Week 9: The U-Shaped Relationship between Exercise and Health Flashcards

1
Q

Who is considered the “pioneer of exercise physiology”?

A

Per-Olof Åstrand.
The first man to note the beneficial effects of exercise on the heart and the negative effects of pro-longed bed-rest.

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2
Q

What are the beneficial effects of exercise (on a cardiovascular level)?

A
  1. Improves blood lipid profile
  2. Increases insulin sensitivity
  3. Aids blood pressure control
  4. Enables weight loss
  5. Reduces risk of coronary artery disease (CAD)
  6. Reduces risk of myocardial infarction
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3
Q

How much does regular exercise reduce the risk of developing CHD (based on general population studies)?

A

30-50% reduction in risk of developing CHD.

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4
Q

What effect does exercise have in heart failure patients?

A

Improves their functional capacity and well-being.

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5
Q

What is AF?

A

Atrial fibrillation - happens when abnormal electrical impulses suddenly start firing in the atria.
- Overrides the hearts natural pacemaker
- Causes highly irregular pulse rates

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6
Q

What is the effect of moderate PA on AF?

A

Moderate PA associated with a reduction in prevalence of AF, especially in older adults.

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7
Q

What difference in longevity is seen in olympic athletes (compared to the general population)?

A

Longevity benefit of 3 years approx.

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8
Q

What mix of PA do adults need to stay healthy?

A

Moderate intensity aerobic activity - at least 150 mins a week.

Muscle strengthening activity - at least 2 days a week.

(If you prefer to do vigorous intensity aerobic activities, like running, then aim for at least 75 mins a week)

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9
Q

What is meant by the “U-shaped curve”?

A

Moderate exercise is better than no exercise, but extreme exercise may be harmful.

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10
Q

Give an example of a study that exhibits this U-shaped curve.

A

A recent study showed…
- Light joggers had lower mortality than sedentary non-joggers
- Strenuous joggers had a mortality rate that was not statistically different to the sedentary group

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11
Q

What did Kokkinos et al. show?

A

A 13% reduction in mortality per MET achieved between 4 and 10 METs, but no additional benefit after 10 METs.

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12
Q

What do we need to be aware of when carrying out an athlete’s ECG?

A

Many physiological changes are at risk of being identified as abnormal.

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13
Q

What are reasons for not mandating ECGs in athletes?

A
  1. Financial cost (large number of tests that would be required)
  2. Resources
  3. Potential for false-positive results
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14
Q

What does clinically effective interpretation in athletes require?

A

The ability to optimally distinguish between normal, training-related changes and pathological changes on the ECG.

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15
Q

What are athletes with high body mass at increased risk of?

A
  1. Elevated systolic blood pressure
  2. Low-density lipoprotein and glucose
  3. Cardiometabolic syndrome (CMS)
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16
Q

What did Baron et al., (1994 and 2012) show in retired American football athletes?

A

46% reduction in all-cause mortality.
HOWEVER,
CVD was increased by 52% in linemen, primarily due to hypertensive heart disease and coronary heart disease.

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17
Q

What did Pelliccia et al., (2017) show in Olympic athletes?

A

Reported an unexpected prevalence of cardiovascular risk factors in power, skill, and mixed discipline with endurance based athletes likely to be free from risk factors.

18
Q

What did Zemski et al., (2019) show in Polynesian rugby players?

A

Elevated risk factors, such as increased visceral fat and unfavourable lipid profiles in rugby athletes of Polynesian decent compared to athletes of Caucasian decent.

19
Q

What is CMS?

A

Cardiometabolic syndrome - a combination of metabolic dysfunctions mainly characterised by insulin resistance, impaired glucose tolerance, dyslipidemia, hypertension, and central adiposity.

20
Q

What is hypertension during adulthood a well-established independent risk factor for?

A

Later life CVD morbidity and mortality.

21
Q

What is essential (primary) hypertension?

A

Abnormally high blood pressure that is not as a result of a medical condition.

22
Q

Where is essential hypertension most commonly seen?

A

Essential hypertension is the most prevalent cause of high blood pressure in athletes.
- Participation in certain sports may be associated with an increased risk of developing hypertension
- E.g., American football

23
Q

What might strenuous static training induce?

A

Unfavourable blood pressure profile.

24
Q

What is hypertension a result on?

A

Complex interplay between genetic determinants and behavioural characteristics.

25
Q

What behavioural characteristics contribute to increased hypertension risk?

A
  1. Dietary habits
  2. Beverages rich in salt and energy drinks
  3. Overuse of dietary supplements
  4. Prohibited substances
  5. Frequent use of NSAIDs
  6. Fatigue, poor sleep
  7. Psychological stress, competitive sport
26
Q

What is SCD?

A

Sudden cardiac death - the abrupt loss of heart function, breathing and consciousness.

27
Q

When does the ESC use the term sudden cardiac death?

A
  1. A congenital/acquired potentially fatal cardiac condition is known to be present during life.
  2. Autopsy has identified a cardiac/vascular anomaly as a cause of death.
  3. No obvious extra-cardiac causes have been identified by post-mortem exam and therefore an arrhythmic event is a likely cause of death.
28
Q

What is SCD in older athletes predominantly due to?

A

Atherosclerotic coronary artery disease.

29
Q

Who in the athletic population are most at risk of SCD?

A

Middle-aged recreational athletes.

30
Q

What have recent studies identified in the muscles after prolonged exercise?

A

A rise in the concentration of biomarkers of myocyte damage.

Note!
- Myocytes = smallest unit of muscular tissues and organs.

31
Q

50% endurance athletes have an elevated
troponin response after exercise. What can such elevations result in?

A

May eventually lead to myocardial fibrosis that manifests as cardiac dysfunction and arrhythmias.

32
Q

What can repeated bouts of endurance exercise lead to?

A

Myocyte necrosis.

33
Q

What is the consequence of increased cardiac damage (occurring as a result of too much vigorous endurance exercise)?

A

Development of arrhythmogenic substrate (forms a prerequisite for the induction of arrhythmia) through adverse myocardial remodelling and myocardial fibrosis.

34
Q

What has been uncovered regarding the prevalence of AF in endurance athletes?

A

High prevalence of AF in middle-aged endurance athletes.
- Athletes engaged in chronic exercises experience a 5-fold risk of AF compared to sedentary population

35
Q

What are the cardiac consequences of using steroids (such as androgen-anabolic steroids, used to increase muscle mass and strength)?

A

They are implicated in adverse lipid and blood pressure profiles, myocardial infarction, arrhythmias, LV (left ventricle) dysfunction, and SCD.

36
Q

What can the use of human growth hormone (used to increase skeletal muscle) lead to?

A

Can cause myocardial hypertension and fibrosis.

37
Q

What can the use of erythropoietin EPO (usually utilised to increase red cell concentration and improve oxygen delivery to tissues) cause?

A

The accompanying rise in haematocrit and dangerous blood viscosity levels may predispose to spontaneous thrombosis and systemic thromboembolism as well as hypertension due to the elevated afterload.

38
Q

What is thrombosis?

A

Local coagulation or clotting of blood within a vein or arteries.
- Results in an embolism
- Can results from use of EPO

39
Q

What is an embolism?

A

A blocked vein or artery caused by a foreign body, such as a blood clot or air bubble.

40
Q

What is systematic thromboembolism?

A

An embolism which travel through the systemic arterial circulatory system.
- Vast majority arise within the heart secondary to atrial fibrillation (altered flow) or thrombus formation over an area of myocardial infarction (altered wall)