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Exercise and Aging Skeletal Muscle

• Reading - Rogers p 65-97• Brooks - end of Ch 19• Nygard - Musculoskeletal Capacity• Outline• Body composition changes• Changes in muscle function• Morphological changes• Metabolic capacity• Adaptations to training

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Aging• Decline of physiological capacity is

inevitable consequence of aging– physical inactivity may contribute to

this decline - not predominant explanation

• Body composition with aging• inc % body fat / dec lean body mass

– studies illustrate selective decline in sk ms protein vs non muscle protein

– body K+ and Nitrogen levels

• muscle peaks at 25-30 yrs– decline in X sec area, ms density

– inc intra-muscular fat

• Resting Metabolic Rate (RMR)– decline associated with dec ms mass

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Muscle Function• Decline in ms strength

– sig loss of max force production

• Fig 3.1 - Cross-sec study ages 11-70 men

– inc strength to 30, constant to 50, then decline (24-36%)

– similar dec in isometric, dynamic and speed of movement

• women - 20-70 yrs – dec 35% in strength, 33% in Xsec area

– dec 15% / decade after 50 yrs

– dec 30% / decade after 70 yrs

• evidence of selective declines in type II fiber area, no change in type I

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Size and Strength• Decline in strength with aging either• loss of muscle mass, or• alteration in ms capacity to generate

force - motor unit activation / contractile properties

• MVC / CSA (max vol vs X sec area)

– older subject ~70% of young

– other studies - women no change

– men 8.7-7.1 with age ~ 20 % weaker

• values for old men similar to women• difference in young men may be

activity related• Fig 3.2 - cadaver study

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Endurance Capacity• Fitts - no difference in fatigability

– 28 vs 9 month old rats

• Human studies – maintenance of MV isometric and

dynamic strength for 1min similar

– at same % of MVC (70 vs young)

• other studies– greater force loss in 30 sec stimulation

– greater relative force loss and reduced capacity to resist fatigue

• observed slow return to resting function following fatigue test– dec rate of twitch force relaxation and

inc half relaxation time

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Morphology

• Muscle fiber types– divisions based on physiological,

ultrastructural and metabolic characteristics

• Distribution with aging– may be result of inter-conversion or

secondary to preferential loss of specific fiber type

• Lexell - cadaver studies– ~50 % type I in all age groups

– found 25% fewer fibers (30-70)

– accounting for 18% decline in strength

• between 20 and 80 - 39% loss of fibers - all types

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Denervation and Fiber loss• What is cause of fiber loss with age

– damage to ms cells without regeneration

– interruption of m neuron connection

• Fig 19-9 Brooks - 47% decline• EMG studies

– # of active motor units dec with age

– low threshold M units that remain become larger

– elderly - lower # of functioning spinal cord motor neurons

• Aging and fiber size– no sig change in type I fiber size

– sig dec in type II fiber size ~26%

– (age 20-80) accounts for dec strength

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Capillarization and Metabolic Capacity

• Observe 25 % dec in cap density• 20-40 % dec in cap / fiber ratio

– * screened for activity level - truly sedentary - still may be confounded

– inconclusive evidence

• Metabolic Capacity and Aging• Study enzymatic activity

– marker enzyme glycolysis, Krebs, ETC, Beta oxidation, ATP synthesis

• Glycolytic Capacity• considerable evidence glycolytic

enzyme activity and high energy phosphates not adversely affected

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Respiratory Capacity• Scandinavian studies - no change in

mito ox capacity B - HAD, CS

• later studies– ~25% dec in men and women

– 40% less O2 uptake capacity

• contrast - Scandinavian may not be truly sedentary - activity inc mito

• Adaptation to Endurance Training• healthy sedentary - ~10% decline per

decade in VO2 max– aging and physical inactivity contribute

• Cartee - relative inc in VO2 max and ms resp capacity is similar old and young

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Endurance Training• Seals - 6 months low and high

intensity training– 30% mean increase in VO2 max 60-70

– others 9-12 months - ~24 % inc

• Oxidative Capacity• Table 3.1 - Suominen

– 20 min 3-5 X/week - 8 weeks- 56-70yrs

– inc 45% in Resp capacity

– inc 12% in VO2 max

• Orlander - no inc - 12 weeks 70-75• Meredith - 128% inc Ox cap, 20 in

VO2 max -young 27 % inc in ox cap

– ** 45 minutes 3 X / week

• Coggan - fig 3.4A - 10 month program

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Endurance Training• Glycolytic capacity - minimal impact

• Capillarization– Coggan Fig 3.4 B

– cap density inc 20 %

– cap / fiber ratio inc 25%

• Fiber type alterations– Gollnick - 30 yrs old - 5 months

– 23 % inc in size of type I

– no change in type II

– no change in % type I

– type II b to a shift

• Cogan - elderly - similar to above– changes that occur function of intensity

and duration of stimulus

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Prolonged Endurance Training

• Animal studies - prolonged wheel running or swimming training– for significant portion of life span

– inc type I fiber mass, dec type II

– 20-40% inc in SDH, CS and B-HAD

• Human Studies– chronic intense endurance training in

master athletes - reduce or eliminate decline in VO2 max over 10 yrs

• compared to performance matched younger athletes– same max (a-v)O2 difference

– 25-30% higher ox enzyme capacity

– cap / fiber inc, cap / mm same

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Resistance Training• Regular resistance tx over sufficient

time period– muscle hypertrophy, inc strength

– alteration in body comp

• older individuals– table 3.3

• Frontera - 12 weeks - 80 % 1RM– Inc 5 % / day (similar to young)

• Fig 3.6 a inc 100 % ext, 200 % flexors

• Fig 3.6 b - 11 % inc in Xsec area– inc type I and II ~30 % each

– inc CS, Cap density, and VO2 max

• very old - 8 weeks high intensity– inc 174 % strength, 15 % X sec area