Aging of muscle - AGHE meeting in San Jose, Feb. 2001
Overhead transparencies by Augustine G. DiGiovanna
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Muscle mass

1. begins to decrease at approx. age 30

2. rate of decrease becomes much faster at age 50

3. decrease in muscle mass is linear after age 50

POSSIBLE significance

1. lower physical abilities (e.g., IADLs, balance, falls)

2. physical disabilities

3. mean longevity/mortality risk

4. quality of life

5. muscle mass VS. muscle strength

6. muscle mass VS. speed, control, endurance, task-specific performance

7. average rates of decline

a. 15% per decade at ages 50-60

b. 30% per decade after age 60.

DEFINITION of sarcopenia

1. no standard definition for sarcopenia

INCIDENCE

1. > 20% for elderly men

2. > 30% for elderly women

POSSIBLE causes

1. reduced exercise

2. malnutrition

3. oxidative stress (free radicals and other ROS)

4. muscle mitochondrial mutations (i.e., mtDNA deletions)

5. changes in specific types of muscle fibers

a. selective atrophy of Type II fibers (perhaps the major factor)

b. selective loss of Types II fibers

c. conversion of Type II fibers to Type I fibers

6. decline in muscle protein

a. decline in muscle protein synthesis

b. decline in certain proteins (e.g., MHC, SR, mitochondria).

c. dysregulation of hormones

7. diseases

a. hyperinsulinemia

POSSIBLE treatments

1. exercise

2. dietary modification

3. hormone supplementation (e.g., testosterone, GH, IGF-I, DHEA)

Free radicals, oxidation, and muscle

1. age-related increases in -

a. membrane lipid peroxides

b. oxidized muscle proteins

c. sarcoplasmic reticulum

d. mitochondria

2. sources of FR damage to mtDNA

3. mtDNA sensitivity to FR damage

4. age-related increase in muscle mtDNA deletions

5. mtDNA heteroplasmy

a. clonal distribution (perhaps clonal replication)

b. not a vicious cycle of FR damage to mtDNA

Effects from mtDNA deletion mutations

1. less energy output

2. more FR production

3. damage to cells throughout body (e.g., atherosclerosis).

4. may affect Type I or Type II preferentially

5. atrophy (may be regional from heteroplasmy)

Effects from damaged mitochondria

1. decline in ATP production

2. mitochondrial signaling proteins (e.g., apoptosis-inhibiting factor)

3. calcium ion regulation

4. sarcopenia (preferential for Type II fibers)

5. "reductive hotspot" hypothesis

Reducing FR damage in muscle

1. exercise

2. antioxidant supplements ??

3. caloric restriction (CR)

Glycation (intracellular)

1. little research

Hyperinsulinemia

1. promoting FR damage to proteins

_a. increasing H₂O₂

b. increasing NO

c. increasing NO-caused mitochondrial damage

d. lipid peroxidation (e.g., mitochondrial membranes)

2. decreasing removal of damaged proteins

a. decreased proteosome activity

3. exercise and GLUT-4 transporters

4. caloric restriction

Muscle proteins

1. types or myosin heavy chains (MHCs)

a. MHCI in Type I fibers

b. MHCIIA and MHCIIb in Type II fibers.

2. age-related declines in MHC synthesis

3. FR damage and proteosomes

4. effects from androgens

Voluntary control of muscles

1. steadiness

2. strategies

3. throat muscles

a. thyroarytenoid muscle

b. laryngotracheal muscle
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Aging of muscle - AGHE meeting in San Jose, Feb. 2001 Overhead transparencies by Augustine G. DiGiovanna Return to Main Site Index Return to Main Site Map Return to Index Page