KNES 454 Exam 1 (NEW)

ageism

refers to the stereotypes (how we think), prejudice (how we feel) and discrimination (how we act) towards others or oneself based on age

Individual (Personal/Casual) ageism

• ideas, attitudes, beliefs

• E.g. stereotypes about older people

Institutional ageism

• knowledge of bias, overt, microaggressions

• E.g. greeting cards that use stereotypes

Unintentional ageism

• without awareness or malintent

• Covid-19 policies, lack of emergency procedures (flood, heat wave, etc.)

Aging

complex biological process, with the passage of time, leads to the progressive loss of physiological function, resilience, and adaptability, and functional performance

Chronological Age

Adult: 25-44 yrs

Middle-Aged: 45-64 yrs

Young-Old: 65-74 yrs

Old: 75-84 yrs

Old-Old: 85-99 yrs

Oldest-Old: 100 yrs +

Primary Aging

• Natural, inevitable, time-dependent changes

• universal age-related changes within a species that are independent of disease or environmental influence

Secondary Aging

accelerated changes and clinical symptoms caused by external factors (environment & disease) and lifestyle choices

Healthspan

The period of life spent free of major chronic disease and disability.

Compression of Morbidity

Increase “healthy life” and shorten the period of illness and disability to the end of life

Population Aging

Driven by several factors:

• Aging baby boomers

• Lower fertility rates

• Longer life spans

3 Theories of aging

biological, psychological, and sociological explanations

Error-Based (Damage) Theories

Aging is the result of the gradual accumulation of damage, errors, or cellular dysfunction

Program- based (Genetic Theories)

Aging may result from biological timetables or developmental processes that continue in later life and become harmful

Damage Theories

accumulation of cell damage causes cellular dysfunction

Wear & Tear Theory

• Key idea: Tissues deteriorate from repeated use, like a machine breaking down.

• Result: Degeneration over time

DNA Damage/Mutation Theory

• Key idea: Accumulation of mutations begins to produce irreversible defects

• Result: Faulty cells, impaired repair systems, disease

Free Radical Theory

Evidence is mixed; the use of antioxidants doesn’t consistently slow aging

• Key idea: Reactive oxygen species can damage proteins, lipids, DNA, and other cellular structures

• Result: Cellular damage builds up, may contribute to dysfunction over time

Cross-Linking Theory

• Key idea: Proteins, DNA, and other molecules become bound together through abnormal chemical bonds called crosslinks

• Result: Crosslinked proteins lose flexibility and function, → stiff tissues and impaired cellular communication

  • May affect the lung, kidney, vasculature, GI system, skin, muscles, ligaments, and tendons

Sun Damage

Cross-Linking impacts the production of collagen and elastin

collagen & elastin

major proteins of the extracellular matrix in many connective tissues

‒ comprise 30-40% of body proteins

‒ present in all body cells; not renewed

‒ affects blood vessels, lung tissues, skin, and cell permeability

‒ an active lifestyle and healthy diet seem to inhibit cross-linking

Program (genetic) Theories

Programmed by our genes

• Aging follows a “biological clock” programmed into each cell

• Suggest aging is not random, but rather follows an internal timetable

Telomere Shortening Theory

Key idea: Telomeres shorten each time a cell divides

• Result: Eventually, cells can no longer divide → “cellular senescence”

• Programmed/genetic perspective: Cell division limits and telomerase activity are biologically regulated

• Damage/error perspective: Progressive telomere loss can be understood as the accumulation of molecular damage

Hayflick Limit

Normal human cells can only divide a limited number of times before they stop dividing ‒ # of cell divisions is fixed and quite constant (40-60 times, then die)

Neuroendocrine Theory

• Key idea: Aging results from changes in hormones and signaling pathways

• Result: Declines in growth hormone, estrogen, testosterone, and melatonin affect repair, metabolism, and sleep

Immunosenescence Theory

• Key idea: Immune system declines with age, reducing ability to fight infections and cancer

• Result: ↑ risk of disease, slower recovery, ↑ chronic inflammation (inflammaging)

Gradual Imbalance Theory

Neuroendocrine & immune systems age at different rates and are highly integrated

• Key Functions:

  • Adaptation to environmental challenges

  • Regulation & integration of cellular activity

  • Malfunctions lead to hormonal imbalances & deficiencies

  • Cascade of negative effects on body functions

• With age: these systems are less coordinated

  • Small imbalances accumulate → functional decline

Rowe and Kahn: “Successful” Aging

• Low risk of disease and disability

• High physical and cognitive function

• Active engagement with life

Limitation of “Successful” Aging

This model may be too narrow if it excludes older adults with chronic disease or disability who still view themselves as aging successfully

heterogeneity

Same chronological age group ≠ same function, health, resources, or life history

Age-group differences

• A snapshot comparison of people at different ages.

• Useful for describing differences between younger and older adults

• Developmentally static

Age-related change Research

• Repeated measurement of the same people over time.

• Better suited to studying the aging process, but slower and more complex.

• Developmentally dynamic

Cross-sectional (Cohort) studies

Useful for:

• Large samples

• Describing group differences

• Generating hypotheses

Be cautious about:

• Cohort effects

• Confusing age differences with age- related change

• Morbidity and disability differences across groups

Longitudinal Studies

Strength:

Can describe within-person change more directly.

Challenges:

Expensive, slow, exposed to repeated testing, cultural change, dropout, and mortality.

Cohort effects (aging research)

People born in different eras may differ in education, health care, nutrition, work, and social conditions.

Attrition (aging research)

Participants who stop participating may differ systematically from those who remain.

Survivor bias (aging research)

The oldest participants are often a selected group who have already lived longer than peers.

Typical Sample of Older Adults (aging research)

• Healthier or more mobile

• More motivated or confident

• Better access to transportation or technology

• Fewer severe health limitations

Within-individual variability

Day-to-day change in the same person

Physiological measures

Often less influenced by motivation, but still affected by health status, medications, protocol, and timing.

Performance measures

Can be influenced by fatigue, pain, learning, anxiety, encouragement, and self- efficacy.

Self-report measures

Can be shaped by recall, interpretation of questions, social desirability, and response burden.

Research design choices

• Collect data at similar times of day when possible

• Use consistent instructions, practice trials, and rest periods

• Document health status, medications, pain, fatigue, and recent activity

• Keep age bands narrow when comparing age groups

• Report variability, missing data, and dropout transparently

Age-related change in Body Shape

• Height (Stature)

  • Curvilinear changes

  • Increases until ~20 yrs./men and 16-18 yrs./women

  • After age 40, height gradually declines

    • approx. 2 - 4 cm (1-1.5 inches) over life course

Age-related changes in body weight

• Accounts for all tissues

• Between ages 40 & 70, typical weight gain is ~ 1 pound/year

• After age 70, weight typically declines (no more than 0.5%/year)

Decrease in Fat-free mass

• ↓ muscle mass

• < 40% in men

• < 30% in women

• ↑ bone mineral loss

• ↓ physical activity

Increase in Relative body fat

• ↑FM (fat mass)

  • 10-25% in men

  • 20-35% in women

• ↑ dietary intake of nutrients

• ↓ physical activity

• ↓ ability to mobilize fat

High FM (curvilinear pattern)

predisposing factor for several negative health outcomes

• Hypertension, elevated cholesterol, insulin resistance, T2DM, cardiovascular disease, certain cancers

Low FM (curvilinear pattern)

may indicate a lack of physiological reserves and may be indicative of sarcopenia or frailty

Body Mass Index (BMI)

Not a direct measure of adiposity

• Higher BMI, more likely the person has high proportion of body fat (BF)…but not always!

  • Very muscular individuals

  • Individuals with very low muscle mass

• Provides no information about fat distribution

  • Visceral adipose tissue poses greatest health risk

Waist Circumference

A strong predictor of all-cause morbidity and mortality

• > 40 inches (103 cm) for men

• > 35 inches (89 cm) for women

Centralized adiposity increases risk for:

• Cardiovascular disease

• Diabetes

• HBP

• Stroke

• Arthritis

• Sleep apnea

• Mobility impairments

Distribution of BF changes w/ age

Waist circumference (WC) increases by ~ 0.7 cm/yr

• Women show greater increase than men

• WC (and total adiposity) can increase despite decrease in BMI

• Corresponds to increases in visceral fat

Decreased hip circumference by age 60

• Progressive inability of body to store fat in subcutaneous adipose tissue mass

• Greater lipid accumulation in non-subcutaneous fat or lean tissue

  • Associated with dyslipidemia, insulin resistance, & ↑ mortality

Lipid accumulation within hepatocytes is associated with aging

Results in impaired hepatic glucose metabolism

• Associated with dyslipidemia, hypertension and insulin resistance, independent of age & BMI

Inter-muscular

• visible fat deposits between muscle fibers

• reduced muscle quality

Intra-muscular

• lipid located within the myocyte

The Obesity Paradox

Higher BMI associated with lower risk of mortality, especially as we age

Optimal survival occurs in the overweight BMI category

• 6% lower mortality rate than normal weight BMI cohort

• Overweight/obese older adults with CVD have a better prognosis than normal- and underweight counterparts

Sarcopenic Obesity

simultaneous presence of high body fat (obesity) and low skeletal muscle mass combined with reduced muscle function (sarcopenia)

• cardiometabolic disease

• increased mortility

• increased physical disability

Osteosarcopenic Obesity

clinical condition defined by the simultaneous loss of bone density, loss of muscle mass and strength, and an excess of body fat

• high fracture risk

• poor functionality

• high mortality

Cortical bone

• Outer layer

• More compact

• Long bones (e.g. femur, humerus)

Trabecular bone

• Spongy bone

• Less dense

• E.g. hip, wrist, vertebral column

Bone Mineral Density (BMD)

Normal peak bone mineral density (BMD) reached at 25-30 years of age

• Bones become more porous, rigid, brittle

• Loss in bone matrix

  • Decline in trabecular bone begins earlier and faster than cortical bone

• Greatest decline in the first 5 years post-menopause

Factors that influence Bone Health

Healthy bones – interaction of exercise, hormones, and diet

• Vitamin D & calcium (inhibits osteoclastic activity; promotes bone formation)

• Sex hormones (promote osteoblastic activity)

• Insulin, thyroid hormones (promote normal bone growth/maturity)

• Mechanical stress (promotes osteoblastic activity)

Aging Endocrine System (Bone Health)

results in lower hormone levels in both men and women, which will impact bone health

• Bone health in both men and women is negatively affected by diminished levels of:

  • Estrogen

  • Testosterone (indirectly)

  • DHEA

  • Growth Hormone and IGF-1

• Physical activity associated with:

  • ↓ testosterone/estrogens – older women

  • ↑ testosterone – older men

  • higher DHEA – both

Primary (age-related) osteoporosis- Type I: Post-menopausal

• High turnover

  • 3-7%/year for 5 years

• Affects 5–20% of women

• Primarily trabecular bone

  • Vertebral column

  • Fractures of hip, wrist, forearm

Primary (age-related) osteoporosis- Type II: Senecescent

• Evident in both men and women

• Primarily affects cortical bone

  • Leg and spinal fractures

Secondary Osteoporosis

caused by conditions/ treatments that disrupt bone reformation

• Disease Processes

• Hormonal Issues

Medications/ Chemicals

Hip fractures

most often occur as the result of a fall from a standing position

• Chronic pain, reduced mobility, disability, and an increasing degree of dependence

  • >50% never regain functional independence

• Incidence increases with age

  • After 70yrs, rate of hip fractures in women is double that of men

  • 20-30% die within one year due to medical complications↑risk of mortality may persist for at least 5 years

Vertebral fractures

caused by mild to moderate trauma that is associated with lifting or changing position

• Crush fractures

  • Spontaneously occur; often clinically silent

  • Pain, loss of height, humpbacked posture (kyphosis), poor circulation, difficulty breathing, immobility, loss of self-esteem, reduced quality of life

Distal forearm fractures

generally occur when trying to break a fall with an outstretched hand(s)

• Occur much more frequently in women compared to men

  • incidence of wrist fractures in women usually increases gradually with age (different than hip and vertebral fractures)

• Only 1% of individuals who have a wrist fracture become dependent

  • However, at 6 months, almost 50% report having poor to fair function

Hormone replacement therapy (HRT)

decreases the risk of fracture by 20-35%

• In women over the age of 60, HRT may increase the risk of:

  • coronary heart disease

  • stroke

  • venous thromboembolism

  • breast cancer

Immovable Joints

e.g. skull bones

− Stronger with age

Slightly movable Joints

e.g. vertebral column, rib cage

− Cartilage and ligaments becomes stiffer

− Intervertebral disks become dry and compressed

Freely movable Joints

all joints in arms, legs, shoulders, hips

− Pieces of cartilage may form in synovial membrane

− Cross-linking of fibers and decreased blood supply to joints causes stiffness and less flexibility

Arthritis

More than 100 forms – osteoarthritis & rheumatoid arthritis are most common

• The word arthritis is a blend of the Greek words arthron, for joint, and itis, for inflammation

• arthritis literally means "joint inflammation"

Osteoarthritis

degenerative joint disease in which joint tissues break down over time

• Articular cartilage erodes, osteophyte formation, joint shape changes, damage to other joint structures

• Hard ends of bones bump and rub each other

• Result is inflammation, swelling, joint dysfunction, pain

Effects of Osteoarthritis (OA)

Symptoms of OA

• Stiffness

• Swelling

• Joint Pain

• Muscle Weakness

• Impaired physical function

Most common sites are:

• Knees, hips, cervical & lumbar spine, fingers

• Lifetime risk of developing symptomatic knee OA is 45%

Effects of exercise on OA

• Little effect on pathological process of OA

• Helps to reduce pain and improve function

Cardiovascular System

Key Functions

• transport of O2 & nutrients

• removal of CO2 & waste products

• thermoregulation

• distribution of hormones and other agents that regulate cell function

• protects the body against blood loss, pathogens, toxins

Arteriosclerosis

thickening and loss of elasticity in the large arteries

• Less responsive to neurotransmitters and hormones controlling vasodilation

  • leads to ↓ vasodilation, ↑ peripheral resistance (1%/yr), ↓ arterial compliance and thus, ↑ systolic blood pressure

• cross-linking of collagen decreases arterial elasticity

• endothelial cells become irregular in shape

  • atherosclerosis & calcification

Atherosclerosis

specific type of arteriosclerosis with a pathogenic origin

• Endothelial damage can include:

  • mechanical, free radicals, high blood glucose, microbes, toxins

• Formation of Plaque

• Stenosis

  • narrowing of the internal section of the vessel

• Thrombosis

  • intravascular coagulation (blood clot) at the level of the plaque occludes the vessel

  • embolism - the detachment of a fragment of the plaque downstream from the plaque

Neural control of the CV system

• Sensitive to epinephrine & norepinephrine

• With aging, there is a loss of beta receptors in arterial system

  • – ↓ vasodilation

  • – leads to ↑ peripheral resistance (1%/yr)

  • – results in an ↑ systolic BP

Baroreceptors (carotid arteries, aortic arch)

– ↓ receptor sensitivity

– orthostatic hypotension

Renal function

primary long-term regulation through control of

blood volume

Summary of key functional changes in blood vessels

increased wall thickening and arterial stiffening + edothelial dysfunction —> elevated systolic pressure (increased afterload) —> left ventricular hypertrophy

Afterload

the pressure that the heart must overcome to maintain blood flow to the body

Left Ventricle Hypertrophy

• thickening of LV wall

  • ↑ collagen; ↓elastin

  • ↑ by 30%, ages 25 – 80 yrs

• response to age-related ↑ in SBP

  • occurs even in normotensive individuals

• greater at the interventricular septum than free wall

  • LV shape changes result in ↓ contractile efficiency and ↓ systolic reserve

Calcification in the valves of the heart

• ↑ thickness and ↓ flexibility

• present in 80% of older adults

• results in restriction of flow (stenosis) and failure to close properly (incompetence)

  • Systolic and diastolic murmurs may result from incomplete valve closures

Diastolic function of the heart

Diastolic filling rate is altered

• reduced LV compliance and prolonged myocardial contraction

• By age 80, early diastolic LV filling is 50% of its peak rate

  • Likely due to ↓ blood volume (↓ preload)

• Heart compensates by increasing strength of atrial contraction – augmented late filling

Conduction system of the heart

• ↓ # cells in SA node

  • At 75 yrs - decreased by 90%

• ↓ in # of Purkinje fibers

  • Replaced with fat & fibrous tissue

• ↑ susceptibility to arrythmias

  • Atrial fibrillation, atrial tachycardia

Autonomic dysfunction results in decreased HR variability

• Cardiac rhythm is regulated by the autonomic nervous system

  • Parasympathetic (Vagus Nerve)

  • Sympathetic

• At rest, autonomic control is well maintained – no change in HR

  • Maximum HR declines by ~30% between 20 & 85 yrs of age

• HR variability ↓ with age due to diminished influence of the parasympathetic NS

VO2 max

The maximal rate at which oxygen can be taken up, distributed and used by the body during PA

Cardiac Output

Volume of blood pumped from the heart each minute

Stroke Volume

Volume of blood pumped from the heart with each beat

Determined by the interaction of 4 physiological systems

• Respiration (lungs)

• Central Circulation (heart and nerve conduction; autonomic nervous system)

• Peripheral Circulation (arteries & veins)

• Metabolism (muscles)

Age-related changes in Chest wall

The aging pump
Reduced ability to expand & contract

• Bones become thinner, change shape

• Increased stiffness, loss of elasticity due to calcification in cartilage

• Decreased respirator muscle mass & strength

Age-related changes in Lung

• Decreased elastic recoil

• Decreased lung size - ↓ alveolar surface area

Age-related changes in Alveoli

# of functional alveoli ↓

• Remainder become flatter, more shallow, resulting in decreased surface area

Loss of tissue elasticity

# of capillaries per alveolus ↓

• Less efficient transfer of oxygen from alveoli to the blood