SENESCENCE
• …ALL POSTMATURATIONALCHANGES AND THE INCREASING
VULNERABILITY INDIVIDUALS FACE AS A RESULT OF THESE CHANGES.
• THE GROUP OF EFFECTS THAT LEAD TO A DECREASING EXPECTATION
OF LIFE WITH INCREASING AGE
3.
SENCESCENCE, CONT’D
• DIFFERSFROM OTHER BIOLOGICAL PROCESSES:
• ITS CHARACTERISTICS ARE UNIVERSAL
• CHANGES COME FROM WITHIN THE INDIVIDUAL
• ASSOCIATED PROCESSES OCCUR GRADUALLY
• CHANGES HAVE A DELETERIOUS EFFECT ON THE INVIDUAL
4.
ULTIMATELY…YOU DIE.
U.S. DEATHRATES:
• LEADING CAUSE AMONG OA’S--HEART DISEASE
• HIGHER FOR OLDER MEN THAN FOR OLDER WOMEN
• HIGHER FOR AFRICAN AMERICANS THAN WHITES
AT AGE 75,THE AVERAGE PERSON,
COMPARED TO AGE 30:
• 92% OF BRAIN WEIGHT
• 84% OF BASAL METABOLISM
• 70% KIDNEY FILTRATION RATE
• 43% OF MAXIMUL BREATHING CAPACITY
• WE ARE NOT THE PEOPLE WE ONCE WERE!
7.
CHANGES IN THESKIN
• “TO MOST PEOPLE, THE CONDITION OF THE SKIN, HAIR, AND
CONNECTIVE TISSUE COLLECTIVELY REPRESENTS THE ULTIMATE
INDICATOR OF AGE”. (KART & KINNEY, P. 74)
8.
SKIN: WRINKLING
• MUSCLESOF THE FACE ARE CAPABLE OF TREMENDOUS MOVEMENT.
“SMILES, LAUGHTER, FROWNS, DISAPPOINTMENT, AGER, RAGE, AND
SURPRISE ARE ALL RECORDED. THE HAND OF TIME CAPTURES THESE
EXPRESSIONS AND OUTLINES THEM ON THE FACE….BY THE AGE OF
40, MOST PEOPLE BEAR THE TYPICAL LINES OF THEIR EXPRESSIONS.”
(KART & KINNEY, P. 75)
9.
SKIN--WRINKLING:
• LOSS OFSUBCUTANEOUS FAT
• > VULNERABILITY TO PRESSURE SORES
• LESS INSULATION OF BODY TO COLD (ALSO AFFECTED BY DIMINISHED
BLOOD FLOW TO SKIN & EXTREMITIES) & HEAT
10.
SKIN & NAILS
•ATROPHIC CHANGES IN SWEAT GLANDS
• THICKENED FINGERNAILS & TOENAILS
• GENERALIZED LOSS OF BODY HAIR AND HEAD HAIR
• DECREASE IN # OF FUNCTIONING PIGMENT-PRODUCING CELLS--
>GRAYING
• SOME REMAINING PIGMENT CELLS ENLARGE--> “AGE SPOTS”
• SKIN CHANGES INCREASE. VULNERABILITY TO INFECTIONS/DISORDERS
11.
SKELETOMUSCULAR SYSTEM CHANGES
•“ARTHRITIS & ALLIED BONE AND MUSCULAR CONDITIONS ARE
AMONG THE MOST COMMON OF ALL DISORDERS AFFFECTING
PEOPLE 65 YEARS OF AGE AND OVER.” (KART & KINNEY, P. 76)
• ARTHRITIS: A GENERIC TERM THAT REFERS TO AN INFLAMMATION OR
DEGENERATIVE CHANGE IN A JOINT
• OCCURS WORLD WIDE & IS ONE OF THE OLDEST KNOWN DISEASES
12.
ARTHRITIS
OSTEOARTHRITIS
• CAUSE NOTKNOWN
• ALSO REFERRED TO AS
DEGENERATIVE JOINT DISEASE
• A GRADUAL WEARING AWAY OF
JOINT CARTILAGE THAT RESULTS
IN THE EXPOSURE OF ROUGH
UNDERLYING BONE ENDS
• CAN DO DAMAGE TO INTERNAL
LIGAMENTS
• MOST COMMONLY ASSOCIATED
W/ WEIGHT BEARING JOINTS
RHEUMATOID ARTHRITIS
• A CHRONIC, SYSTEMIC,
INFLAMMATORY DISEASE OF
CONNECTIVE TISSUE
• 2-3 TIMES MORE COMMON
AMONG WOMEN THAN MEN
• CURRENTLY VIEWED AS AN
AUTOIMMUNE DISEASE
• MAY OCCUR AT ANY AGE -- MOST
COMMON ONSET BETWEEN 20 &
50
13.
MUSCULOSKELTAL, CONT’D:
OSTEOPENIA -->
OSTEOPOROSIS:
•GRADUAL LOSS OF BONE
THAT REDUCES SKELETAL MASS
WITHOUT DISRUPTING THE
PROPORTIONS OF MINERALS &
ORGANIC MATERIALS
• FOR MANY, IT IS
ASYMPTOMATIC
• BONES MOST CRITICALLY
INVOLVED: VERTEBRA, WRIST,
HIP
SARCOPENIA:
• LOSS OF MUSCLE MASS THAT
OCCURS WITH AGING
• CAUSE NOT COMPLETELY
UNDERSTOOD
• PREVENTABLE/REVERSIBLE WITH
REGULAR PHYSICAL ACTIVITY
14.
GASTROINTESTINAL SYSTEM
• ATROPHYOF SECRETION MECHANISMS
• DECREASING MOTILITY OF THE GUT
• LOSS OF STRENGTH/TONE OF MUSCULAR TISSUE & SUPPORTING
STRUCTURES
• CHANGES IN NEUROSENSORY FEEDBACK
• ENZYME & HORMONE RELEASE
• INNERVATION OF THE TRACT
• DIMINISHED RESPONSE TO PAIN & INTERNAL SENSATIONS
15.
• THE PHENOMENONOF REFERRAL IS COMMON IN THE GI--I.E. SIGNS
& SYMPTOMS OFTEN ASSOCIATED WITH ONE PART OF THE TRACT
MAY ACTUALLY BE ASSOCIATED WITH ANOTHER PART OF THE TRACT.
“DISCOMFORT PERCEIVED AS ORIGINATING IN THE STOMACH MAY
ACTUALLY BE COMING FROM THE LOWER GI TRACT.”
• THE GI SYMPTOMS OFTEN HAVE THEIR ORIGINS IN PSYCHOSOCIAL
FACTORS
16.
CARDOPULMONARY SYSTEM
• INTHE ABSENCE OF DISEASE, THE HEART TENDS TO MAINTAIN ITS SIZE
• HEART VALVES TEND TO INCREASE IN THICKNESS WITH AGE
• BP TENDS TO GO UP WITH AGE
• SYSTOLIC STABILIZES AT ABOUT AGE 75
• DIASTOLIC STABILIZES AT ABOUT 65 THEN MAY GRADUALLY DECLINE
17.
ATHEROSCLEROSIS VS.
ARTERIOSCLEROSIS
ATHEROSCLEROSIS
• DEVELOPEDBY AN OVERWHELMING #
OF PEOPLE IN INDUSTRIALIZED NATIONS
• A NARROWING OF ARTERIAL
PASSAGEWAYS AS A RESULT OF THE
DEVELOPMENT OF PLAQUES ON THEIR
INTERIOR WALLS
• REDUCES THE SIZE OF THE
PASSAGEWAY--EVEN TO THE PT OF
CLOSING IT OFF. A CAUSE OF ISCHEMIC
HEART TISSUE (TISSUE DEPRIVED OF
ADEQUATE BLOOD SUPPLY)
ARTERIOSCLEROSIS:
• A GENERIC TERM REFERRING TO
THE LOSS OF ELASTICITY OF
ARTERIAL WALLS
• OFTEN REFERRED TO AS
“HARDENING OF THE ARTERIES”
• CONSIDERED A GENERAL
AGING PHENOMENON
18.
RESPIRATORY CHANGES
• AIRWAYS& TISSUES BECOME LESS ELASTIC & MORE RIGID WITH AGE
• OSTEOPOROSIS MAY ALTER THE SIZE/SHAPE OF THE CHEST CAVITY
• POWER OF RESPIRATORY & ABDOMINAL MUSCLES BECOMES
REDUCED--HINDERS DIAPHRAMATIC MOVEMENT
19.
URINARY SYSTEM
• “THEBLADDER OF AN ELDERLY PERSON HAS A CAPACITY OF LESS
THAN HALF (250ML) THAT OF A YOUNG ADULT (600 ML) AND OFTEN
CONTAINS AS MUCH AS 100 ML OF RESIDUAL URINE”. (P. 81)
• MICTURATION REFLEX IS DELAYED-- USUALLY ACTIVATED WHEN
BLADDER IS HALF FULL; IN OAS, NOT UNTIL BLADDER IS NEARLY AT
CAPACITY
GENITAL SYSTEM CHANGES
•“THE GENITAL SYSTEM IS CHARACTERIZED BY A NUMBER OF AGE-
RELATED CHANGES IN PHYSIOLOGY AND ANATOMY. ON THE
WHOLE, VERY FEW AGE-SPECIFIC DISORDERS ARE ASSOCIATED WITH
THIS BODY SYSTEM. WITH THE EXCEPTION OF DECLINING LEVELS OF
TESTOSTERONE, MOST OF THE PROBLEMS OF SEXUALITY AND AGING
ARE SOCIOGENIC OR PSYCHOGENIC”. (P. 83)
22.
FEMALE GENITAL TRACT
•EXTERNAL GENITALIA
FOLDS BECOME LESS PRONOUNCED
SKIN BECOMES THINNER
VASCULARITY & ELASTICITY DECREASE
BECOMES MORE SUSCEPTIBLE TO TISSUE TRAUMA & ITCHING
• INTERNATAL REPRODUCTIVE ORGANS
UTERUS DECREASES IN SIZE & BECOMES MORE FIBROUS
UTERUS HAS FEWER ENDOMETRIAL GLANDS
CERVIX REDUCED IN SIZE
UTERINE TUBES BECOME THINNER
OVARIES TAKE ON AN IRREGULAR SHAPE
OVULATION STOPS--MENOPAUSE (50% BETWEEN AGES 45 AND 50)
23.
MALE GENITAL SYSTEM
•CONTINUES TO PRODUCE GERM CELLS (SPERM) AND TESTOSTERONE
WELL INTO OLD AGE, DECLINING WITH ADVANCING AGE
• SIZE & FIRMNESS OF THE TESTES DECREASE
• REDUCED SPERM PRODUCTION DUE TO AGE-RELATED FIBROSIS
WHICH CONSTRICTS THE BLOOD SUPPLY
24.
PHYSIOLOGICAL RESPONSE TO
EXERCISEIN ELDERLY
• THE TERM ‘ELDERLY’ IS APPLIED TO THOSE INDIVIDUALS BELONGING TO AGE 60
YEARS AND ABOVE, WHO REPRESENT THE FASTEST GROWING SEGMENT OF
POPULATIONS THROUGHOUT THE WORLD. THE MAGNITUDE OF PHYSIOLOGICAL
RESPONSE DEPENDS ON SEVERAL FACTORS SUCH AS
• AGE, SEX, INITIAL FITNESS STATUS AND THE SPECIFIC TYPE OF TRAINING. LET US
DISCUSS THE RESPONSE TO
• EXERCISE INVOLVING THE COORDINATED INTERPLAY BETWEEN THE
PHYSIOLOGICAL SYSTEMS, ESPECIALLY,
• CARDIOVASCULAR SYSTEM, RESPIRATORY SYSTEM AND MUSCULOSKELETAL
SYSTEM IN ELDERLY INDIVIDUALS.
25.
CARDIOVASCULAR SYSTEM
• THEPHYSIOLOGICAL RESPONSE OF CARDIOVASCULAR SYSTEM TO
EXERCISE MAY BE CONSIDERED AS EITHER
• CENTRAL OR PERIPHERAL IN ORIGIN. CENTRAL ADAPTATIONS WITH
EXERCISE TRAINING INCLUDE CHANGES IN CARDIAC OUTPUT, BLOOD
VOLUME AND ARTERIAL OXYGEN-CARRYING CAPACITY WHEREAS
SKELETAL MUSCLE BLOOD FLOW AND CAPILLARIZATION ARE THE
PERIPHERAL ADAPTATIONS.
26.
AGE-RELATED STRUCTURAL CHANGESIN
THE HEART
• STRUCTURAL CHANGES WITH AGING INVOLVE THE MYOCARDIUM,
THE CARDIAC CONDUCTION SYSTEM, AND THE ENDOCARDIUM. THERE
IS A PROGRESSIVE DEGENERATION OF THE CARDIAC STRUCTURES
WITH AGING, INCLUDING A LOSS OF ELASTICITY, FIBROTIC CHANGES
IN THE VALVES OF THE HEART, AND INFILTRATION WITH AMYLOID.
27.
AGE-RELATED PHYSIOLOGICAL CHANGESOF
HEART RATE, STROKE VOLUME, EJECTION
FRACTION, CARDIAC OUTPUT, AND BLOOD
PRESSURE
• HEART RATE :SUPINE RESTING HEART RATE IS WIDELY REPORTED TO BE UN
CHANGED BY AGING. IN CONTRAST, SITTING-POSITION HEART RATE
DECREASES WITH AGE. RESPIRATORY SINUS ARRHYTHMIA, WHICH IS THE
VARIATIONS IN HEART RATE DUE TO RESPIRATION (DURING INSPIRATION
HEART RATE INCREASES), AND HEART RATE VARIABILITY DECREASE WITH
AGING.
• STROKE VOLUME: IS CHANGED LITTLE BY AGING; AT REST IN HEALTHY
INDIVIDUALS, THERE MAY EVEN BE A SLIGHT INCREASE.
• EJECTION FRACTION: DOES NOT SHOW ANY AGE-RELATED CHANGE.
• CARDIAC OUTPUT: AT REST IS UNAFFECTED BY AGE. MAXIMUM CARDIAC
OUTPUT AND AEROBIC CAPACITY ARE REDUCED WITH AGE. THERE IS A LINEAR
DECLINE THROUGH THE ADULT YEARS, SO THE AVERAGE 65-YEAR-OLD HAS
30% TO 40% THE AEROBIC CAPACITY OF A YOUNG ADULT.
28.
AGE-RELATED PHYSIOLOGICAL CHANGESOF HEART RATE,
STROKE VOLUME, EJECTION FRACTION, CARDIAC OUTPUT,
AND BLOOD PRESSURE
• BLOOD PRESSURE: IS DETERMINED BY CARDIAC OUTPUT AND BY TOTAL
PERIPHERAL RESISTANCE. SINCE CARDIAC OUTPUT IS LITTLE
ALTERED BY AGE IN THE HEALTHY OLDER ADULTS, BP INCREASES WITH AGE ARE
LIKELY TO REFLECT MAINLY ALTERATIONS IN TOTAL PERIPHERAL RESISTANCE
AND DIMINISHED AORTIC COMPLIANCE.
BP = CARDIAC OUTPUT X TOTAL PERIPHERAL RESISTANCE
• SYSTOLIC BLOOD PRESSURE VS. DIASTOLIC BLOOD PRESSURE: BOTH
SYSTOLIC AND MEAN BLOOD PRESSURES SIGNIFICANTLY INCREASE FROM 20
TO 80 YEARS. SPECIFICALLY, SYSTOLIC BLOOD PRES
SURE TENDS TO INCREASE
WITH AGE THROUGHOUT LIFE, WHEREAS DIASTOLIC PRESSURE INCREASES
UNTIL THE AGE OF ABOUT 60 YEARS AND THEN STABILIZES OR EVEN FALLS.
29.
AGE-RELATED CARDIOVASCULAR
RESPONSE DURINGEXERCISE
• HEART RATE AND EXERCISE :THE MAXIMUM ACHIEVABLE HEART RATE WITH
EXERCISE DECREASES LINEARLY WITH AGE AND MAY BE CALCULATED
EMPIRICALLY, USING 220 BEATS PER MINUTE AS THE MAXIMUM IN THE ADULT.
THE AGE CHANGES CAN BE CALCULATED BY SUBTRACTING THE AGE OF THE
INDIVIDUAL FROM THE 220 VALUES. THUS, IN AN 8O-YEAR-OLD THE MAXIMAL
HEART RATE THAT CAN BE ACHIEVED WHILE EXERCISING IS 220 - 8O = 140
BEATS/MIN.
• THE STROKE VOLUME: DURING EXHAUSTING WORK IS THUS 10% TO 20%
SMALLER THAN IN A YOUNG ADULT. THE ABILITY TO INCREASE STROKE VOLUME
IN THE OLDER ADULT DURING EXERCISE IS ACHIEVED WITH AN INCREASE IN END-
DIASTOLIC VOLUME THROUGH THE FRANK-STARLING RELATIONSHIP. THE FRANK-
STARLING RELATIONSHIP LINKS THE VOLUME AND PRESSURE OF BLOOD IN THE
VENTRICLE (FILLING PRESSURE) TO THE FORCE OF CONTRACTION OF THE
VENTRICULAR MUSCLE SO THAT AN INCREASED FILLING OF THE VENTRICLE
CAUSES AN INCREASED STRETCH OF THE WALL AND RESULTS IN AN INCREASED
FORCE OF CONTRACTION.
30.
CARDIAC OUTPUT ANDEXERCISE
• CARDIAC OUTPUT INCREASES SIMILARLY WITH INCREASING WORK LOADS IN
VARIOUS AGE GROUPS; HOWEVER, THE MECHANISM OF AUGMENTATION OF
CARDIAC OUTPUT IS DIFFERENT BETWEEN THE AGE GROUPS
31.
2. IN COMPARISONTO AGE-MATCHED
SEDENTARY INDIVIDUALS:
• ALTHOUGH, LOW INTENSITY EXERCISE ELICITS MARGINAL CHANGES,
BOTH LOW AND HIGH INTENSITY REGULAR EXERCISE IS EFFECTIVE IN
RETAINING THE CARDIOVASCULAR FUNCTION IN ELDERLY
INDIVIDUALS, WHEN COMPARED TO AGE-MATCHED SEDENTARY
SUBJECTS.
32.
3. IN COMPARISONTO PREVIOUS
YEARS OF LIFE:
• IN A LONG-TERM STUDY (STUDY PERIOD = 10 YEARS), IT WAS
OBSERVED THAT AT AGE 55, PREVIOUSLY ACTIVE MEN HAD
MAINTAINED THE SAME VALUES FOR BLOOD PRESSURE, BODY
WEIGHT AND MAX VO2 AS AT AGE 45.
33.
REPIRATORY SYSTEM
• WHENCOMPARED TO CARDIOVASCULAR AND MUSCULOSKELETAL SYSTEMS, THE EXTENT OF ADAPTATION
TO EXERCISE BY THE RESPIRATORY SYSTEM APPEARS TO BE VERY LIMITED.
1. IN COMPARISON TO YOUNGER INDIVIDUALS:
THE EFFECTS OF EXERCISE TRAINING ON RESPIRATORY SYSTEM OF ELDERLY PERSONS ARE SIMILAR TO THAT
OF THE YOUNG ADULT, NAMELY:
– RESTING PULMONARY VENTILATION IS UNCHANGED AFTER EXERCISE TRAINING.
– ENDURANCE TRAINING LOWERS THE VENTILATION AT SUB MAXIMAL WORK RATES, MAINLY DUE TO
REDUCTION IN LACTATE AND CO2 PRODUCTION.
– EXERCISE TRAINING INCREASES THE MAXIMAL VENTILATION DURING EXERCISE.
2. IN COMPARISON TO AGE-MATCHED SEDENTARY INDIVIDUALS:
– OLDER ENDURANCE ATHLETES HAVE GREATER PULMONARY FUNCTIONAL CAPACITY THAN SEDENTARY
PEERS.
– EXERCISE TRAINING REDUCES THE BREATHLESSNESS EXPERIENCED BY ELDERLY, SENSE OF EXERTION AND THE
PERCENTAGE OF MAXIMAL VENTILATION USED DURING EXERCISE.
34.
RESPIRATORY SYSTEM
• THEEFFECTS OF EXERCISE TRAINING ON RESPIRATORY SYSTEM OF
ELDERLY PERSONS ARE SIMILAR TO THAT OF THE YOUNG ADULT
WHICH ARE RESTING PULMONARY VENTILATION, ENDURANCE
TRAINING, EXERCISE TRAINING INCREASES THE MAXIMAL
VENTILATION
• THE ATHLETES OVER THE AGE OF 60 HAVE VALUES FOR VITAL
CAPACITY, TOTAL LUNG CAPACITY, RESIDUAL VOLUME, MAXIMUM
VOLUNTARY VENTILATION ARE BETTER AS COMPARE TO SEDENTARY
ELDER POPULATION, LOSS IN PULMONARY FUNCTION MAY LEAD TO
VENTILATORY LIMITATION IN EXERCISE IN ACTIVE ELDERLY, LIMITING
THE ABILITY.
35.
AGE-RELATED CHANGES INSKELETAL
MUSCLE
• MUSCULOSKELETAL ADAPTATIONS ARE PROBABLY MOST IMPORTANT
FROM PHYSICAL THERAPY PERSPECTIVE.
• SIGNIFICANT CHANGES OCCUR IN MUSCULAR PERFORMANCE, BODY
COMPOSITION AND SKELETAL SYSTEM OF ELDERLY PERSONS AFTER
EXERCISE TRAINING:
36.
1. MUSCULAR PERFORMANCE:
GIVENAN ADEQUATE TRAINING STIMULUS, OLDER ADULTS CAN
MAKE SIGNIFICANT GAINS IN STRENGTH. IT DEPEND ON DURATION,
INTENSITY AND TYPE OF EXERCISE.
DURATION: WITH MORE PROLONGED RESISTANCE TRAINING, EVEN
A MODEST INCREASE IN MUSCLE SIZE IS POSSIBLE.
INTENSITY: HIGH-INTENSITY RESISTANCES THAT USE 70% - 80% OF
1RM PRODUCE MORE PREDICTABLE INCREASES IN SHORTER PERIOD
OF TIME, BUT LOW TO MODERATE RESISTANCES ALSO PRODUCE
IMPROVEMENTS.
TYPE OF EXERCISE: RESISTANCE TRAINING IS MUCH MORE EFFECTIVE
IN STRENGTH IMPROVEMENTS THAN AEROBIC EXERCISE SUCH AS
CYCLING, SWIMMING OR JOGGING.
37.
AGE-RELATED CHANGES INSKELETAL
MUSCLE
• REDUCTIONS IN MUSCLE MASS: AGING IS ASSOCIATED WITH
DECREASES IN TOTAL MUSCLE CROSSSECTIONAL AREA,
AMOUNTING TO APPROXIMATELY 40% BETWEEN THE AGES OF
20 AND 80 YEARS.
• REDUCTION IN MUSCLE FIBER NUMBER: THE TOTAL NUMBER OF
MUSCLE FIBERS IS SIGNIFICANTLY REDUCED WITH AGE,
BEGINNING AT ABOUT 25 YEARS AND CONTINUE AT AN
ACCELERATED RATE THEREAFTER.
• CHANGES IN MUSCLE FIBER SIZE: THE SIZE OF FAST-TWITCH
TYPE II FIBERS DECREASES , WHEREAS THE SLOW-TWITCH TYPE I
FIBER SIZE DOES NOT CHANGE.
38.
MUSCULOSKELETAL SYSTEM
2. BODYCOMPOSITION:
ALTHOUGH IT IS COMMON TO SEE THAT MOST “NORMAL” INDIVIDUALS
GROW FATTER WITH INCREASING AGE, INDIVIDUALS WHO ENGAGE IN HEAVY
RESISTANCE TRAINING INCREASE THEIR LEAN BODY MASS AND DECREASE FAT. THIS
HEALTHY BODY COMPOSITION IS CRITICALLY IMPORTANT FOR EXPERIENCING THE
JOY THAT OPTIMAL HEALTH CAN BRING.
3. SKELETAL SYSTEM:
IN VIEW OF THE FUNCTIONS AND AGE-RELATED CHANGES IN BONE, IT IS
REASONABLE TO BELIEVE THAT SUFFICIENT MECHANICAL LOADING AND MUSCULAR
ACTIVITY IS REQUIRED TO IMPROVE AND PRESERVE BONE STRENGTH IN THE
LOCOMOTORS SYSTEM. THE STRENGTH TRAINING COULD BE A POTENTIAL THERAPY
TO IMPROVE FUNCTIONAL ABILITY AND QOL IN OSTEOPOROTIC PTS.
39.
AGE-RELATED CHANGES INSLEEP
PATTERNS
• SLEEP PATTERNS : BEGIN IN THE 4TH
DECADE. VARIABILITY OF SLEEP PATTERNS IS
EVIDENT WITH AN IN
CREASE IN THE AMOUNT OF TIME SPENT SLEEPING, A
CHANGE IN THE STAGES OF SLEEP, AND AN INCREASE IN THE NO: OF
NIGHTTIME AWAKENINGS. BY THE 6TH
DECADE, DEEP SLEEP IS ALMOST GONE.
WITH ADVANCING AGE THERE IS A GRADUAL INCREASE IN THE TOTAL AMOUNT
OF SLEEP TIME, IN THE AMOUNT OF NAP TIME, AND IN WAKE EPISODES AFTER
SLEEP ONSET. AFTER THE AGE OF 85 YEARS, GOING TO SLEEP OFTEN TAKES
LONGER. AN ELDER'S MENTAL ACUITY AND OVERALL ABILITY TO FUNCTION ARE
AFFECTED BY PROBLEMS OF SLEEPLESSNESS OR CHANGES IN SLEEP PATTERNS.
THEREFORE, ATTENTION TO SLEEP PATTERNS MAY HELP A PRACTITIONER
UNDERSTAND A PT'S AFFECT, COMMUNICATION STYLE, AND RESPONSE TO
TREATMENT.
40.
TYPICAL MUSCLE CHANGESWITH
AGING
• DECREASED MUSCLE MASS, REPLACED BY INCREASED FAT MASS
• DECREASED MUSCLE STRENGTH (PARTICULARLY LOWER EXTREMITIES)
• SLOWING OF MUSCLE CONTRACTILE PROPERTIES AND RATE OF FORCE DEVELOPMENT
• REDUCED RATE OF CROSS-BRIDGE CYCLING
• ALTERATIONS ON EXCITATION AND CONTRACTION COUPLING
• INCREASED COMPLIANCE OF MUSCLE’S TENDINOUS ATTACHMENT MUSCLE FIBER
CHANGES
• TYPE II (FAST TWITCH) ATROPHY MORE THAN TYPE I (SLOW TWITCH)
• FIBER NECROSIS
TYPICAL GAIT CHANGESIN OLDER
ADULTS
• DECREASED GAIT SPEED
• DECREASED STEP OR STRIDE LENGTH
• INCREASED STANCE TIME AND DOUBLE-LIMB SUPPORT TIME
• INCREASED VARIABILITY OF GAIT (OPERATIONALLY DEFINED AS
VARIABILITY IN STEP OR STRIDE TIME, LENGTH, WIDTH, FREQUENCY,
OR VELOCITY)
• DECREASED EXCURSION OF MOVEMENT AT HIP, KNEE, AND ANKLE.
43.
CHANGES THAT OCCURIN AEROBIC
TRAINING
SKELETAL MUSCLE
• ↑IN CAPACITY TO GENERATE ATP AEROBICALLY
• ↑IN THE NUMBER AND SIZE OF MITOCHONDRIA
• ↑IN ACTIVITY OF AEROBIC ENZYME FUNCTION
• ↑ IN SKELETAL MUSCLE MYOGLOBIN CONTENT
(INCREASE QUANTITY OF OXYGEN AVAILABLE)
• ↑ IN BLOOD FLOW WITHIN THE MUSCLE
• SKELETAL FIBER HYPERTROPHY (SLOW-TWITCH
TYPE I FIBERS)
• ↑ IN MUSCLE'S CAPACITY TO MOBILIZE FAT,
OXIDIZE CARBOHYDRATE
CARDIAC MUSCLE
• ↑ IN WEIGHT AND VOLUME ( IN THE SIZE OF THE
↑
LEFT VENTRICLE WALL AND CAVITY)
• ↑ IN TOTAL HEMOGLOBIN AND PLASMA VOLUME
• DECREASE IN RESTING AND SUBMAXIMAL EXERCISE
HEART RATE
• ↑IN STROKE VOLUME AT REST AND DURING
EXERCISE
• INCREASE IN DIASTOLIC FILLING
• INCREASE IN MAXIMAL CARDIAC OUTPUT
• ↑ IN CAPACITY TO EXTRACT OXYGEN FROM THE
CIRCULATING BLOOD
• DECREASE IN SYSTOLIC AND DIASTOLIC BP AT REST
AND SUBMAXIMAL EXERCISE
Editor's Notes
#29 SV: Volume of blood ejected per heart beat
EDV: volume of blood in ventrical before contraction