13. Aging

Learning Objectives

• By end of class, student should be able to:
  • Recognize implications of normal aging for daily life & clinical care
  • Describe extrinsic (environmental) and intrinsic (genetic) factors that affect aging
  • Discuss & apply major theories of aging
  • Compare / contrast body-system changes that accompany aging
  • Identify how physical-therapy (PT) intervention mitigates or compensates for these normal, yet pathological, changes

Definition & Implications of Normal Aging (Senescence)

• Senescence = irreversible, cumulative physiological change produced by interaction of genes + environment over time
• Core clinical point: differentiate "normal" age-related decline from disease so appropriate prevention / intervention can be planned

Extrinsic (Environmental) Factors Influencing Aging

• Diet quality (nutrient density, caloric balance)
• Physical activity / exercise profile
• Supplements (positive or negative depending on evidence-based use)
• Exposure to toxic chemicals & pollutants (e.g., heavy metals, air quality)
• Socio-economic stress (chronic cortisol load → faster wear/tear)
• Ultraviolet sun exposure (photo-aging, skin cancers)
• Smoking example:
  • Causes dry skin, premature wrinkles, erectile dysfunction, muscle atrophy, ↓ circulation
  • Dark/thick mucus production → pulmonary clearance problems
  • URL given: aginginplace.org/how-smoking-can-affect-the-elderly (patient-education reference)

Intrinsic (Genetic) Factors Influencing Aging

• DNA polymorphisms & gene expression patterns
• Epigenetic modification across lifespan
• Familial clustering of longevity / early mortality

Theories of Aging

• Two primary philosophical families:
  • Damage-Based (stochastic)
  • Programmed-Based (deterministic)
  • Plus modern Telomerase focus

Damage-Based Theories

• Emphasise environmental assaults ⇨ accumulated molecular/cellular damage
• Four classic sub-theories:
  1. Error Theory – informational molecules (DNA/RNA) sustain unrepaired errors → mis-transcription & faulty protein synthesis
  2. Wear-and-Tear Theory – repeated use gradually degrades cells, tissues, organs
  3. Free Radical Theory – progressive build-up of reactive oxygen species damages DNA, lipids, proteins
  4. Neuro-Endocrine Theory – age-related decline of hormone production reduces cellular regulation & repair

Programmed-Based Theories

• Aging coded into genome; timing controlled by biologic “clocks”
  1. Programmed Longevity – sequential gene on/off switching; aging = period when senescence genes dominate
  2. Endocrine Theory – neuro-endocrine clock controls pace through hormonal signals
  3. Immunologic Theory – immune system genetically programmed to wane ⇒ ↑ vulnerability, morbidity, mortality

Telomerase Theory

• Telomeres = nucleotide caps at chromosome ends (shoelace tip metaphor) preventing fraying/fusion
• With each mitosis, telomeres shorten until critical length reached ⇒ replicative senescence
• Lifestyle factors (healthy diet, exercise, adequate sleep) slow telomere attrition
• PT takeaway: behaviour modification can modulate biological aging rate

Body-Composition Changes with Aging

• Fat
  • ↑ total body fat after age 30, especially visceral/abdominal
  • Sub-cutaneous fat ↓; redistribution to trunk, away from limbs
  • Ectopic fat deposits accumulate in liver & skeletal muscle
• Bone
  • Overall bone shrinks, loses density ⇒ weaker, fracture-prone
  • Intervertebral discs dehydrate & flatten ⇒ stature ↓ (height loss)
• Muscle
  • ↓ strength, endurance, flexibility ⇒ balance & coordination deficits
  • Decline in both mass & quality (fiber type shift)
• High-metabolic-rate organ mass (brain, heart, kidneys, spleen) ↓ with age except heart weight may stay stable or rise (wall thickening)

Muscular System & Sarcopenia

• Definition: age-related loss of skeletal muscle mass, strength, endurance & regenerative capacity
• Epidemiology
  • Muscle mass loss ≈ 4\text{–}6\% per decade starting at 40 y in females, 60 y in males; steepest after 70 y, accentuated by inactivity & illness
  • Females: proportionally greater lean-tissue loss
  • Both sexes can maintain strength into 80s with regular exercise

Etiology (Multifactorial)

• Altered muscle metabolism (↓ protein synthesis, mitochondrial dysfunction)
• Endocrine changes (↓ GH, testosterone, estrogen, IGF-1)
• Nutritional inadequacy (protein, vitamin D, energy)
• Genetic predisposition
• Physical inactivity accelerates onset & severity

Pathogenesis

• ↓ alpha-motor neuron capacity to re-innervate regenerating fibers
• ↓ total fiber number & size (particularly type II fast-twitch)
• Impaired excitation–contraction coupling ⇒ slower contraction velocity
• ↓ high-threshold motor-unit recruitment; motor-unit drop-out pronounced after \ge 70 y

Functional & Clinical Effects

• Progressive weakness ⇒ slower gait, impaired ADLs, poor balance reaction, falls, fractures
• Post-injury recovery protracted ⇒ spiral of deconditioning & comorbidity
• One-year mortality after hip fracture 3\text{–}4× higher vs. general older adult population (Morri 2019)

Exercise Intervention

• Progressive Resistance Training (PRT) can alter/slow/reverse muscular aging
  • ↑ strength ⇒ ↓ fall risk & sequelae
  • Combine resistance, aerobic & stretching for comprehensive benefit
• Clinical pearls
  • Baseline via PT evaluation; monitor vitals; progressive overload is safe & needed

Joints & Connective Tissue

• Joints: ↓ flexibility, ↑ stiffness, ↓ proprioception (knee, ankle)
• Articular cartilage: thinning, dehydration, ↑ stiffness ⇒ osteoarthritis risk ↑
• Tendons: altered collagen, ↓ tensile strength; slower force transmission, higher injury risk

Bone & Osteoporosis

• Aging bone: ↓ mass, density & mineral content; brittle
• Postural adaptations: forward head, rounded shoulders, ↑ thoracic kyphosis, variable lumbar lordosis, flexed limbs; height ↓; balance centre of gravity shifts ⇒ fall risk

Osteoporosis

• Definition: chronic, progressive skeletal disorder of low bone mass + micro-architectural deterioration ⇒ fragility fractures
• Prevalence: 10\text{ million} US; 43\text{ million} additional with osteopenia
• High-risk fracture sites: vertebral bodies, hip, ribs, distal radius, femur, humerus, pelvis
• Compression (vertebral) fractures = most common osteoporotic fracture
• Classification
  • Primary: most common; post-menopausal women & later-life men
  • Secondary: medication‐ or disease-induced (e.g., corticosteroids, endocrine disorders)

Diagnosis / Screening / Management

• Tools: medical Hx, physical exam, labs, imaging (DEXA)
• Bone Mineral Density (BMD) interpretation (T-score vs. young adult mean):
  • Normal: \ge -1 SD
  • Osteopenia: -1.0 to -2.5 SD
  • Osteoporosis: < -2.5 SD
• Calcium & Vitamin D optimisation (Age-based RDA)
  • 31!\text{–}!50 y: 1000\,\text{mg/day}
  • 51!\text{–}!70 y males: 1000; females: 1200
  • >70 y: 1200
• Early intervention crucial; exercise prescription (weight-bearing + resistance) supports BMD maintenance

Sensorimotor & Peripheral Nervous System

• Loss of motor & sensory neuron cell bodies; ↓ myelinated & unmyelinated fiber count (myelinated afferents most affected)
• Altered myelin quality ⇒ slower nerve conduction velocity (NCV)
• ↓ action-potential amplitude may drop below threshold ⇒ functional conduction block (“nothing happens”)
• ↓ neurotransmitter synthesis ⇒ ↑ peripheral neuropathy incidence, slower nociceptive processing, prolonged reaction time, ↓ dual-task ability ⇒ balance/fall implications

Cardiovascular System

• Aging structural changes
  • Heart chambers enlarge while walls thicken ⇒ chamber volume ↓
  • Atrial pacemaker cell apoptosis ⇒ intrinsic HR slows
  • Arterial stiffness & aortic thickening ⇒ systolic hypertension
  • Progressive vascular plaque ⇒ narrowed arteries; ↑ risk of MI, HF

Functional Impact

• General trend table (aging effect relative to youth):
  • Maximal aerobic capacity: ↓
  • Max HR: ↓
  • Max end-diastolic volume: ↑ (compensation)
  • Ejection fraction & cardiac output: ↓
  • Exercise capacity & cardiac response: ↓
• Exercise benefits: endurance training partially preserves function, elevates HDL, lowers vascular resistance & resting BP

Respiratory System

• Pulmonary changes
  • ↓ alveolar surface area ⇒ ↑ physiologic dead space
  • ↓ elastic recoil; ↑ chest wall stiffness
  • Volumetric shifts: ↓ vital capacity, ↑ residual volume + FRC, ↓ expiratory flow
  • Respiratory muscle strength & central drive decline
• Exercise prescription
  • Aerobic conditioning slows VO_2\max decline, boosts endurance
  • Strengthening: global & inspiratory muscle focus
  • Education re: breathing mechanics & pacing

Sensory Systems

• Vision: ↓ corneal sensitivity, smaller pupils, presbyopia, cataracts, dry eyes, lens yellowing/stiffness, orbital fat pad loss
• Hearing: ↓ speech discrimination, cerumen accumulation; conductive vs. sensorineural components affect social participation
• Taste (hypogeusia): ↓ taste-bud count, atrophy, membrane changes; saliva ↓
• Smell (hyposmia): sensitivity decline after \approx60 y → affects appetite/nutrition
• Somatosensation: receptor & pathway loss ⇒ higher stimulus threshold

Integumentary System

• “Paper-thin” skin: dermal thinning, reduced vascularity & hair follicles
• Impaired thermoregulation & inflammatory response
• ↓ melanocytes → less UV protection, ↑ skin cancer risk, Vitamin D deficit risk
• ↓ sweat glands & neural innervation
• Wrinkle pathophysiology: elastin fiber loss, collagen weakening, ↓ sub-cutaneous fat

Cognition & Neurodegeneration

• Aging linked with global cognitive decline; \approx\tfrac13 of adults >65 die with Alzheimer’s or related dementia
• Projection: 9\text{ million} US adults with AD by 2030

Alzheimer’s Disease Pathology

• Extracellular amyloid-β plaques + intracellular tau neurofibrillary tangles cause synaptic dysfunction & neuronal death
• Multifactorial prevention strategies required (vascular, metabolic, lifestyle)

Exercise & Brain Health

• Aging gray-matter volume drop mitigated by higher cardiorespiratory fitness
• Longitudinal evidence:
  • Mid-life fitness delays dementia onset (40-y study, Neurology Today 2018)
  • High physical activity ↔ lower cognitive-decline risk (BMC Public Health 2014)
  • Walking >72 blocks/week (~3.5 mi) predicts greater gray-matter volume across 9 y (Neurology 2010)
  • Strength training 1×/week ↑ cerebral perfusion (Neurosci Lett 2014)
  • Aerobically fit women outperform sedentary peers cognitively (Adv Physiol Educ 2015)
• Hypothesised mechanism: exercise-induced vascular & neurotrophic enhancements

Clinical Practice / PT Implications (Cross-System)

• Thorough evaluation distinguishes normal aging from pathology; screening tools (e.g., DEXA, fall-risk tests, cognitive screening) essential
• Exercise is central, evidence-based intervention across systems:
  • Resistance & balance for sarcopenia & fall prevention
  • Weight-bearing & impact loading for osteoporosis
  • Aerobic conditioning for cardiovascular, respiratory & cognitive preservation
  • Flexibility & joint-specific mobilisation to address connective-tissue stiffness
• Education: lifestyle modification (smoking cessation, diet, stress management) linkage to telomere health & disease prevention
• Vital-sign monitoring & progressive loading encourage safe but challenging programmes even in advanced age groups

Ethical / Philosophical Considerations

• Normal aging processes are “physiological,” yet cause disability; clinicians must balance age-acceptance with advocacy for modifiable change
• Socioeconomic determinants (access to nutritious food, safe exercise environments) intersect with biological theories

Real-World Relevance & Integration

• Rising aging population ⇒ increased healthcare utilisation; prevention via PT lowers societal cost
• Awareness of intrinsic/extrinsic factors empowers patient-centred interventions
• Interdisciplinary management (nutrition, psychology, medicine, PT) required to optimise aging trajectory

Key Numerical / Statistical References (quick lookup)

• Muscle mass loss: 4\text{–}6\% / decade (from 40 F, 60 M)
• Hip-fracture 1-y mortality: 3\text{–}4\times general population
• Osteoporosis prevalence: 10\text{M}; Osteopenia: 43\text{M} US
• BMD T-score cut-offs: Normal \ge -1; Osteopenia -1\text{ to }-2.5; Osteoporosis < -2.5
• Walking >72 blocks/week ≈ 3.5 mi linked to ↑ gray matter

Concluding Clinical Pearls

• Aging is inevitable; rate & functional impact are modifiable
• Regular, progressively challenging physical activity is the most potent, low-cost intervention spanning musculoskeletal, cardiovascular, respiratory, sensory & cognitive domains
• PT role: assessor, educator, exercise prescriber, advocate for holistic healthy aging