hormonal Imbalance
- Increase parathyroid hormone (increase resorption)
- Decrease estrogen (normally inhibits osteoclasts)

64
Q

Osteoporosis

A

Reduction in bone mass/density
- Loss of bone tissue and mass
- Bone becomes more porous

65
Q

Osteoporosis Development

A

Mid 30s
- Bone density starts to decline

Osteopenia
- Bone loss not as severe as osteoporosis

Osteoporosis
- Not usually detected until a break or develop the classic Dowager’s hump

66
Q

Based on the physiology of age-related declines in bone mass and quality, describe ideas for treating osteoporosis.

A
  • Supplements – vitamin D and calcium – both are needed for calcium to be deposited in the bone
  • Increase antioxidant intake to help neutralize ROS which will help maintain bone marrow which means can maintain production of osteoblasts
  • Hormone replacement therapy – estrogen
  • With osteopenia it depends on the situation but dietary intake of calcium/vitamin D or a high-risk female might prescribe estrogen
  • Can loading be used? Yes it can!
  • Including aerobic exercise to increase blood flow which is critical to these processes
  • Parathyroid hormone inhibitor – reducing amount of parathyroid hormone (can be part of HRT as well) – would reduce osteoclasts activity
  • Anti-inflammatories would help reduce chronic inflammation which helps restore some of the bone healing processes which involve blasts and clasts.
  • Chronic exercise would help to reduce inflammation and ROS. Improved blood flow but also loading.
  • Preventative measures of trying to build up bone in younger years – still dropping off, but starting at a higher point
67
Q

Effects of resistance training on bone density

A

Overall, we can get an increase in bone density but not always
- In the spine we can see that roughly half the studies show a decrease in bone density after a resistance training intervention. Roughly half show an improvement. Not very conclusive results from this.
- In the hip then the results are more consistent. Pretty consistently we see a beneficial effect of that resistance training on bone density.
- One consideration is how we are loading that bone. It’s hard to do resistance training that specifically loads the spine. A lot easier to load the hips. Some of these differences are likely due to difference in actual exercise protocol (type, load, etc.) that was used.
- Is the rate of deterioration between diff bones different? It is! Differences in blood flow, rate of loss of bone marrow, inflammation rates all are contributing factors. So are differences in use – how much we are loading specific bones over time.

Takeaway here is that resistance training can increase bone density but the effectiveness of that resistance training on bone density depends to some degree on which bone we are trying to improve.

68
Q

Arthritis

A
  • Inflammation of the joints
  • Can affect one or multiple joints
  • Involves pain, swelling, decreased range of motion
  • Not directly related to loss of bone mass/density
  • Anything that increase inflammation is more detrimental to older adults than young!
  • Knees are often affected
  • Pain especially with movement
69
Q

Osteoarthritis

A

Most common type
- Long-term degeneration of cartilage exposing bone surface
- The cartilage gets worn down from years of use. Every time you bend the knee get some rubbing of femur on tibia and with that repeated use over time the cartilage starts to wear away in the joint. The cartilage is protecting the ends of the bone so the bones aren’t rubbing against each other. When cartilage rubs away bones are exposed and that is painful especially during movement.

70
Q

Rheumatoid Arthritis

A

Auto-immune disease
- Immune cells attack synovial membrane creating grainy fluid
- Grainy fluid abrades cartilage

In RA, the immune system creates antigens for some unknown reason, which start to break down the synovial membrane which is in between (within) the joints. Acts as a lubricant between bones in a joint allowing them to slide over each other quite easily. The immune system attacks the fluid and then that fluid becomes grainy. A grainy substance between the joints – when the bones of the joint move over each other that graininess starts to wear away that cartilage. No longer a nice substance that helps the bones slide over each other.

-The grainy fluid is the byproduct of the immune system attacking the synovial fluid. Fluid is still there just with a different consistency than before. See swelling/inflammation

71
Q

Compare/contrast osteoarthritis and rheumatoid arthritis, based on the theories of aging that would best explain each.

A
  • Both lead to exposed bone and pain. Both involve swelling and inflammation.
  • In both there is some wear and tear happening
  • Cartilage is being broken down in both cases
  • Negatively effects physical activity in older adults.
  • Decreased ROM in both cases
  • RA involves synovial fluid leading to breakdown of cartilage and OA is the rubbing of cartilage over other cartilage.
  • In OA genetics can play a role, the way you have used your joints can play a factor, runners are more likely to develop OA and more likely to recover from surgical interventions to fix it. This is looking at the fact that not everyone gets OA. Some ppl are better at repairing lost cartilage. Ppl who are overweight are more likely to get it b/c of the way they are loading their joints.
  • OA is wear and tear theory primarily! There is inflammation, and hormones can play a role in how susceptible you are to that damage but not the main theory.
  • In OA could be programmed longevity component as some cartilage cells are programmed to die so won’t repair themselves.
  • RA it would be primarily the immunological theory. There is some wear and tear involved but the initial degradation is happening b/c of a faulty immune response.
  • Getting an increased immunological response – it’s attacking
  • Often athletes have a higher rate of OA – have higher loading over time the more you use your joints. But have better immunological response and lower ROS. That exposure over time can contribute to a higher incidence. Not uncommon to see in older runners.
72
Q

Effects of physical activity in patients with arthritis

A
  • Can’t regrow cartilage once it’s lost so not looking at effects on cartilage growth so looking at pain and QOL.
  • Pain is largely improved by exercise! Not in all cases but most of the time
  • Quite effective at improving subjective ratings of QOL. This is looking strictly at exercise as the intervention
  • Exercise decreases chronic inflammation which helps with pain. Can get antioxidants to the area. Reduction in pain usually comes from reduction in swelling. Not rebuilding that cartilage but are reducing the swelling/inflammation in the area.
  • Moving more regularly is better than being still for a longer period of time and then moving (would be stiffer). Releases endorphins which can be a pain reliever which is separate from the tissue.
73
Q

Sarcopenia

A

Age related decline in muscle mass and strength

74
Q

Proof that sarcopenia involves strength

A

The change in muscle size doesn’t follow the same curve as the change in strength. Strength slope is steeper so it declines faster than muscle size. This tells us that muscle size is not the only thing contributing to that reduction in strength. If it was the only contributor then the curves would look identical. It is a big contributor but not the only

75
Q

2 impacts of motor units

A
  • Recruitment
  • Rate coding
76
Q

Motorneuron death

A
  • Motor neurons typically die off before the muscle fibers do
  • MN die and when they die there can be 2 consequences of their muscle fibers
  • Muscle fibers that no longer have input are called orphan fibers. Ideally the MN of a nearby muscle fiber will generate a new branch of an axon that will re-innervate that orphaned muscle fiber
  • Primarily motor neurons supplying type 2 muscle fibers die off: decrease type 2 muscle fibers and increase # type 1 muscle fibers/MU
77
Q

Reinnervation

A
  • Type 1 MN are the ones mostly doing the reinnervating. When they reinnervate those previously type 2 muscle fibers that muscle fiber will start to take on the characteristics of the other fibers in the unit (i.e., type 1).
  • If a muscle fiber is not reinnervated it will die b/c it is not functional without nervous system input
  • So we are losing type 2 muscle fibers by cell death and are converting some of the reaming ones to type 1 so end up with a decrease in the total number of type 2 fibers so greater proportion of type 1 fibers.
  • Innervation ratio goes up because a type one fiber is now innervating more fibers through re-innervation.
  • Strong connection between nervous system input and response of muscle fibers
78
Q

Why do motorneurons die?

A
  • Increase inflammation
  • Increase ROS
  • Decrease astrocyte function (maintains health of nervous system)
  • Why might motoneurons die? – Hayflick’s limit not applicable but encoded time of death could be, maybe motoneurons that supply type 2 fibers are more susceptible to ROS over time
  • Astrocytes help repair damage to neurons but with age the ability to do that is reduced
  • DISUSE is a huge factor here! When we don’t use these MN they become even more susceptible to damage due to the 3 things on the slide. If not using it, doesn’t get maintained as well!! More susceptible to damage from things like ROS
  • Heneman’s size principle – recruit MU from smallest to largest. Smallest MN typically innervate type 1 (small slow muscle fibers) fibers.
  • Those smallest MU which are the first to be recruited due to size principle are typically innervating slow type 1 muscle fibers. Largest MU/MN are typically innervating type 2. The ones that are first recruited are recruited much more frequently than the larger MU. Young people tend to fully recruit their MU much more frequently than older adults. Even in tasks of daily living more likely to use full recruitment range. This means that the larger MU connecting with type 2 fibers are least likely to be used.
  • This is a big reason as to why they are more susceptible to that cell death.
79
Q

Twitch and reinnervation

A
  • When we have that branching/re-innervation. When this MU fires an AP we get a twitch force as a result of the muscle contracting in response to that MN firing an AP.
  • Before the reinnervation in this example we had 2 fibers contributing to an AP in that MU. One MU firing rate you are now recruiting more muscle fibers so twitch force goes up per motor unit.
  • Now have 3 muscle fibers in this MU so when we have an AP coming down the MN we get a twitch force at all 3 fibers so overall getting more force. Force produced by one MU is now greater than it was before reinnervation. Summing twitch force from more muscle fibers.
  • Makes simple movements more chaotic – especially fine control – much more variable

We all have some variability in our force – the older individual is also trying to hold their force steady. See more jumping around. Much more variability in the ability to hold steady force. This is b/c every time this MU fires it is producing a bigger jump in force than it was in a younger muscle.
- Now have more muscle fibers per motor unit (especially early recruited ones).

80
Q

What are the functional outcomes of reinnervation?

A

Reductions in strength and harder time controlling force during fine control are functional outcomes!

81
Q

Tibialis Anterior and Biceps with age

A

Why is there a bigger loss of MU in their biceps?
- People walk using the tib ant – don’t use the biceps as often
- Biceps has higher proportion of type 2 muscle fibers (those are the motor neurons more likely to die off)
- Use dependence – every time we stand, we use tib ant to some degree so less likely to suffer from disuse
- Those are the 2 main reasons!
- There is data to support that there is a use dependence
- Master runners – MU numbers are sig greater than older healthy adults who don’t run. MR are people who run a lot and are 70 and older. If you actively use the muscle to some degree you can maintain those numbers
- MR biceps – slightly different in biceps but not significantly different. Not different from healthy normal adults. They are runners so aren’t using biceps a ton more.

82
Q

Rate coding and older age

A

How often AP’s fire
- The shorter the time between the AP’s the greater the force. This is b/c of summation.
- Every time a MU fires and AP you get a twitch force in response. If there is a long time between APs the force will fully relax and with the next AP we get another twitch force.
- See a decrease in firing rate in older adults

83
Q

Changes with motor units and age

A
  • Have a reduction in nerve conduction speed
  • Reduction in motor unit firing rate (isn’t necessarily coupled with first point)
  • Loss of motor neurons
  • Have branching and re-innervation as a result of the motor neuron loss
  • As well as death of some muscle fibers so decrease in fiber size and increased fat within muscle
  • Fibers that do remain are smaller because of less protein in those fibers
  • See decreased fibre size

End up with older muscle, fewer muscle fibres, less contractile tissue, slower MU firing rates and more type 1 MF proportionally than young. Type 1 uses more oxidative energy sources.

84
Q

How might the slower twitch properties be advantageous to the older muscle? (Hint: think about MU firing rates).

A
  • Slower relaxation so for a lower firing rate will get greater summation (this is b/c contractile properties are slow)
  • In older muscle the next AP can be further away (longer time between firing rates) and still get that summation. If there were no changes to the twitch force it would fully relax before we got next AP, but older muscle has slower contractile properties (longer to reach peak force and to relax) so when you get next AP even though it’s further apart than it is in young you are still able to get summation in force b/c contractile properties of muscle are slower. If all that changed was MU firing rate would have less summation of force.
  • Slower properties is advantageous b/c it allows them to summate forces regardless of decrease in firing rate
  • Makes things smoother b/c you’re summating not going up and down repeatedly
85
Q

Given the changes in the neuromuscular system with advanced age, what differences would you expect in muscle fatigue?

A

At an equivalent relative contractile force will have a longer period before fatigue. Fatigues more slowly!! If you take younger and older adults older ones aren’t reaching same absolute force (muscle size and strength goes down. So young has higher maximal force but not necessarily the ability to maintain that force for a longer period of time. So, if contracting to same relative force (not absolute) - older adults’ fatigue less

86
Q

What is the difference between mechanical and electrical response of muscle?

A

Need motor neuron and muscle fire to repolarize before you can get another AP but that is different than mechanical response where we want next twitch force to come before it lowers completely

87
Q

Knee extension exercise and power remaining

A

Young and older adults producing 3 minutes of repeated knee extension. Isometric contraction – kick out and relax (not actually moving though) for 3 minutes.
- Percent of initial power (so relative) that is remaining at the end of the 3 minutes of exercise. At the end of the 3 minutes the older adults have a greater percent of their initial power remaining. Meaning they fatigued less. Fatigue in this case is a drop in power or force/strength not a measure of endurance/time. This is also true if we go to a dynamic concentric contraction as well. This is 90 degrees per second but we get the same result. Older adults have more of initial power remaining meaning they fatigued less.

This is partly b/c of the summation – do get a slowing of MU firing rate with fatigue and in older adults they are better matched to maintain that force (are used to summating with more distance between APs – b/c of type 1). The muscle fibers in older adults are more oxidative as well so are better built for fatigue resistance.

88
Q

Functional Consequences in Neuromuscular System

A
  1. Decreased strength
  2. Slower muscle contractile properties
  3. Greater reliance on oxidative ATP
  4. Greater fatigue resistance (b/c of numbers 2 and 3) at isometric and slow contractions
  5. Slower conduction velocity
  6. Reduced power
  7. Greater fatigue (high velocity contractions)
89
Q

Disability threshold

A
  • Neuromuscular system has decrease in strength and mass. To function independently need to be able to produce enough force in your muscle.
  • Functional capacity – have a low one when born (can’t do anything on our own) and that increases through our early childhood and peaks in adulthood. As everything we have discussed starts to change (reductions in cardiac function, endocrine, neuromuscular, etc.). The goal with healthy aging is to stay above disability threshold.
  • If your functional capacity drops below, you need assistance to perform activities of daily living
  • One neuromuscular factor that is a good predictor of being above threshold (best) is power (how much you can produce with your muscles). Power is force x velocity.
90
Q

How is force effected in the power equation?

A

Fibres shorten which generates force –> in adults have a decrease in number and size of fibres (loss of protein)

This leads to sarcopenia

In the power equation see a reduction in force that is contributing to reduction in power when looking at loss of muscle mass/size and number of fibers (these contribute to loss in force).

91
Q

How is velocity effected in the power equation?

A

Calcium release from SR/calcium binds to troponin –> in adults have decreased Ca in SR and decreased Ca sensitivity for binding which leads to reaching high forces slower and relaxing slower
- Lots of things effect muscle contractile velocity. One is firing rate of MU. Faster MU firing rates contribute to higher contractile velocities. Lots of factors within the muscle that have to do largely with how fast we can bind and release calcium
- Faster you can cycle calcium the faster you can move through cross bridge cycling.
- Less to be released from SR and less sensitivity on troponin for the calcium. Less available and less able to bind to binding sites. Together these lead to the slower contractile properties of the muscle. Limits how fast muscle can contract b/c the faster you can bind calcium and get to binding site faster you can cycle through binding cycle.

Summary: calcium needs to be released from SR and bind to troponin to open up binding site for myosin. Faster Ca cycles the faster you can cycle through cross bridges. How fast it can bind is dependent largely on how fast you can cycle the calcium. In older muscles have less Ca and less sensitivity to takes longer to bind and cause conformational change that allows myosin head to bind so maximal contractile velocity is slower b/c you aren’t cycling calcium as quickly.

92
Q

Relative torque and angular velocity graph

A
  • Faster you contract the less torque or force you can produce. See this decrease in both young and old.
  • Drops off much more quickly in older adults than in younger
  • If we look at a high velocity contraction younger adults can produce more torque relative to their max torque than older adults at this higher velocities.
  • When you are trying to contract very rapidly need rapid neural input. Not getting higher force that you get out of type 2 fibers. Need that calcium binding to produce force at high contraction velocities. All 3 of those factors combine to limit amount of force older adults can produce at higher contraction velocities.
  • *Think back to power being best predictor of functional capacity in older adults. Already know there is a reduction in force in older adults. Absolute force is lower at any contraction velocity and maximal velocity of contractions is limited in older adults. So power the best predictor is substantially reduced in older adults – b/c of reduction in force and velocity.
  • Already have reduction in force so any small reduction in velocity is compounding the already reduced force.
93
Q

What are the 3 contributing factors to decreased torque as we age?

A
  1. Slower maximal motor unit firing rates
  2. Greater proportion of type 1 muscle fibres
  3. Reduced Ca2+ in SR and reduced Ca2+ sensitivity
94
Q

List 3 neuromuscular factors that change with advanced age and describe how each factor contributes to sarcopenia.

A

Sarcopenia – decrease in muscle size and strength
- Less calcium in the SR – limitation in velocity of contraction. At a given velocity there is less strength produced (less force produced) in older adults. That is the curve with circles we just looked at.
- Loss of muscle fibers – lost muscle fibers b/c with advanced age there is motor neuron death (so if not reinnervated will die). Will contribute to loss of muscle size and strength!
- Reinnervation of orphan muscle fibers by branching of motor neurons – typically those muscle fibers that are reinnervated are converted to type 1 muscle fibers. We know that type 1 MF produce less force than type 2 so that contributes to reduction in strength which is part of sarcopenia definition.

Kinesiology (5 decks)

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