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Exercise Physiology and Pharmacology > Exercise, Aging, and Disease > Flashcards

Exercise, Aging, and Disease Flashcards

1
Q

Physical activity

A

Muscular movement that increases energy expenditure.

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2
Q

Physical inactivity

A

Any decrease in body movement that produces decreased energy expenditure toward basal level.

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3
Q

Exercise

A

Planned structured and repetitive physical activity designed to improve physical fitness.

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4
Q

Physical fitness

A

How well one performs physical activity (specified for a type of activity).

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5
Q

Health

A

Physical, mental, and social well-being (not just absence of disease).

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6
Q

Healthspan

A

Duration of a person’s life that they remain in excellent health.

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7
Q

Lifespan

A

Duration of a person’s life.

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8
Q

What is SeDS?

A

Sedentary death syndrome which is death due to a lack of regular physical activity and a poor diet.

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9
Q

What diseases result from a lack of physical activity and a poor diet?

A

Obesity, diabetes (type II), cardiovascular disease, and cancer.

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10
Q

Does exercise prevent disease? How much is needed?

A

Around 150 minutes of exercise a week lowers:
- CVD = 40%
- high blood pressure = 50%
- stroke = 27%
- type 2 diabetes = 50%
etc.

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11
Q

How does exercise benefit the economy?

A

There would be improved productivity and reduced mortality rates, less sick leaves, and health care costs; thus helping the economy with $28 billion/year (US).

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12
Q

What balance is required for your body weight?

A

It results from a balance between the amount of food that you intake and the amount of energy that you expend.

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13
Q

What is adaptive thermogenesis?

A

The ability for the body to adjust itself to increase/decrease its energy expenditure in response to food intake and temperature.

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14
Q

What is adaptive thermogenesis controlled by?

A

The hypothalamus which detects signals from blood nutrients or the hormone leptin released from white adipocytes.

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15
Q

What is obligatory energy expenditure?

A

The minimal amount of energy we must expend in order to maintain cellular and organ function.

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16
Q

What hormone do white adipocytes produce?

A

Leptin

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17
Q

How does leptin levels relate to the amount of triglycerides?

A

The more triglycerides you have stored, the more leptin you produce.

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18
Q

What receptors does leptin bind to in the brain? Where?

A

It binds to the Ob-Rb receptors in the hypothalamus, particularly in the arcuate nucleus.

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19
Q

What happens when leptin binds to Ob-Rb receptors?

A

Hypothalamic outputs decrease the drive to eat so less food intake and an increase in energy expenditure through adaptive thermogenesis which provides altered behavioural, neuroendocrine, and autonomic output (sympathetic).

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20
Q

What is an ob/ob mice?

A

An overweight mice.

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21
Q

What gives the phenotype of an ob/ob mice?

A

A mutation in the gene encoding leptin, thus no leptin or dysfunctional leptin.

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22
Q

Why are the ob/ob mice extremely overweight?

A

They overeat (hyperphagia) and have a reduced energy expenditure (not mobile).

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23
Q

Hyperphagia

A

An abnormally great desire for food.

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24
Q

What is leptin resistance?

A

There is less sensitivity to leptin when it binds to the Ob-Rb receptor and thus the feedback mechanism is lost = overweight.

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25
Q

What contributes to obesity?

A

We are eating too much and foods that are in high caloric intake.

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26
Q

Where is protein stored in the body?

A

A very limited amount in all cells.

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27
Q

Where is lipid storage unlimited?

A

Adipose tissue

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28
Q

What happens to the fat of excess carbs or protein?

A

Converted to fats where it’s stored in unlimited amounts in adipose tissue.

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29
Q

Explain the food intake of hunter-gatherers.

A

They had just enough food to support the energy expenditures of their daily activities.

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30
Q

What happened when hunter-gatherers rested?

A

They conserved energy because they didn’t have much excess food.

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31
Q

What is the theory behind food consumption that led to obesity?

A

Weight gain by people in modern society was due to behaviours developed when food was scarce. This is attributed when hunter-gatherers rested to conserve energy. Nowadays, we overrest. In addition, to the open availability of food and the ease of getting it without spending too much calories (walking versus driving).

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32
Q

What is glucose detected by?

A

The beta cells of islets of langerhans in the pancreas.

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33
Q

What does insulin do?

A

It controls glucose uptake and storage.
- muscle take 70% of glucose load and converts it to glycogen
- liver converts it to glycogen
- adipose takes the excess and converts into triglyceride

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34
Q

What is type 2 diabetes?

A

You can still produce insulin, but you become insulin resistant.

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35
Q

What type 1 diabetes?

A

The pancreatic beta cells cannot produce insulin and therefore, you are reliant upon insulin injections.

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36
Q

What receptor does insulin act on?

A

Tyrosine kinase receptors

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37
Q

What is the PI-3K signalling pathways of insulin binding?

A
  1. Synthesis of lipids, proteins, glycogen
  2. Cell survival and proliferation
  3. GLUT4 insertion into membrane
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38
Q

What is the MAP kinase signalling pathway of insulin binding?

A

Cell growth, proliferation, and gene expression.

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39
Q

What is the link between obesity and insulin resistance?

A
  1. Increasing diabetes = increasing in circulating free fatty acids
  2. These free fatty acids inhibit several points within the insulin dependent pathways (PI-3K signalling reduced) and the GLUT4 transporters (inhibit insertion and directly inhibit)
  3. Insulin resistance
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40
Q

Why store fat instead of glycogen?

A

It’s an efficient way of storing energy since you can store twice as much energy per gram as triglycerides compared to glycogen.

41
Q

What happens if you decrease your body weight to solve your obesity problem?

A

There is a decrease in free fatty acids = decrease in insulin resistance = improved glucose control = decrease the stress of pancreatic beta cells and less chance of progressing to insulin-dependent diabetes

42
Q

What happens if you have prolonged stress on pancreatic beta cells?

A

You can develop type 1 diabetes because if you force them to generate more and more insulin to respond to high glucose levels, then the pancreatic beta cells will give up.

43
Q

What is atherosclerosis?

A

A progressive, chronic inflammatory disease in which there’s a build up of lipid deposits and plaques within the blood vessel walls of medium-large arteries.

44
Q

What disease can atherosclerosis under lye?

A

Cardiovascular diseases.

45
Q

What happens with an increase of lipid deposition in blood vessel walls?

A

Endothelial activation = immune cell recruitment

46
Q

What does the immune cell recruitment of atherosclerosis release?

A

The release of pro-inflammatory cytokines, which can lead to foam cells forming.

47
Q

Why are foam cells bad?

A

They can acquire large amount of lipids which leads to increasing size of plaques.

48
Q

Where does the inflammation occur in atherosclerosis?

A

It’s chronic and local.

49
Q

What is the theory behind the progression of atherosclerosis?

A

Whether it develops is up to a balance of pro-inflammatory and anti-inflammatory cytokines.

50
Q

What does the narrowing of arteries in atherosclerosis do?

A

It decreases the amount of blood that can pass through the medium-large arteries. It alters blood pressure.

51
Q

What happens if a plaque ruptures?

A

It leads to platelet activation and thrombus formation, and if the thrombin block the blood supply, it can either lead to a heart attack or stroke.

52
Q

What are the anti-inflammatory cytokines?

A

TGF-beta and specific interleukins (IL-6).

53
Q

What are the pro-inflammatory cytokines?

A

Tumour necrosis factor-alpha (TNFa).

54
Q

Who risks mortality more due to chronic disease?

A

Greater in individuals with a normal BMI and poor physical fitness versus those with a high BMI and good physical fitness.

55
Q

What is the mechanism that displays that regular exercise can reduce chronic disease in terms of trained muscle?

A

As you train muscle, it increases your muscle mass and thus your ability to store glycogen; your insulin sensitivity increases; and your ability to use lipid as an energy source increases. As a result, there is a reduction in the conversion of glucose to fat, circulating fats, and the storage of fat.

56
Q

What is the mechanism that displays that regular exercise can reduce chronic disease in terms of physical fitness?

A

The increase in physical fitness increases your overall health, well being, brain health, and metabolic health. This resists the effects of pathogens, disease, stress, and aids in recovery.

57
Q

What is the mechanism that displays that regular exercise can reduce chronic disease in terms of inflammation?

A

There is a reduced amount of inflammation because of anti-inflammatory cytokines released from the muscle (myokines). Most chronic disease have an inflammatory basis.

58
Q

Myokines

A

Anti-inflammatory cytokines released from contracting skeletal muscle.

59
Q

How was the idea that contracting skeletal muscle release humoral factors that control various organs?

A

Electrically inducing cycling in patients with spinal cord injury and healthy individuals with a spinal block showed that the injured had the same physiological changes as the same activity in the uninjured.

60
Q

What are the functions of myokines?

A

Endocrine, paracrine, and autocrine factors.

61
Q

Why do myokine mediate the effects of physical activity?

A

Because they are produced upon contraction.

62
Q

What do myokines act on?

A

White adipose tissue to inhibit the release of pro-inflammatory adipokines.

63
Q

Myostatin

A

A myokine that acts locally and distantly by regulating skeletal muscle hypertrophy (increase in size), metabolic homeostasis, and adipose tissue mass.

64
Q

BDNF (brain-derived neurotrophic factor)

A

A myokine released from skeletal muscle that connects skeletal muscle and brain health by promoting neuronal growth and activity.

65
Q

IL-6

A

A myokine that talks with adipocytes, releases cortisol from the adrenal cortex, and increases insulin sensitivity.

66
Q

How does IL-6 increase after exercise?

A

It increases in the blood by 100 fold.

67
Q

What does BDNF increases in the brain?

A

The release of serotonin and dopamine and brain plasticity (thus new connections between cells are opened up).

68
Q

What is the mechanism that displays that regular exercise can reduce chronic disease in terms of myokines?

A

Specific anti-disease reduction by myokines. For example, exercise mediated BDNF improves cognitive function thus proven a therapy in Parkinson’s and Huntington’s disease.

69
Q

What is the mechanism that displays that regular exercise can reduce chronic disease in terms of acute activation?

A

Exercise results in the acute activation of body stress responses (the hypothalamus/pituitary/adrenal gland axis, the sympathetic ANS, and the immune system). The relaxation effects and overall training effect prepares the body to cope better with stresses of diseases.

70
Q

What are the three systems that respond to stress?

A
  1. Autonomic nervous system (sympathetic)
  2. Hypothalamus, pituitary, and adrenal axis
  3. Immune system
71
Q

What is the problem when you chronically activate the stress systems?

A

Dysregulation of multiple body systems leading to weakened stress responses and immune supression.

72
Q

Where is stress picked up in the brain?

A

The amygdala

73
Q

What does the amygdala do if it detects stress?

A
  1. Increase in activation of adrenal medulla, which releases more adrenaline
  2. Increase in sympathetic nerve output
  3. Both act on various organs to increase heart rate, mobilise energy stores, breathing rate
74
Q

Explain the hypothalamic, pituitary, adrenal axis.

A
  1. Hypothalamus detects stress and releases corticotropin releasing hormone (CRH) via the hypophyseal stalk portal blood system
  2. Anterior pituitary is influenced and releases ACTH via the blood
  3. Adrenal cortex is targeted by ACTH and releases cortisol in the blood
  4. Cortisol negatively feeds back
  5. Cortisol increases the mobilization of energy stores and immune cells
75
Q

What does long term stress release?

A

Constant cortisol levels

76
Q

How does a constant release of cortisol relate to obesity?

A

It increases appetite and thus consequently fat storage.

77
Q

What are the effects of constant cortisol release?

A

It reduces cortisol resistance, which reduces your ability to combat stress. Also, weakened immune system.

78
Q

How does long term stress lead to artherosclerosis?

A
  1. Repeated adrenaline surges
  2. Increase in blood pressure
  3. Endothelial injury
  4. Promotes artherosclerosis
79
Q

What are the brain pleasure rewards released during exercise?

A

Dopamine and serotonin.

80
Q

How does exercise reduce chronic long term stress?

A

The release of serotonin from exercise provides relaxing effects that inhibit the chronic long term stress, thus inhibiting outputs from the hypothalamus.

81
Q

Sacropenia

A

Age-related involuntary loss of skeletal muscle mass.

82
Q

What does sarcopenia result in?

A

A loss in muscle mass results in a loss of strength.
ex. 100 m running time increases as you get older

83
Q

What is sarcopenia a result of?

A
  1. A decrease in the number of muscle fibres (hypoplasia)
  2. A decrease in the area of each muscle fibre (atrophy)
    Both accompanied by an increase in fat and connective tissue in the lost muscle space (fat deposition; myosteatosis).
84
Q

What are sarcopenia and myosteatosis accelerated by?

A

Physical inactivity

85
Q

Explain the neuropathic processes that are responsible for sarcopenia.

A
  1. Loss of alpha motoneurones in skeletal muscle
  2. The leads to a loss of muscle denervation and loss of motor units
  3. The loss of muscle innervation leads to denervation muscle atrophy = muscle fibers die off as they aren’t being stimulated (apoptosis)
86
Q

What happens to the remaining nerve fibers for muscle?

A

They can generate axonal sprouting (giant motor units), thus leading to some reinnervation of some denervated muscles.

87
Q

What does axonal sprouting result in? Why may it lead to sarcopenia?

A

With giant motor units, this decreases the number of fine motor unit recruitments when regulating force. Typically, an increase in muscle strength results from an increase in action potentials/recruitment of motor units.

88
Q

Explain how growth factors are responsible for sarcopenia.

A
  1. Decreases in growth factors with age
  2. Somatopause = progressive decline of pituitary function in making insulin-like growth factors
  3. Decrease in muscle size (atrophy) due to loss of satellite cell activation/proliferation (GFs promote satellite cells to aid in muscle strength)
  4. Decrease in capacity for motor unit remodelling (natural on-going process involving selective denervation + sprouting axons + motor endplate regeneration)
89
Q

What muscle fibers are more susceptible to sacropenia?

A

Type II

90
Q

How does nutrition affect sarcopenia?

A

A reduction in food intake means that there is less nutritional supply to maintain status quo for muscle. Less strength = sarcopenia.

91
Q

What happens with myosteatosis?

A

There is an increase in the infiltration of fat cells and deposits and connective tissue with age in skeletal muscle where those fibers die off.

92
Q

How does myosteatosis affect sarcopenia?

A

With less motor units this increases the load on specific muscle groups/units. Increase load = increase stress. There is an increase in pro-inflammatory adipokines promotes sarcopenia by promoting chronic inflammation = increase insulin resistance.

93
Q

How does obesity enhance myosteatosis?

A

More circulating free fatty acids that lead to pro-inflammatory adipokines, which myosteatosis promotes and leads to sarcopenia.

94
Q

What is the known treatment for sarcopenia and myosteatosis?

A

Exercise

95
Q

What is the correlation between exercise and fat reduction?

A

When you double your physical activity, you double the reduction of intramuscular level of fat and connective tissue.

96
Q

What exercise reduces sarcopenia?

A

Resistance training using weights or bands.

97
Q

Why does resistance training reduce sarcopenia?

A

Sarcopenia is having a preferential effect on the loss of type two fibres compared to type I. This is because type II fibres tend to atrophy (decline) more with age. This type of training trains the fast twitch fibers.

98
Q

What can endurance training help with?

A

It can limit the normal loss of aerobic power and VO2max.

99
Q

Disability threshold

A

It’s the point at which you’ve lost so much muscle strength that you’re not able to support your own body.

Exercise Physiology and Pharmacology (9 decks)

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