Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sports Science Y3 S1 > Physiology lectures > Flashcards

Physiology lectures Flashcards

You may prefer our related Brainscape-certified flashcards:
Sports Trivia flashcards Biology 101 flashcards
1
Q

Why is there a declining CVD mortality? Consequences?

A

BEtter acute management, better control of RFs e.g. hypertension and cholesterol.
More people living with chronic CVD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is CVD

A

Diseases affecting the heart and vascular/ circulatory system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How many deaths is CVD reponsible for?

A

27% in Uk in 2004 according the BHF, 2015

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Economic implications of CVD

A

16.1bn in 2014
19.8bn in 2020
Centre for economics and business research, 2014

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the process of atherosclerosis

A

Response to injury hypothesis
Endothelial damage
Lipid accumulation in intima
Migration and proliferation of SM
Oxidation of lipid.
Immune cell migration and proliferation/ immune response - T cell activation (enhance platelet aggregation and adherence).
Uptake of lipid by macrophage (from recruitment of monocytes monocyte) to form foam cell.
Forms plaque
Proliferation of smooth muscle cells and further uptake of lipid.
Forms fibrous plaque and may become calcified (reducing elasticity).
May haemorrage, thrombosis, embolise, total occlusion
Symptoms at 45% stenosis - clinical horizon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe stages of CVD and reference

A 
3000 autopsied bodies
10-20yrs fatty streak begins
20-30yrs - fibrous plaque
40 yrs calcification
45+ clinical symptoms
McGill et al 2000
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Prevalence of atherosclerosis in Korean War and source

A

77% of yound men (22.1yrs) autopsied after Korean war. Varied from fibrous thickening to complete occlusion of one or more of the main branches
Enos et al 1953

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Early work showing PA links to CVD mortality, references and limitations

A

Professor Jeremy Morris and the London Bus studies.
Conductors vs drivers
Conductors had half the number of heart attacks than drivers, occured later and were less severe.
Cross sectional - self selection bias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Example of dose response between PA and CVD

A

Morris et al 1990
Whitehall studies
9k civil servants followed for an average of 9 years.
Those that do vig activity >6 MET or considerable amountsof cycline or walking pace >4mph had less than half non fatal or fatal CHD than those that do not.
Also showed a dose response between number of bouts of vig sport and age adjusted rate of CHD. Accounted for confounders including fx, stature, health attitude, smoking, BMI, history of disease. Relationship not found for non-vig PA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Example of change in PA and CVD risk.

A

Paffenbarger et al 1993
Harvard alumini health study.
Asked activity in 1963/66, asked again 12 yrs later in 1977. Recorded activity ‘yes’ or ‘no’ - very arbitary.
Those tha did MV sports ‘no’ ‘yes’ decreased RR by 43%. vs no no.
PA index >2000kcal/week no-yes decrease by 17%. vs no no
Lowest overall risk in yes-yes.
Adjusted for smoking hypertension, BMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Example of exercise intensity and link to CHD

A

Lee et al 2003
Harvard Alumini
Intensity of exercise has a strong relationship with risk of CHD independent of total energy expenditure.
Limited as not objective but VAS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Example of dose response between fitness and CHD

A

Barlow et al 2012 - Dallas Texas
Fitness determined on maximal treadmill test.
+11,000 individuals ages 30-50 followed up 27 yrs.
.29HR between fittest quintile and unfittest.
1MET increase in baseline cardioresp fitness associated with 18% reduction in CVD deaths after adjusting for confounders

Framingham “low risk” people only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is fitness possibly a better marker of PA, possibly not?

A

Objective measure.
Collerates well with PA
Influence of genetics.
More correct categorisation.
INcreases precision of measurement.
Increases chances that true findings will not be missed.
Supported by fitness being better predictor that PA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

General point on dose response between PA and CHD

A

Hardman & Stensel 2003 noted that 30 studies, 2/3 of studies support dose, more in fitness. Some show increased risk at high levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Example of change in fitness and change in risk of CHD

A

Blair et al 1995
Physically active should remain active
Physically inactive should become active
5yr between maximal treadmill testing and 5 yr follow up.
Reduction in mortality of 44% if became fit.
Reduction in CVS risk of 52% if become fit.
Arbitatory - fit or unfit?
However also seen between quintile 2/3 but less strong.
Dose response - Each increase in minute between treadmill times resulted in a decrease of 7.9% risk of mortality.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Summary of evidence on PA/ fitness vs CVD. Way to strengthen?

A

All cohort/ prospective.
Strengthens association but proving? Self selection and subclinical disease causing sedentariness?
Randomised needed but unethical with disease endpoints. Affect on other RFs - direct and indirectly show improvement to help ‘prove’ increase in activity reduces CVS. Also provide evidence for biological plausibility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Link between sitting time and CVD mortality?

A

Katzmarzyk et al 2009
54% increase in CVS mortality between no sitting and sitting all day
17000 canadian men 12 yrs independent of other factors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Evidence for the effect of non modifyable risk factors on CVS mortality

A

Genetics
Khera et al 2016.
50 polymorphisms associated with CHD.
Low, mod or high depending on which ones were present.
Lifestyle also low mod or hig.
Genetics has an independent association - 75% higher risk than low risk.
Regardless of genetic risk PA can decrease risk by approx 50% - no obesity, regula PA, healthy diet and smoking status

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explaination of why PA lowers CVD

A

Genes evolved in a active/ hunter gatherer way of life. genes that decreased mortality with PA became favorable, only recently that genes that cause decreaes in mort with sendentary lifestyle have become unfavorable.
PA through direct or indirect (other RFs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the relationship between lifestyle RFs and clinical endpoints and evidence

A

Lifestyle risk factors (PA, smoking and diet) effect both novel risk factors and established e.g. endothelial function, inflammatory pathways, thrombosis/ coagulaton, arrhythmia and blood pressure, lipids and adiposity. These then cause subclinical vasc disease, onto symptoms and diability (clinical endpoints)
Mozaffarian et al 2008.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Risks of different modifiable RFs and MI in men

A 
Pa similar to BP, high cholesterol and smokng risk of MI in men
Hypertension 2.1
high cholesterol 2.4
Smoking 2.5
Powell et al 1987
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Cross sectional evidence on the effect of PA on lipid profile?

A

Countries
Increasing average cholesterol level causes increased total serum cholesterol and decreased HDL-cholesterol
Simons 1986

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Effect of HDL on CHD mortality

A

Increase in 0.26mmol/l increases CHD risk by 50%

Kannel 1983

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Evidence between HDL and PA

A

Cross sectional
LaPorte 1983
Increasing sedentary lifestyle decreases HDL.
Runners highest, then joggers, sedentary, chronic pain, Old SCI, recent SCI, New SCI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Can exercise intervention improve cholesterol levels main reference?

A

Slentz et al 2007
240 sedentary overweight ppl randomised to 6 months to control or exercise intervention.
Vig intensity better than mod intensity at decreasing HDL (increase in 3mg/dl) and small LDL. Mod is better at decreasing VLDL-TAG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Back up reference.

A

Wood et al 1985 smaller study, non randomised intervention but similar results

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Does the reduction in cholesterol as a result of exercise result in less CHD?

A

Kramsch et al 1981 - diet and exercise on cholesterol and CHD in monkeys.
HDL lower in exercise
LDL + VLDL - only slighly improved with exercise.
However
35% to 10% coronary artery narrowing in both left and right coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe anecdotal evidence regarding the benefits of exercise on blood flow

A

Clarence DeMar (Mr Marathon)
Currens & White 1961
2-3x diameter of CAs
Some artherosclerosis but no impairment of blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Observational evidence regarding the BP lowering effects of exercise

A

Kuung Bushmen in Botswana
Truswell et al 1972
Maintain in SBP and DBP in bushmen with age in mena nd women - BP does not invariably increase with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why is BP reduced by exercise

A

After exercise Co falls but arterial vasodilation takes longer
BP = CO x TPR
longer life with lower BP
Also reduces symp tone at rest due to catecholamine release in response to exercise
May modify baroreceptor effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Evidence that exercise effects BP from old stuff. - observational

A

Harvard - Paffenbargar 1983 - vig exercise decrease in 35% hypertension in 6-10yr follow up. (only men)

Aerobic centre
Blair et al 1984
52% more likely in least fit quintile compared with most fit to develop hypertension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

experimental studies that show that exercise and BP in African Americans

A

Kokkinos et al 1996
46 men with severe hypertension.
stationary cycling 3x a week
Sig decrease in DBP and IV septum thickness and LV mass at 16 weeks (better function)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Experimental design and exercise and SBP

A

Miyashita et al 2008.

Walking 10 x 3 mins or 1 x 30mins a day can lower SBP approximately 17mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Meta analysis of treatment of BP

A

Meta analysis in 2001 average or 3.4/2.4 decrease in BP, 3x more if high BP at baseline.
Fargard 2001

35
Q

How does exercise improve coronary blood flow?

A

Less lipid so less atherosclerosis, recruitment of coronary collaterals, endothelial function - No in response to exercise/ shear stress force exerted by blood from and SM dilatin - flow induced arterial vasdilation. Endothelial dysfunction occurs in early atherosclerosis and can trigger myocardial ischaemia (gielen et al 2001)

36
Q

Cross sectional evidence that exercise helps dilating capacity?

A

Althetes greater dilating capacity than inactive

Haskell et al 1993

37
Q

Effect of HIIT on dilation of CAs

A

Hambrecht et al 2000
Exercise vs control
Vessel diameter with angiography
6 sesh/ week, 10min/session, 80% HR max 4 weeks
Sig imporvement with dilation in response to ach

38
Q

Effect of acute exercise on endothelial function

A 
Gill et al 2004
Improved endothelial function by approximately 15% - fasting and post prandial.
20 middle aged men
90 min walking at 50% VO2max
Doppler
39
Q

Inflammatory mechanism by which exercise decreases CHD

A

Via CRP decreases and other inflam markers. Ford 2002. INcrease CRP may decrease NO bioavailability in endothelial cells, increase PAI and independently related to insulin sensitivity.

40
Q

How may exercise effect coagulation and fibinolysis acutely

A

Pro coagulant state
Increased fibrinogen, thrombin, platelet activation, haemoconc.
Explain Cardiac events.
Followed by rapid increase in fibrinolytic activity.
Imhof and Koenig 2001
Rauramaa et al 2001.

41
Q

How may exercise effect coag and fibrinolysis long term

A

Decrease PAI, INcrease t-PA, reduced platelet agg, reduced fibrinogen.

42
Q

How may exercise effect insulin resistance?

A

Well established it enhances sensitivity and counters insulin resistnace (direct and indirect)
Ivy 1997

43
Q

exercise and overweight and obesity?

A

May prevent.

Obesity - direct and indirect CVS also.

44
Q

Why does high LDL lead to more cholesterol laden macrophages

A

Normally regetor down regulated but returned in macrophages hence foam cells. - higher addinity if oxidised too

45
Q

Regulation of Insulin in lipids

A

Activate lipoprotein lipase postprandial - removes TGs when they are highest.

46
Q

Describe lipoprotein lipase saturation and reults

A

Does both chylo and VLDLs. More affinity for chylomicros. IF low VLDL then faster clearence of chylo.
Insulin supresses VLDL output, resistance causes increases VLDL (even if broken down shell becomes LDL too) and atherosclerosis, incrased chylomicrons/ TG. so more in intima/ exposed to endothelial cells

47
Q

Relationship between TGs and HDL

A

Increased TG = decreased HDL

As TGs rich lipoproteins break bown they form the shell components to HDL

48
Q

Why are smaller denser LDLs worse?

A

More likely to leave circ and entre intima.

Break down of VLDL and low HDL associated with these

49
Q

What is PA?

A

Howley 2001

PA - Any bodily movement produced by skeletal muscle that substantially increases energy expenditure

50
Q

What is exercise?

A

Exercise - A sub category of leisure time PA in which planned, structured and repetitve movements are performed to improve or maintain one or more components of physical fitness.

51
Q

Describe primary cause of SCD in <35 yrs

A 
HCM - hyperobstructive cardiomyopathy
Inherited disease of the heart muscle
Left and right ventricle muscle wall is thickened
Compromise cardiac function
Lead to dangerous arrythmias
1 in 500
British Heart FOundation
52
Q

How is Sudden CVS event linked to amount of vigorous exercise? Prospective and limitations

A

Albert et al 2000
21,000 physicians
12 years
122 sudden deaths
Absolute risk is very low 1 per 1.5 mil episodes.
Inreased in vig exercise and up to 30 mins after RR = 16.9.
Higher the number of Vig exercise per week, the lower the risk <1/wk = 74.1 and >5 = 10.9.

Limit:

  • Only men
  • Only physicians
  • Fewer cases than other

Positives
- Long follow up, large study

53
Q

How is MI risk linked to amount of vigorous exercise? Retrospective and limitations

A

Mittleman 1993
Case control style
Contacted people for interview 4 days average after MI.
Ask about frequency of vig exercise. Compared with simialr controls.
Risk raised in vig activity. Lower risk if more frequence.
+100RR if av frequency of 0.
Vig exerertion transiently increase risk of AMI/ SCD particularly among habitually sedentary persons with occult or known CAD performing unaccustomed, vig PA.

Positives:
-more cases than albert, didnt do 0 frequency in his

Limitations:

  • Recall bias - although only 4 days
  • C
54
Q

Describe incidences of cardiac arrest during long distance runners and causes

A 
Kim et al 2012
More in marathon than half
More in older
More in men
.54 per 100,000 participant-hours
As much as 50% due to HCM
55
Q

What does Thompson et al 2007 show? main statements

A

Consensus statements

Overall risk of SCD/ ACM is very low

Both highest in inactive performing unaccustomed exercise.

Athero in older
SCD in young

HCM and anomolous Cas are not improved by vig exerices unlike CHD

56
Q

Types of hereditary or congentital CVS abnormalities

A

HCM, CA abnormalities, arrhythmias/ conductio disorders e.g. long QT syndrome, AS, Aortic dissection and ruture from CT disroder e.g. Marfans, mitral prolapse.
Arrhythmia is COD

57
Q

Suggested triggering mechanism in asymptomatic people of atherosclerotic disease Thompson?

A

Exercise induced CA spasm
Increased wall stress from increased HR and BP
Flexing of atherosclerotic epicardial CAs
Plaques disruption or erosion
Deepening of Coronary fissures in plaques
Catecholamine induced platelet aggregation

58
Q

Suggested triggering mechanism in symptomatic ppl?

A

Iscaemia-induced VF from plaque
1 - decreased perfusion due to shortened diastole
2 - increased demand to to increased HR and CO - catecholamine repsonse
3 - decrease perfusion after exercise due to lower venous return/ BO as lower TPR

59
Q

How can time of day, activity and temp affect risk?

A

Most common in the early morning hours
Young mostly in afternoon but varies on cause.

Cold increases angina.

Increased higher rate-pressure products with activity such as snow shovelling vs treadmill

60
Q

Variation in incidence of sudden cardiac events?

A

Massive due to population studies - heteroguity, very low incidence, random chance plays a big role.
Often lack power ad have large CIs.

61
Q

Potential treatments/ preventative measures for SCD? problems with this?

A

Preparticipation screening, teaching of athletic staff to deal e.g. defibrillation, recognition of prodromal symptoms (fairly common and ignored), graded exercise programs, warm up and cool down periods, exclusion of high risk participants from certain activities.
No systemic evaluation of any of this

62
Q

Can screening help lower SCD?

A

Decrease in sudden death among athletes decreased 89% over 24 years in Italy among athletes - so many confounders

63
Q

How is SCD risk linked to distance?

A

Harris et al 2010
Increases with increased distance swam.
Increased incidence over time

64
Q

Why might running over 7.5miles per hour be for some other reason than living longer?

A

O’Keefe et al. 2012
Long term excessive endurance exercise may induce pathological structural remodeling of the heart and large arteries.
Elevation of biomarkers in extreme endurance events
Fibrosis - particularly in atria and IV septum and RV
Can get A or V arrhythmias

65
Q

Early evidence that large amounts of PA may increase RR of death?

A

Paffenbarger 1986
Increase in age adjusted RR of death over 3499kcal/week Pa expenditure from 3000-3499. Stil lower than <500.
Only Harvard peeps and males

66
Q

Link between daily PA and all cause mortality? Positives and negatives of study

A 
Wen et al 2011
Vig exercise more beneficial for ACM than mod or total PA.
Peak benefit at 40-50min/day of vig at 45%
MOderate at 90mins with 30% reduction
Largest improvement form 0
Limitations
-Taiwanese
-Questionnaire

Postiive

  • 400,000ppl
  • 8 years follow up
  • 5 cateories
67
Q

Link between cardioresp fitness and CVD mortality among men with diabetes

A 
Church et al 2005.
Benefit in ACM (lower death vate) with fitness at baseline up to >13 MET when death rate increases from 12-12.9 METs
2,300 men
15.9 yrs
Aerobic Centre
Limitations
-obese/ overweight DM patients only
- Men only
68
Q

Link between all cause mortality and running distance per week in a U shaped relationship

A

Cited in O’Keefe and Lavie 2012
U shaped relationshup between fitness and morality and morbidity,
Fintess levels above 12METS do not seem to translate into additional gains in CV health and longevity.
Increase in morality after 20miles/week

69
Q

Why did the BBC report that ‘Training very hard is as bad as no exercise at all’

A

Schnohr et al 2015
Dose of jogging and long-term mortality
underpowered, only 2 deaths in strenuous group.
Classified into light moderate or strenuous based on self reported pace and frequencey.
Adjusted for age, sex, smokig, alcohol, education and DM status there was not a signficicant result (>5% due to chance)

70
Q

Describe anecdotal evidence regarding dangers of running too much

A 
Michah True's Death
Died from heart disease
Ran 25-100 miles a day
Died on 12 mile training run
Autopsy = unclassified cardiomyopathy
71
Q

Evidence of cardiac damage in marathon runners?

A

Eijsvogels et al 2016

Elevated Cardiac Troponin suggesting myocardial damage and troponin

72
Q

Evidence of pathological changes in rates

A

Rats ran 60 mins a day for 16 weeks
Fibrosis thickening and scarring, particularly in RV free wall, IVS and LVFW.
LEads to arrhythmias

Benito et al 2011

73
Q

Summary of general points from Eijsvogels et al 2015

A

A safe upper-dose limit of exercise potentially exists
Chronic intense sustained exercise can cause patchy myocardial fibrosis particularly in atria, IVS and RV leading to arrythmias
Chronic can also lead to artery calcification, diastolic dysfunction adn large-artery wall stiffening.
Veteran endurance athletes have a 5 fold increase in the prevalence of AF
Excessive show markers of myocardial injury e.g. troponin and BNP correlated with transient reductions in RV ejection fraction

Eijsvogels et al 2015

74
Q

Definition of AF and risk of stroke

A

Chaotic electrical activity that replaces normal sinus rhythm and eliminates the contribution of atrial contraction to LV filling

Eijsvogels et al 2016

Af lead to 5x increase in risk of stroke

75
Q

UK prevalence of AF?

A

2% of pop in UK
One in four lifetime risk
Atrial fibrillation association 2011

76
Q

Incidence of AF in endurance athletes?

A

Animal models show long term intensive exercise training induces fibrosis in both atria and susceptibility to AF.
There is a variable but high prevalence in different elite athlete populations compared with control
RR 5.5 to 14.4
Wilhelm et al 2012

77
Q

Changes and reversibility of AF and structure in endurance atheleties

A

Guasch et al 2013
Programme in rats after 8-16 weeks on treadmill
Time matched controls
AF inducibility increased after 16 weeks and rapidly returned to baseline with detraining.
Atrial dilation and fibrosis after 16 weeks of training and failed to fully recover following 4-8 week cessation
Autonomic changes, atrial dilation and fibrosis and potential mechanisms. Vagal promotion - augmented baroreflex responsiveness.

78
Q

Case report of normal sturcture of heart with exericse

A 
De arujo et al 2014
Case report on a six time ultraman winner and a normal heart
47 yr old
50,000h of training and competition
35yr career.
Normal ECG, Echocardiogram and MRI
79
Q

Does AF from long distance affect mortality?

A

Moderate levels of exercise reduce AF risk and even though risk is increased in very high, there is no effect on mortality. No firm threshold or guideline from existing literature
Bosomworth 2015

80
Q

Relationship between exercise capacity and AF

A

Andersen et al 2015
U shaped relationship between exercise capcity and muscle strength and risk of arrhythmia driven by a direct association with risk of AF and U shaped association with bradyarrhythmia

81
Q

Risks of stroke, death and recurrent stroke from AF

A

Despite higher AF and potential strok risk. Death and recurrent stroke is similar to nonskiers. HIgh incidence of AF but lower risk of recurring stroke
700,000 people
600 incidences of stroke
Hallmarker et al 2015

82
Q

Is there a sufficient amount of evidence to provide guidelines for risks of AF?

A

no

83
Q

Arguments against screening atheletes

A

Small proportion of yong athletes at risk of SCD
Poor sensitivity of health questionnaires and physical examination but ore elaborate are costly
ECGs can detect (not CAD) but some causes however vary on activity, age, race, sex and skilled docotrs are needed to avoid large num of false positive test results
- implementation hampered by lack of resources and infrastructure and connot be regarded as cost effective in most countries.

Sports Science Y3 S1 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions