KINE 1020-All Lectures 1-30-Winter Term

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York University
Kinesiology & Health Science
KINE 1020
Angelo Belcastro

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 cant 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/ doesnt allow the fragmentation of DFF40 to occur Caspase-3 (agent)- an enzyme that gets activated during apoptosis 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- O 2used 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. McArdls disease (glycogen storage problem, not enough fuel), Forbes Disease 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 2. Peripheral Nerves Disease (peripheral neuropathies or polyneuropathies) Symptoms usually begin in the hands and feet and progress toward the body- also associated with sensory disturbances Peripheral neuropathies- degeneration of the axons o Axons can regenerate but only at a rate of one to two millimetres per day o Damage to blood vessels, nerves can cause these peripheral neuropathies Myelin Sheath- can degenerate o Symptoms are similar to axonal neuropathies Major difference is muscles rarely atrophy o Recovery can be very quick o Causes: diabetes, heredity c) N-M junction disease These disease are associated with weakness and fatigability with exercise Diseases of the neuromuscular junction typically involve the generation of an end plate potential that is too low to cause an action potential in the muscle fibre Causes: heredity, autoimmune disorder Muscular Dystrophies- are a group of hereditary disorders (n=9) characterized by progressive muscular atrophy and weakness. In most varieties the muscles of the limb girdles- the pelvic and should muscles- are involved Progressive loss of muscle size, and strength which is caused by loss of muscle proteins laer changing to muscle fibre death and tissue death Assessments Include: 1. Measurement of the activity of creatine kinase in the blood 2. Analysis of a muscle biopsy (structural), and 3. Recordings from an electromyography frequently establish that the muscle weakness is due to primary degeneration of the muscles Nine Types of Muscular Dystrophy 1. Steinerts Disease or Myotonic Muscular-muscles remain in spasms or become stiffened 2. Duchenne Muscular Dystrophy- happens in males 2- 6 yrs, will live up to 20 yrs old a. Associated with Becker- differ by severity of muscle disease-milder and symptoms can appear up till 25 years of age- have some heart problems and only impacts males 3. Emery- Dreifuss- only affects males from childhood to teen years- affects the muscles of pectoral, upper and lower arm, and lower leg 4. Limb Girdle- in both males and females in t
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