4. Cardiopulmonary Adaptations to training in older adults Flashcards

1
Q
  • aerobic capacity is the single best measure of what? (also known as what?)
  • what does aerobic capacity represent?
  • determined by what?
  • can be measured in (2) terms)
  • usually measured how (3)
A
  • measure of cardiovascular function (also known as work capacity)
  • represents ability of cardiopulmonary system to deliver oxygen and E substrates (to tissues) to perform work during maximal physical stress
  • determined by measuring submaximal OR maximal oxygen uptake (VO2)
  • can be measured in absolute terms (L/min) or relative terms (mL/kg bw/min)
  • usually measured while subjects walk or jog on a treadmill or ride a cycle ergometer (dif protocols exist!)
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2
Q

why is aerobic capacity so important for aging?
- explain
- result?

A
  • Cardiorespiratory fitness is one of the strongest predictors of independent living and mortality risk!!
  • due to the age-related decline in aerobic capacity, many activities of daily living represent a higher relative intensity
    IE: With a VO2max of 20 mL/kg* min, activities costing 12-15 mL/kg*min (e.g., housework, gardening), represent 75% of VO2max

RESULT:Various daily activities are difficult or impossible to perform, and individuals can become progressively less active and eventually, fitness declines and dependence increases –> vicious cycle!

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3
Q

cross-sectional and longitudinal studies show similar rates of increase/decline in VO2max –> ranging btw __-___% per _______ after the age of _____
- age-related increase/decline in cardiorespiratory fitness is expected to be most evident by age ___-_____
- more pronounced increase/decline in VO2max in what populations? suggesting what?

describe graph! vo2max vs age for trained vs sedentary

A
  • decline in VO2max –> 10-15% per decade after age 40
  • decline –> 70-80
  • decline in sedentary individuals, suggesting the importance of optimal exercise participation during aging
  • linear decrease in VO2max whether trained or sedentary
  • sedentary line is lower though –> will reach threshold for dependence earlier (ie 85 yo) than trained (105)
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4
Q

what is the fick equation? define its components

A

VO2 = Q x A-VO2 diff

Q (cardiac output) = SV x HR
- determines central O2 delivery variable
A-VO2 diff (arterial-venous O2 difference)
- O2 consumption variable

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5
Q
  • what happens to resting HR as men and women age? supine position vs sitting position
  • what about max heart rate? normal vs masters athlete? WHY? (2)
A

resting HR in supine position is unaffected
- some age-related effects are observed in seated position –> increase resting HR, since venous return is involved

  • max HR is reduced with aging (decrease 5-10 bpm/decade)
  • some longitudinal studies have noted a smaller reduction in max HR with aging in Master’s athletes

WHY reduced HR?
1. decrease number and excitability of sinoarterial node cells (initiate depolarization)
2. decrease responsiveness to sympathetic stimulation

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6
Q
  • what is often used as a measure of work intensity to determine training HR?
  • why is it problematic? (4 ish)
    solution?
A
  • maximal heart rate!
    1) Traditional equation (HRmax = 220 – age) underestimates HRmax in individuals over age 40
    2) Tanaka equations represent more accurate equations (especially after 40)
    3) Some medications affect heart rate (e.g., beta-blockers)
    4) if underestimating –> individual might not be working hard enough!

SOLUTION: Rating of perceived exertion (RPE) or the Talk Test are alternative methods for determining exercise intensity

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7
Q
  • what happens to RESTING stroke volume as we age? BUT what is something important to take into account? (2)

BUT big consequence?

A
  • SV mostly unaffected by age BUT diastolic dysfunction (caused by enlarged atria) may be present especially at older age
  • slower myocardium relaxation time (bc of changes in ion/Ca2+ channels and SA node cells) leads to REDUCED EARLY DIASTOLIC FILLING RATE in left ventricle (50% decrease by age 80)

BUT late diastolic filling is greater due to an increased blood volume in enlarged atria = CATCH-UP/compensates for lower filling rate (maintains end diastolic volume at rest!)
SO structural changes in heart mitigate lower filling rate –> same preload when older and younger!

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8
Q

what happens to stroke volume during SUBMAXIMAL AND MAXIMAL EXERCISE?
trained vs untrained
older vs younger

WHY? (5)

A
  • reduced in older trained and untrained men compared to younger adults
    *as exercise intensity increases, SV decreases

1) Reduced preload (left ventricular filling) –> doesn’t keep up during exercise (vs at rest)
2) Increased afterload (bc peripheral changes = increase peripheral resistance)
3) Reduced left ventricular contractility –> SA node, Ca2+ release
4) increased left ventricular stiffness –> less able to stretch
5) Prolonged contraction time

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9
Q

what happens to cardiac output in older vs younger adults?
a) during supramaximal exercise? (2)
b) at maximal exercise intensity

A

a) CO for a given intensity will be similar or slightly lower in older vs younger adults
- can be maintained at the expense of an increased heart rate compensating for a reduced stroke volume
b) older adults (vs young endurance athletes) have age-related decrease in max CO due to lower max HR and lower stroke volume
*depends on fitness level

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10
Q

a-VO2 difference an aging
- what happens?
- what plays an important role after age 65%?
- why? (5 ish)

A
  • lower a-VO2
  • decline in ability of mitochondria to consume O2 plays an important role!
  1. aging vascular system is less able to redirect blood from inactive tissue to working muscle (lower vascular tone)
  2. lower O2 uptake by muscle mitochondria:
    a) decrease mitochondria density, volume, respiration capacity (promotes ATP prod)
    b) decrease oxidative enzyme activity
    c) decrease capillary-to-fiber surface ratio (less gas exchange ratio)
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11
Q

early studies on _________ training in older adults demonstrated that cardiovascular fitness (ie WHAT?) improved by around ___% after ___-____ months of training
- more recent studies indicate that similar improvements in ________ occur after ___ weeks of _________ training
- CONCLUSION?

A

on endurance training –> ie VO2max –> improved by about 20% after 6-12 months
- improvements in VO2max occur after 12 wks of aerobic training

older adults are capable of improving their CV function in response to aerobic training!

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12
Q

Effects of aerobic training interventions
- following ____ months of aerobic training that progressed from low (____% HRR) to high (____% HRR) intensities of _________ exercise –> increase in VO2max of ___% was possible for both older women and men btw ___-____ yo
- THEREFORE, even though WHAT, WHAT?

A
  • 12 months of aerobic training –> 40% (for 1st 6 months) to 75% HRR (for last 6 months) of continuous exercise –> increase in VO2max of 30% –> 60-70yo
    THUS: even though low intensities of exercise can produce small but significant increases in VO2max –> higher training intensities can result in more pronounced increases in VO2max! –> intensity matters!
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13
Q

MA of controlled clinical trials evaluating effect of aerobic exercise on VO2max in adults aged 60 years +
- 80 studies used ________ as primary training modality
- improvements in VO2max were observed at what intensity, frequency and duration&

A

WALKING!
- >=60% VO2max
- >=3days/wk
- >= 16 wks

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14
Q

EFFECTS OF AEROBIC TRAINING ON HR AND SV:
> ___ months of mod-intensity aerobic training (>___% VO2max) is associated with LOWER/HIGHER HR at rest and submaximal workload
- what happens to max HR after training? and SV?
WHY? (3)

A

> 3 months at >=60% VO2max –> lower HR
- Max HR generally remains unchanged after training BUT an increase in SV can be observed (especially at higher intensities)

  1. increase sensitivity to circulating catecholamines (ie NE)
  2. decrease peripheral vascular resistance (important for determining MAP)
  3. increase peak rate of ventricular filling rate (increase end-diastolic volume)
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15
Q

EFFECTS OF AEROBIC TRAINING on a-VO2 difference
- after > ___ weeks of (what intensity) aerobic training, what happens to a-VO2 difference at rest and during submaximal and maximal exercise in older adults?
HOW?

A

> 12 weeks –> INCREASES!
HOW: increase mitochondrial density, volume and function –> enables working muscles to extract more O2 from blood
*especially important for older adults with the lowest levels of cardiorespiratory fitness (greater benefits for them!)

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16
Q

EFFECTS OF EXERCISE TRAINING ON BP:
- what is the effect of exercise training on systolic and diastolic pressure for older adults with normal or high BP?
- greater effects are typically observed if what occurs?
- what can also help modify BP? though effect is more profound in which population?

A
  • improved systolic and diastolic BP!
  • greater effects if weight loss occurs (shows importance of nutrition and PA!)
  • resistance training also reduces blood pressure –> effect more profound in those with hypertension
17
Q

MA of 44 RCTs –> influence of exercise training on BP responses in normo or hypertensive subjects 21-79 yo
- weight net increase/reduction of BP in response to exercise training >___ weeks –> how much SBP/DBP?
- exercise training at what frequency, time, intensity?

A
  • reduction in BP, > 4 weeks –> 3.4/2.4 mmHg (quite clinically relevant)
  • 3-5 sessions/wk
    -30-60min/session
  • 40-50% max exercise performance leads to BP benefits
18
Q

SUMMARY: effects of exercise training on CV system
- changes in the ________ of VO2max contribute to a linear increase/decline in aerobic capacity and WHAT with aging
- (2) components play a role in the impairment of aerobic capacity commonly observed in aging
- aerobic training interventions can improve both (2) CV responses to exercise –> results in important implications for (2)

A
  • determinants of VO2max –> linear decline in aerobic capacity AND exercise tolerance
  • central (CO) and peripheral (a-VO2 diff) components
  • improve both maximal and submaximal CV responses to exercise –> important implications for functional independence and quality of life
19
Q

maximal oxygen uptake (measured through which variable) is a stronger predictor of mortality than (3)

A

hypertension, smoking and diabetes!

20
Q

Cardiovascular disease stats:
- which leading cause of death in Canada? vs worldwide?
- claims lives of approx. __________ canadians per year
- ____ M Canadians live with CV disease or effects of stroke
- risk of developing CVD is greater for _______ but with increasing age, _____ have a higher incidence
- what is an independent non-modifiable risk factor for CV disease?

A
  • 2nd!
  • 70 000
  • 1.6M
  • greater for males, but with increasing age, females have a higher incidence
  • older age!
    *ppl are living until older –> need to be PROACTIVE vs reactive
21
Q

defining CV disease
- can refer to several conditions affecting (2), including (4)
- which 3 are often grouped together as CVD?

A

affecting heart and blood vessels
- Coronary artery disease
- cerebrovascular disease or stroke
- peripheral vascular disease
- chronic heart failure

  1. heart/vascular disease
  2. stroke
  3. hypertension
22
Q
  • what are 4 non-modifiable risk factors for CVD?
  • reducing risk factors before a 1st CVD event can prevent or postpone ____% of all _________
  • risk factors can present as early as age ____!!
A
  • age, sex/gender, family history, ethnicity
  • 33% of all deaths
  • 20!
23
Q

Non-modifiable CVD risk factor: AGE
- aging is associated with ___________ cardiorespiratory fitness due to (2)
- with aging, VO2max ________ by ___-___% per decade
- at age 80, a person’s VO2max is roughly _____% of that age 20!!
- recall, what are age-related cellular, structural and functional changes in heart and blood vessels? (7)

A
  • decrease cardiorespiratory fitness due to declines in VO2max and structural deterioration of heart and blood vessels
  • declines by 10-15% per decade
  • by roughly 50% of that at age 20!!
  • myocardial hypertrophy
  • reduced left ventricular compliance
  • arterial stiffening
  • endothelial dysfunction
  • imbalance in the autonomic nervous system function
  • systolic hypertension
  • increased susceptibility to conduction system disorders
24
Q

Non-modifiable CVD risk factor: SEX/GENDER
- risk for men? WHY?
- risk for women? WHY?
- which subpopulation of women have a greater risk?
- are men or women more likely to die within the year following a heart attack?

A
  • men are 3-5x more likely to have CVD than premenopausal women –> bc men have bigger hearts, bigger body, metabolic predisposition for plaque accumulation, no protective estrogen
  • after menopause, risk for CVD increases for women to almost the same level as men –> bc no more estrogen = no more CV protection
  • younger women who have diabetes are at the same risk for heart disease as age-matched men
  • women!
25
Q

____________ is the #1 killer of women over the age of 35 worldwide, accounting for more deaths every year than all cancers combined
WHY? (4)

A

heart disease!

  • ANATOMICAL FACTORS: Women generally have smaller hearts/blood vessels than men –> more prone to blood clots/blockages and more difficult to repair
  • Traditional risk assessment underestimates risk for heart disease in women –> need to also consider female-specific conditions (i.e., pregnancy complications (preeclampsia, GDM), menopause, polycystic ovary syndrome)
  • Heart attack symptoms present differently in women, leading to under-recognition (e.g., upper back/stomach ache, shortness of breath, fatigue) (vs chest tightness in men)
  • Diagnosis and treatment of heart disease differ in women –> Leads to women being under-diagnosed and under-treated!!!

*overall lack of research!!!

26
Q
  • define menopause? typically when?
  • why does CVD risk increases during menopause?
  • who has even greater risk of CV health issues later in life?
  • how to reduce risk of CVD?
A
  • Menopause = time when menstrual periods permanently stop, marking the end of reproductive ability (typically occurs between the ages of 45 and 55)
  • Menopause can increase risk of CVD due to hormonal changes (estrogen levels decline) associated with higher blood pressure, higher blood glucose, and less favourable lipid profiles
  • Women who experience menopause before age 45
  • Monitoring women’s health during midlife can help identify risk factors and implement early intervention strategies to reduce the risk of CVD
27
Q

Non-modifiable CVD risk factor: FAMILY HISTORY
- family history of CVD is a strong indicator of personal risk of CVD
- positive family history involving first-degree relatives is associated with __-fold increase in risk for CVD
- what are 4 aspects of family history that indicate higher risk for CVD?

A
  • 2-fold!
  • Early onset of CVD — e.g., coronary artery disease in men younger than 55 and women younger than 65
  • CVD in 2-3 relatives on the same side of the family
  • Late onset of CVD on both sides of the family
  • Loss of a family member to sudden cardiac death
28
Q

Non-modifiable CVD risk factor: RACE AND ETHNICITY
- ethnicity and race can have (2) influences that predispose individuals to CVD
- which ethnicities (3) are at higher risk?
WHY? (2)

A
  • genetic and environmental
  • Indigenous, African-American and Asian
  1. high BP and diabetes are more common (genetic predisposition)
  2. cultural differences in lifestyle factors (ie physical inactivity, diets that are higher in sat fat and sodium) play an important role –> quite modifiable though
29
Q

what are 8 modifiable risk factors for CVD?
- cumulative effect?

A
  1. high BP
  2. obesity
  3. diabetes
  4. elevated stress
  5. tobacco use
  6. high cholesterol
  7. physical inactivity
  8. excessive alcohol use
  • increase number of risk factors = increase risk of CVD!
  • as you get older, more and more risk factors accumulate ish
30
Q

case study:
Shirley is a 75-year-old African-American woman and experienced a heart attack two years ago caused by coronary atherosclerosis. Shirley has not participated in any exercise since she moved from the area where she attended a supervised cardiac rehabilitation program for 3 months. She is cautious about physical activity because she fatigues easily and can get out of breath with daily activities and exercise. Shirley has stage 2 uncontrolled hypertension (160/100 mmHg) and a BMI of 26 kg/m2. She quit smoking shortly after her heart attack but still drinks a moderate amount of alcohol (~2-3 drinks/day). Shirley has joined the local walking group with her neighbour, but does not know the frequency, intensity, and duration for which she should be exercising.

  1. What modifiable and non-modifiable risk factors are contributing to Shirley’s cardiovascular disease (CVD)?
  2. What frequency, intensity, and duration of walking should Shirley participate in to observe improvements in her maximal aerobic capacity (VO2max)?
A

1.
MODIFIABLE:
- physical inactivity
- alcohol
- hypertension
- overweight
- history of smoking ish
NON-MODIFIABLE:
- age: 75 (nearer threshold for decreased independance)
- women: more risk after menopause + after 65
- ethnicity (african american)
- history of heart attack ish

  1. F: 3-5 days/week: starting with 3, depending on her level of tolerance
    I: moderate to high, RPE >7, 75% HRR, 60% of VO2max ish –> want her HR to be higher, increased breathing rate, difficulty talking
    T: walking
    T: 30-60min, ultimate goal: 150min/wk –> at least 12 wks to see benefits in VO2max