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physiology > Exercise, Inflammation & CVD risk > Flashcards

Exercise, Inflammation & CVD risk Flashcards

1
Q

What is meant by the term inflammation?

What are the 2 functions of inflammation?

A

Local immune response to physical injury/damage (cell or tissue) or infection : redness, pain, swelling

(1) to destroy infected or damaged tissue (phagocytic cells)
(2) stimulate tissue repair ‘cytokines’ released by immune cells (in the tissues), endothelial cells and adipocytes stimulate the liver to release acute phase proteins such as C-reactive protein (CRP) and fibrinogen

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2
Q

What is chronic inflammation?

What are some reasons for chronic inflammation?

A
  • ‘Chronic (long‐term) low‐grade inflammation’ - for months/years
  • Dysfunction of this repair response leads to long‐term (chronic) release of inflammatory cytokines by immune cells
    Causes include sustained tissue damage caused by:
  • FFA uptake by immune cells
  • High levels of toxins/pollutants in the circulation
  • Unresolved infection / autoimmune response
  • Local tissue hypoxia (e.g. in obesity)
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3
Q

What happens when there is a positive energy balance and physical inactivity?

A
  • causes visceral fat accumulation = chronic inflammation
  • increases proinflammatory adipokines(IL-6, TNF-α)
  • increases triglycerides, LDL and FFA
  • increased risk of atherosclerosis, T2DM and tumour growth
  • Reduces longevity
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4
Q

Name some long-term conditions associated with chronic inflammation?

A
  • Inflammatory bowel disease
  • Stroke
  • Diabetes
  • Lung disease
  • Chronic kidney disease
  • Heart disease
    M2 macrophages - clear out damage from the cell
    Tissue goes into hypoxia as there is not enough O2 in the cell(reduced blood flow)
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5
Q

What affects can activated immune cells have on the body e.g.: TNF-α and IL-6?

A
  • liver - insulin resistance, sustained acute CRP
  • adipose tissue - adipokine production, immune cell infiltration
  • brain - build up of amyloidogenic proteins
  • endothelial cells - endothelial dysfunction, atherosclerosis
  • skeletal muscle - sarcopenia, insulin resistance
  • bone - bone remodelling, osteoporosis
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6
Q

Explain how a stimulus initiates the biomarkers of chronic inflammation:

What are the diagnostic levels of blood cytokines?

A
  • stimulus: infection, injury
  • Endothelial cells and activated immune cells release pro-inflammatory cytokines(TNF-α, IL-6)
  • These are transported to the liver
  • Liver releases acute phase proteins(fibrinogen)
  • 0.5-1 g/ml normal
  • 3g/ml in obese
  • 8g/ml in chronic inflammation patients
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7
Q

How is IL-6 associated to CVD risk factors in women?

Can this be influenced by exercise?

A
  • IL-6 increases with risk factors of CVD in women
  • the more CVD risk factors present the higher the persons IL-6 level
  • LPA and MVPA were related to better cardiometabolic biomarkers and that associations with triglycerides and blood pressure were stronger in women
  • Greater sedentary time was associated with higher CRP and IL-6 and associations were stronger in women than men
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8
Q

Are inflammatory markers higher just because someone has more adipose tissue?

A
  • Most IL-6 comes from amount of adipose tissue
    Most active had lowest IL-6 inflammatory markers
  • Inflammatory markers are lower with increased activity and reduced sedentary time
  • Lower CRP and IL-6 with increased MVPA and light PA
    Higher with increasing sedentary time
    • Fat mass is a key mediator for inflammatory markers, but not only mediator
  • Decreased numbers of inflammatory immune cells infiltrating adipose tissue, because there a fewer they are unable to be released from inflammatory tissues
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9
Q

Can moving more affect immune cell migration?

A
  • monocyte migration was lower in those with obesity but who moved more - exercise can stop the movement of inflammatory cells into the tissue
  • Exercise suppressed inflammatory immune cell infiltration of adipose tissue
  • becuase adipose tissue released less cytokines which attract macrophages, causing pro-inflammatory cytokines to be lower in blood
  • Decreased amounts of adipose tissue & number of inflammatory immune cells infiltrating adipose tissue
  • ↓ production of pro‐inflammatory cytokines (e.g. TNF‐α, IL‐1β, IL‐6)
  • increased production of anti‐inflammatory cytokines (e.g. IL‐1ra, IL‐10)
  • High fat diet/obese sedentary had a lot more macrophages than HFD exercise
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10
Q

What is the impact of exercise on pro-inflammatory proteins release into the blood?

A
  • monocyte/macrophages and lymphocytes
  • decreased production of pro‐inflammatory cytokines IL-6
  • increased release of anti‐inflammatory cytokines IL-10
  • At higher intensities, skeletal muscle releases of large amounts of pro‐inflammatory IL‐6
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11
Q

how did monoclonal antibodies effect CVD risk?

A
  • monoclonal antibodies block IL-1β pathways
  • reduces CRP which is the end stage of chronic inflammation
  • decreases risk of atherosclerosis & CVD events
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12
Q

How does muscle-derived IL-6 release change during intense exercise?

A

With high intensity/prolonged exercise large (10‐20% increases) amounts in IL‐6 are released from muscle into the circulation.
- This stimulates the release of anti‐inflammatory cytokines (e.g. IL‐1ra, IL‐10) from immune cells in the blood to ‘switch off’ the response
- Regular performance of higher intensity or longer duration exercise can lead to a persistent elevation in levels of IL‐10 in the blood
- IL-10 released in large amounts creates an anti-inflammatory response

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13
Q

How does fat mass mediate the release of pro-inflammatory markers?

A
  • total effects of activity on IL-6 and CRP is mediated by fat mass index
  • Inflammatory markers are lower with increased activity and reduced sedentary time
  • Lower CRP and IL-6 with increased MVPA and light PA
  • Higher with increasing sedentary time
  • Fat mass is a key mediator for inflammatory markers, but not only mediator
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14
Q

Why is long-term PA associated with anti-inflammatory effects?

A
  • Adipose tissue is the biggest source of circulating IL‐6 at rest
  • inflammatory markers are lower even if fat mass isn’t changed, so this can’t be the only reason…
  • Decreased numbers of inflammatory immune cells infiltrating adipose tissue, because there a fewer they are unable to be released from inflammatory tissues
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15
Q

What factors determine the level of screening needed for an individual in the ACSM algorithm?

A
  • current level of fitness
  • family history, presence of signs/symptoms of CVD of metabolic disease
  • level of intensity they want to work at

these are risk modulators of exercise-related CVD events

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16
Q

Why age is not included as a specific consideration within the ACSM algorithm?

A
  • algorithm is applicable to any age
  • not to waste health care time by elderly patient referrals
17
Q

Why does algorithm include initial assessment of CVD risk factors e.g.: BP, cholesterol, triacyglycerol?

A
  • these factors are very generic and a patient that displays abnormal BP, cholesterol and TAG may not actually have CVD
18
Q

What is the ACSM definition of being active?

A
  • ‘active’ is based of the presence or absence of exercise in the past 3 months
  • at least 30 mins of moderate intensity on at least 3 day per week for 3 months
19
Q

What are the major sign or symptoms that are suggestive of CVD, metabolic and renal disease?

A
  • hypertension, diabetes(1&2)
  • symptoms: pain, chest discomfort & in arms, neck resulting in ischemia(reduced blood flow to these body parts)
  • shortness of breath and dizziness
20
Q

In people with type 2 diabetes why is it necessary to inspect the skin, particularly in the lower extremities?

A
  • loss of sensation in feet so numbness is caused, can lead to infections and amputation
21
Q

Why should a physical examination include the inspection of the lower limbs for edema(swelling from fluid retention) and presence of arterial pulse?

A
  • fluid could put pressure on the arteries causing them to narrow leading to hypertension which is a CVD symptom
22
Q

what types of medication would be particularly concerning when an individual is about to embark on an acute exercise bout?

A
  • blood thinners, diuretics, caffeine causes increased HR, contraceptives.
  • anti-depressants cause excess sweating
  • sleeping pills and laxatives
23
Q

What is an ECG?
What does it do?

A
  • electrocardiogram examines the heart’s electrical activity and is
  • used to determine whether an individual has any abnormalities in electrical rhythms that could relate to structural/functional changes in the heart
24
Q

cut off for hypertension?

Maximum blood pressure for males & females?

A

140/90

  • Males: 210/110
  • Females: 190/110
25
Q

What do cardiac physiologists look out for on a resting ECG as part of screening procedure pre-research studies?

A
  • electrical conductivity(speed up in HR: coffee, stressed, or is baseline high)
  • Bradycardia(slow HR, are they fit, beta-blocker meds) - symptomatic: dizziness, low BP
  • Atrial Fibrillation is most common
  • ectopics –> abnormal heart beats out of the blue(>2 is problematic), depends on where in the heart they occur
26
Q

What do cardiac physiologists look out for on an exercising ECG as part of screening procedure pre-research studies?

A
  • electrical conductivity –> what happens when the heart is under stress
  • coronary arteries –> is there enough supply to meet demand
27
Q

Explain the physiology underpinning exercise-related hypertension in certain patient groups

A
  • exercise-related hypertension could be due to the patient displaying any CVD risk factors.
  • stress can also increase BP during exercise visceral fat

physiology (10 decks)

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