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KIN 335 > Refuting Myth of Non-Response and Exercise Amount > Flashcards

Refuting Myth of Non-Response 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What is subsequently activated when the parasympathetic vagal tone is withdrawn during the cardiac response to exercise?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
  • no decrease in blood plasma
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17
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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18
Q

What does an increase in blood concentration of CK indicate?

A
  • Cell damage with membrane injury
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19
Q

Why cant CK exit the cell?

A
  • Their size
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20
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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21
Q

What is the troponin complex composed of?

A
  • Subunits
  • Troponin C
  • Troponin T
  • Troponin I
22
Q

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

A
  • Troponin C
23
Q

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

A
  • Troponin I
  • Troponin T
24
Q

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

A
  • Detecting Cardiac Damage
25
What activity types have studies observed exceeding levels of cardiac troponin compared to those used to diagnose acute myocardial infarction?
- Marathons - Triathlons - Endurance Cycling - Ultra-endurance races
26
Why might there be increases in cardiac troponin following endurance activity?
- 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
27
Describe the remodeling of left and right ventricles due to endurance training
- Mild/moderate eccentric LVH and RV dilation - Biatrial enlargement - Normal to slightly reduced resting LVEF - Normal/Enhanced Early LV Diastolic Function - Normal/Enhanced LV twisting/untwisting
28
What remodeling of left and right ventricle occur from strength training?
- Mild concentric LVH/ No RV remodeling - Normal/Mild enlarged Left atrial size - Normal/hyperdynamic resting LVEF - Normal/Slight reduced Early LV Diastolic Function - Compensatory Increase in late LV diastolic function
29
What is myocardial fibrosis characterized by?
- Accumulation of collagen in the extracellular matrix of the heart
30
When does myocardial fibrosis most commonly occur?
- After Myocyte injury from ischemia - But can have nonischemic causes
31
What is myocardial fibrosis divided into?
- Reactive interstitial fibrosis - Infiltrative Interstitial fibrosis - Replacement fibrosis
32
What studies are needed regarding fibrosis and athletes?
- determine if it is reversible with exercise cessation - Determine clinical significance of persistent fibrosis in athletes
33
What did the rats who did endurance training equivalent to 10 human years develop?
- eccentric cardiac hypertrophy - Diastolic dysfunction - Atrial dilation - Collagen deposition at right ventricle and both atria
34
What biochemical evidence suggests myocardial fibrosis in elite middle-aged endurance athletes?
- Increased plasma markers of collagen syntheses and degradation
35
What is the QT interval?
- electrocardiographic measurement of the time between depolarization and repolarization of cardiac ventricles
36
What is the QT interval generated by?
- Passage of calcium, potassium, and sodium ions through cardiac ion channels
37
What leads to Long QT Syndrome? What can that lead to?
Abnormal increase in QT interval - Lead to sudden cardiac death
38
What gene defect is most prevalent for producing Long QT syndrome?
- KCNQ
39
What type of gene defects produce LQTS?
- Cardiac ion channel genes - 10 Identified
40
What percentage of LQTS - 1 individuals cardiac events occur during exercise?
75%
41
What percentage of LQTS 2&3 individuals' cardiac events occur during exercise?
5%
42
What do studies suggest increase the risk of ventricular tachycardia and sudden cardiac death in LQTS - 1 patients?
- Enhanced Vagal Tone
43
How does exercise training reduce heart rate?
- Increasing parasympathetic or vagal tone
44
What do studies suggest the increases in vagal tone from exercise training could do?
- Increase arrhythmia risk in individuals with genetic predilection for LQTS-1.
45
What are the potential acute cardiovascular risks to acute and chronic endurance exercise?
Increased - Risk of Sudden Cardiac Death - Risk for Acute Myocardial Infarction Decreased - Ventricular Function of the Heart
46
What potential acute myocardial injury could occur from acute and chronic endurance exercise? | list biomarkers
* CK and CK-MB Concentrations -membrane damage * Cardiac Troponin Concentration -oxidative stress -mechanical stress -ischemia * BNP and NT-proBNP concentration -membrane damage
47
What potential cardiac remodeling occurs from acute and chronic endurance exercise?
Increased - Dimensions of right and left ventricle - Dimensions of right and left atria - Wall thickness
48
What Potential Cardiac Maladaptations could occur from acute and chronic endurance exercise?
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
49
What potential longevity effects occur from acute and chronic endurance exercise?
- Increased life expectancy - Decreased risk for cardiovascular mortality
50
What did the comparisons between the Dallas Bedrest and Training Study + the 30 yrs study observe?
- A more profound impact on cardiovascular capacity observed in bedrest than 30 yrs of aging

KIN 335 (14 decks)

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