Lecture Notes Semester 2.docx

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Lecture Notes Semester 2
Why is Strength Important?
-Health related
- Lowers risk of functional limitations
o Prevents injury and infirmity
o Is a predictor of advanced age disability
o Reduced chronic low back pain
- Lowers risk of chronic diseases
o Improved blood sugar control, slows/prevents osteoporosis, increases metabolic
rate
- Good for psychological health
- Helpful in emergencies
-Performance related
- In sport
- May help individuals to fill job/occupational requirements (
o Reduces risk of injury/increases productivity
Decreasing Muscle Strength with Aging
-Sarcopenia is the loss of muscle mass and strength due to the aging process
- Increases functional limitations
- Involves apoptosis a decreased number of muscle fibres/mass/strength
-Sarcopenia is a result of Programmed Cell Death which is characterized by:
- DNA fragmentation (DNA falls apart)
o Caused by a protein called DNA Fragmentation Factor (DFF) 40
o Under normal circumstances DFF45 is present instead, which inhibits DFF40
preventing the degradation it causes
If DFF45 is damaged/altered, DFF40 can become active
o Influenced by Caspase-3 protease that breaks down DFF45 (more of this =
active DFF40 = more fragmentation)
- Nuclear condensation (nucleus dissolves) occurs in stages
o Influenced by Apoptosis-Inducing Factor (AIF)
Starts the condensation process (disassembly of the nucleus) at the ring
stage
o Leads to the disintegration of cells which are engulfed by macrophages but do not
induce an inflammatory response (therefore cannot be saved)
-Potential causes of Sarcopenia (still being identified)
- Main idea: apoptotic pathways (involving caspases and AIF) lead to cell
death/sarcopenia
o Caspase-dependent process (impacts initiation of apoptotic pathways):
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Initiator caspases (procaspases) are inactive in muscle: Caspase-8, -10,
Caspase-9, Caspase-12 which turn on ↓
Effector caspases (active): Caspase-3, Caspase-6, -7 which cause DNA
fragmentation and protein breakdown
Procaspases are activated by:
o IONIC IMBALANCE: Increased calcium in muscle
because of leaky sarcoplasmic reticulum
Turns on caspase-12 (maybe -8 and -10 too)
o OXIDATIVE STRESS: Increased levels of Reactive
Oxygen Species (ROS) from mitochondria, reduces
mitochondria‟s functionality
Caused by the increased levels of calcium
Turns on caspase-8, -10
o MITOCHONDRIAL DYSFUNCTION: a decline in ATP
levels and increase in oxygen free radicals causes
mitochondrial membrane leakage, leading to released
cytochrome C, which is regulated by Bax (release) and
Bcl-2 ( release, “plugs the leak”, a good thing)
Cytochrome C has to bind with Apaf1, creating
cytochrome c-Apaf-1-ATP or Apoptosomes
(which indicate cell death)
Turns on caspase-8
Bax/↓ Bcl-2 = Cyt.C = Apoptosomes
o Caspase-independent process:
Mitochondrial dysfunction AIF (released from the leaky mitochondria)
results in nuclear condensation (primarily) and DNA fragmentation
- Loss of hormonal adaptations (muscles can‟t grow if there are decreases in testosterone
and growth hormone levels)
- Loss of neurological influences (selective loss of type 2 motor units resulting in clusters
of type 1 muscle fibres with age)
-Impact of training (strength and endurance) on apoptotic pathways in the elderly:
- Improves calcium handling, reducing accumulation
- Increases Bcl-2/Bax ratio to decrease the amount of cytochrome C leakage
- Decreases Apaf -1, decreasing the amount of apoptosomes that can be formed
- Improves mitochondrial function
- Reduces AIF
Muscle Diseases: Definitions and Types
-Muscle disease: any disorder that affects the human muscle system
- Primary muscle disease: the pathology originates with the muscle
- Secondary muscle diseases (predominant): the pathology originates in other systems
o Nerve neuromuscular disease/disorder; ex: Parkinson‟s disease
o Bone/joint
o Inflammatory
o Immune autoimmune muscle disease/disorder; ex: Multiple Sclerosis
-Symptoms/indications of muscle diseases
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- Muscle atrophy (decreased size) with muscle weakness
- Pain
- Tetany: involuntary contractions (spasms) because of changing calcium levels
o Generally in the larger muscle of the arms and legs
- Twitching: single motor units firing due to loss of nerve cells, typically close to the
surface of the skin
- Muscular hypertension with increases in stiffness: increased size in muscle due to
increased amounts of fat there
o A form of muscular dystrophy (weaken the musculoskeletal system and hamper
locomotion)
- Biochemical parameters
-Primary indicator of muscle disease - Muscle weakness: failure to develop an expected force
-Classifications of muscle diseases associated with muscle weakness:
- Upper motor neuron disease
o Contrary to lower motor neuron disease, you don‟t experience atrophy
o Causes include tumors and spinal cord injury
o Ex: Stroke: producing weakness on one side of the body; the arm is typically
flexed, the leg is extended and the limbs have increased tone, some movement
may be preserved but the use of the hand is particularly limited
- Lower motor neuron disease flaccid (limp) muscle weakness
o Can happen at the spinal cord - muscle wasting causes shrinkage and eventual
death of neurons
Paralysis is rapid and death comes within 3 years (1year in infants)
Ex: amyotrophic lateral sclerosis (ALS) and Lou Gehrig disease
No known cause therefore no cure is available
o Can happen at the peripheral nerves (leaving the spinal cord, going to the
muscles) diseases called peripheral neuropathies/polyneuropathies
Symptoms usually begin in the hands and feet and progress towards the
body; also associated with sensory disturbances
There is a degeneration of the axons
Axons can regenerate but only at a rate of one or two mm/day,
making injury recovery very slow
Axonal types of neuropathy are caused by damage to blood
vessels
There can also be a degeneration off the myelin sheathes (covering of the
axons) “demyelinating neuropathy”
Muscles rarely atrophy, recovery can be rapid
Other causes of peripheral neuropathy can include diabetes, nerve trauma,
inherited factors, chronic renal failure
- Neuromuscular (N-M) disease
o Associated with weakness and fatigability with exercise
o Typically involve the generation of an end-plate potential that is too low to
propagate an action potential in the muscle fibre
Not enough Ach or Ach receptors
o May be acquired or inherited; may be the result of autoimmune disorders,
congenital disorders or toxins
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