KINE 1020 Study Guide - Final Guide: Bulimia Nervosa, Retrovirus, Pasteurization

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Lecture 1- Jan.04.12
Why is Strength Important?
Performance Related
o Sport
More power, speed, and balance, reduce demands on cardiovascular system
o Job
Reduced risk of injury
Productivity
Health Related
o Lower risk of functional limitations
Avoiding injuries, predictor of advanced age disability, reduces chronic low back pain
o Lower risk of chronic diseases
Improved blood sugar control, retard/ prevents osteoporosis, incr metabolic rate
o Psychological Health
Improved self-image
o Emergencies- fight or flight situations
Muscle Fibre Types for Sport Performances
Endurance (distance running)- higher % of type 1 slow fibres
Strength ( ice-hockey) - lower % of type 1, therefore; more fast fibres
o Having these characteristics does not determine the performance in a sport
Health Related
Study by Brill- Higher percentage in functional limitation with lower strength
Study by Ratanen- Muscle Strength as a predictor of old age disability
Walking speed and rising from a chair- those with lower strength had more limitations
Training when done in an appropriate manner will result in gains, and levels are retained
There is always a decline in strength as we age; improving strength will only slow it down
Decreasing Muscle Strength with ageing
Sarcopenia- loss of muscle mass and strength due to aging
o 1-2% muscle mass per year past 50 yrs of age- loss of strength varies
Prevalence
o Impacts 10-25% of 70 years and 40% above 80 yrs
o 80 yrs a loss of 30-40% of muscle fibres
( Hypolasia of muscles containing type 2 muscle fibres)
Concerns
o Risk of functional limitations
Sarcopenia is result of Apoptosis (Programmed Cell Death)
o Characterized by DNA fragmentation and nucleus starts to disintegrate/ condense
o When cell death starts to occur, you can’t go back; cells start to shrink
o Narcosis starts an inflammatory response to try to save the muscle
Lecture 2- Jan.06.12
DNA Fragmenation Factor (DFF40)- degrades/ fragments the DNA
DFF45- inhibits/ doesn’t allow the fragmentation of DFF40 to occur
Caspase-3 (agent)- an enzyme that gets activated during apoptosis
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Nuclear condensation/ disassembly
o Uncondensed-> Ring -> necklace-> collapse/ disassembly
o AIF ( Apoptosis- Inducing Factor)- happens during the Ring stage- starts the condensation
process
Potential Causes of Sarcopenia ( still being identified)
1. Activation of apoptotic pathways- Caspases and AIF ( most popular school of thought)
2. Loss of hormonal adaptation
3. Loss of neurological influence- change in neural pattern- loss of motor neurons- more
relevant to type 2 fibres (fast)
Apoptotic Pathways
In muscle caspases are inactive and they are referred to as Procaspases
When activated they activate other caspases and can result in DNA fragmentation and
degrading protein
o Three factors to activate caspases
Increased calcium in muscle- leaky sarcoplasmic reticulum- impact leakiness of
mitochondria
Increased Reactive Oxygen Species (ROS) from mitochondria- O2 used to make ATP
Cytochrome c will be released from a leaky mitochondria
Procaspases- Initiator Caspases- Caspase-8, 10, 9, 12
o Activation
Increased calcium affects 12 ( perhaps 8 and 10)
Increased ROS affects 8 and 10
Cytochrome C affects 9
Combination of Cyt C and Apaf1- ATP creates Apoptosome which then activates
Caspase 9
Bax and Bcl-2 slows down the release of Cyt C
Active Caspases- Effector Caspases- Caspase-3, 6, 7
o Caspase- 3 is important because it affects the protein that keeps the DNA intact
I. Caspase-dependent
a) Ionic Imbalance (accumulation of intracellular calcium)
b) Oxidative stress (accumulation of reactive oxygen species (ROS) which are considered
damaging)
c) Mitochondrial dysfunction (a decline in ATP levels, increase in oxygen free radicals
membrane leakage)
II. Caspase-Independent
a) Mitochondrial dysfunction apoptosis-inducing factor (AIF) results in DNA
fragmentation
Impact of training (strength and endurance) on apoptotic pathways in the elderly
Improved calcium handling, and mitochondrial function
Increased Bcl-2/ Bax ratio- therefore les Cyt C release, decreased Apaf-1
Reduced AIF ( Apoptotic Inducing Factor)
Muscle Disease/ Disorder- a disease or disorder that affects the human muscle system
Primary Muscle Disease- the pathology originates with the muscle ( internal membranes/
metabolic) disorders
o Ex. McArdl’s disease (glycogen storage problem, not enough fuel), Forbe’s Disease
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Secondary Muscle Disease- the pathology/ cause comes from other systems
o Nerve- neuromuscular disease or disorder
Parkinsons
o Bone/ Joint- musculoskeletal disease or disorder
o Inflammatory system- inflammatory muscle disease or disorder
o Immune System- autoimmune muscle disease or disorder
Muscle Diseases: Symptoms/ Indications
1. Muscle Atrophy (decrease size) and accompanying muscle weakness
2. Pain- no pain receptors in muscle- defects in cardiovascular system
3. Tetany- spasms involuntary contractions b/c of changing calcium levels
4. Twitching- singular motor unit loss
5. Muscular Hypertrphy- increase in size is a form of muscular dystrophy
6. Biochemical parameters- reduced muscle glycogen; mitochondrial oxidative potential;
increased myoglobin, acid maltase
Lecture 3- Jan.09.12
Muscle weakness- failure to develop an expected force which can be attributed any one of the
processes required for force generation. This is associated with all types and examples of muscle
diseases/ disorders
Muscle contraction results from a chain of events that begins with a:
1. Nerve impulse traveling in the up motor neuron from the cerebral cortex in the brain to
spinal cord
2. The nerve impulse then travels in the lower motor neuron from spinal cord to
neuromuscular junction
3. Where the neurotransmitter acetylcholine is released. Acetylcholine diffuses across the
neuromuscular junction, stimulating acetylcholine receptors depolarize the muscle
membrane
4. The result is the contraction of the muscle fibre
Contraction depends on the integrity of each of these parts; disease or disorder in any part
causes muscle weakness
Classification:
a) Upper Motor Neuron Disease- a problem from cerebral cortex down to the spinal cord
CV- stroke producing weakness of one side of the body. The arm is flexed, leg
extended, and the limbs have increased tone
With the upper motor neuron disease the muscle bulk is usually well preserved
Other causes of upper motor neuron disorders include tumours and spinal cord
injury
b) Lower motor neuron disease- flaccid muscle weakness- can happen at two levels; spinal
cord and peripheral nerves
1. Spinal cord- motor neurons are lying in the spinal cord- you get muscle wasting,
shrinkage and eventual death of neurons, and denervation
Generally between 50- 70 years of age and have upper and lower motor neuron
weakness- paralysis progresses rapidly, and death within three years
Infant amyotrophic lateral sclerosis is fatal within one year
No cause is yet known, and no cure
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