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KIN 335 > Refuting Myth and Exercise Amount > Flashcards

Refuting Myth and Exercise Amount Flashcards

1
Q

What is the strong evidence regarding individual differences in response to physical activity?

A
  • Considerable heterogeneity in the responsiveness to physical activity
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2
Q

What was found to not be a major determinant of human responses to regular physical activity?

A
  • Age
  • Sex
  • Ancestral Background
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3
Q

What was found to have a considerable impact on human response to regular physical activity?

A
  • Pre-training phenotype
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4
Q

What is habitual employment or leisure time physical activity associated with?

A
  • Reduced Cardiovascular Disease Risk
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5
Q

What do recent studies suggest about lifelong endurance activity?

A
  • Might increase cardiovascular disease risk
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6
Q

What does regular, intense exercise cause regarding the heart?

A
  • Structural, functional, electrical cardiac adaptations
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7
Q

What is more commonly found in older athletes compared to their inactive peers?

A
  • Atrial fibrillation
  • Myocardial fibrosis
  • Coronary Artery Calcification
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8
Q

Describe Athlete’s Heart

A
  • Increase in Heart Mass & Volume
  • Greater LVEDV during rest/exercise
  • Myocardial cell enlargement
  • Increased LV cavity (eccentric hypertrophy)
  • Modest Thickening of walls (concentric hypertrophy)
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9
Q

What can increase the risk of sudden cardiac death?

A
  • Vigorous exercise
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10
Q

What was the overall occurrence of cardiac arrest during long distance running?

A
  • 1 in 184k participants
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11
Q

What is the initial response of the cardiovascular system to exercise?

A
  • Withdrawal of parasympathetic vagal tone
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12
Q

What is subsequently activated when the parasympathetic vagal tone is withdrawn during the cardiac response to exercise?

A
  • Sympathetic Nervous System
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13
Q

What is the evidence that the sympathetic nervous system is subsequently activated when the parasympathetic system withdrawals in a cardiac response to exercise?

A
  • Catecholamine release at nerve endings
  • Spill Over of epi- and norepinephrine into the systemic circulation
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14
Q

What do epinephrine and norepinephrine do following sympathetic activation following cardiac response to exercise?

A
  • Increase heart rate
  • Increase cardiac contractility
  • Increase stroke volume
  • Increase cardiac output
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15
Q

When does cardiac output increase during endurance exercise?

A
  • Initial phases
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16
Q

What is cardiac fatigue in endurance exercise?

A
  • Reduced cardiac output during prolonged endurance exercise
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17
Q

What distinguishes cardiac fatigue from cardiovascular drift?

A
  • Decrease in stroke volume with preserved blood volume
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18
Q

What does Creatine Kinase (CK) catalyze?

A
  • Transfer of phosphate group from creatine phosphate to ADP
  • producing ATP
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19
Q

What are the two subunits of Creatine Kinase (CK)? What do they reflect?

A

M
- Muscle Predominance
B
- Brain Predominance

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20
Q

What does an increase in blood concentration of CK indicate?

A
  • Cell damage with membrane injury
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21
Q

Why cant CK exit the cell?

A
  • Their size
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22
Q

What does the evidence on elevated CK-MB levels following endurance exercise suggest?

A
  • Originate from skeletal muscle damage
  • Does not represent acute myocardial injury
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23
Q

What is the contractile apparatus of striated muscle composed of?

A
  • Troponin Complex
24
Q

What is the troponin complex?

A
  • Actin based thin filament
  • Myosin-based thick filament
  • Tropomyosin
25
Q

What is the torponin complex composed of?

A
  • Subunits
  • Troponin C
  • Troponin T
  • Troponin I
26
Q

What subunit of troponin are identical in skeletal and cardiac muscles?

A
  • Troponin C
27
Q

What subunits of troponin are specific for either cardiac or skeletal muscle?

A
  • Troponin I
  • Troponin T
28
Q

What does the specificity in cardiac Troponin I and T make them suitable for?

A
  • Detecting Cardiac Damage
29
Q

What activity types have studies observed exceeding levels of cardiac troponin compared to those used to diagnose acute myocardial infarction?

A
  • Marathons
  • Triathlons
  • Endurance Cycling
  • Ultra-endurance races
30
Q

Why might there be increases in cardiac troponin following endurance activity?

A
  • Increased cardiomyocyte membrane permeability by mechanical stress
  • Production of oxidative radicals
  • Cardiac ischemia could cause proteolysis of Troponin complex, permitting troponin degrading products to pass through the cellular membrane
31
Q

What is the remodeling of left and right ventricles due to endurance training?

A
  • Mild/moderate eccentric LVH and RV dilation
  • Biatrial enlargement
  • Normal to slightly reduced resting LVFE
  • Normal/Enhanced Early LV Diastolic Function
  • Normal/Enhanced LV twisting/untwisting
32
Q

What remodeling of left and right ventricle occur from strength training?

A
  • Mild concentric LVH/ No RV remodeling
  • Normal/Mild enlarged Left atrial size
  • Normal/hyperdynamic resting LVFE
  • Normal/Slight reduced Early LV Diastolic Function
  • Compensatory Increase in late LV diastolic function
33
Q

What is myocardial fibrosis characterized by?

A
  • Accumulation of collagen in the extracellular matrix of the heart
34
Q

When does myocardial fibrosis most commonly occur?

A
  • After Myocyte injury from ischemia
  • But can have nonischemic causes
35
Q

What is myocardial fibrosis divided into?

A
  • Reactive interstitial fibrosis
  • Infiltrative Interstitial fibrosis
  • Replacement fibrosis
36
Q

What studies are needed regarding fibrosis and athletes?

A
  • determine if it is reversible with exercise cessation
  • Determine clinical significance of persistent fibrosis in athletes
37
Q

What did the study on rats doing endurance training suggest?

A
  • accelerated myocardial fibrosis
38
Q

What did the rats who did endurance training equivalent to 10 human years develop?

A
  • eccentric cardiac hypertrophy
  • Diastolic dysfunction
  • Atrial dilation
  • Collagen deposition at right ventricle and both atria
39
Q

What biochemical evidence suggests myocardial fibrosis in elite middle-aged endurance athletes?

A
  • Increased plasma markers of collagen syntheses and degradation
40
Q

What is the QT interval?

A
  • electrocardiographic measurement of the time between depolarization and repolarization of cardiac ventricles
41
Q

What is the QT interval generated by?

A
  • Passage of calcium, potassium, and sodium ions through cardiac ion channels
42
Q

What leads to Long QT Syndrome? What can that lead to?

A

Abnormal increase in QT interval
- Lead to sudden cardiac death

43
Q

What gene defect is most prevalent for producing Long QT syndrome?

A
  • KCNQ
44
Q

What type of gene defects produce LQTS?

A
  • Cardiac ion channel genes
  • 10 Identified
45
Q

What percentage of LQTS - 1 individuals cardiac events occur during exercise?

A

75%

46
Q

What percentage of LQTS 2&3 individuals’ cardiac events occur during exercise?

A

5%

47
Q

What do studies suggest increase the risk of ventricular tachycardia and sudden cardiac death in LQTS - 1 patients?

A
  • Enhanced Vagal Tone
48
Q

How does exercise training reduce heart rate?

A
  • Increasing parasympathetic or vagal tone
49
Q

What do studies suggest the increases in vagal tone from exercise training could do?

A
  • Increase arrhythmia risk in individuals with genetic predilection for LQTS-1.
50
Q

What are the potential acute cardiovascular risks to acute and chronic endurance exercise?

A

Increased
- Risk of Sudden Cardiac Death
- Risk for Acute Myocardial Infarction
Decreased
- Ventricular Function of the Heart

51
Q

What potential acute myocardial injury could occur from acute and chronic endurance exercise?

A

Increased
- CK and CK-MB Concentrations
- Cardiac Troponin Concentration
- BNP and NT-proBNP concentration

52
Q

What potential cardiac remodeling occurs from acute and chronic endurance exercise?

A

Increased
- Dimensions of right and left ventricle
- Dimensions of right and left atria
- Wall thickness

53
Q

What Potential Cardiac Maladaptations could occur from acute and chronic endurance exercise?

A

Increased
- Prevalence of myocardial fibrosis
- Risk for atrial fibrillation
- Risk for Bradycardia
- Aortic Diameter
- Progression of ARVC
Decreased
- Carotid Intima-Media Thickening
Increased or Decreased
- Coronary Artery Calcification

54
Q

What potential longevity effects occur from acute and chronic endurance exercise?

A
  • Increased life expectancy
  • Decreased risk for cardiovascular mortality
55
Q

What did the comparisons between the Dallas Bedrest and Training Study + the 30 yrs study observe?

A
  • A more profound impact on cardiovascular capacity observed in bedrest than 30 yrs of aging
56
Q
A

KIN 335 (12 decks)

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