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Lecture

Kine 1020 ALL WINTER TERM NOTES .doc

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Department
Kinesiology & Health Science
Course
KINE 1020
Professor
Jennifer Kuk
Semester
Winter

Description
January 4 Lecture Topic 4 Why is strength important Performance related - Sport Greater power, speed, balance Reduce demands on cardio - Job/occupational requirements Reduced risk of injury Productivity Health Related - Lower risk of functional limitations Avoid injuries Predicts advanced age disability Reduces chronic low back pain - Lower risk of chronic diseases Improved blood sugar control Prevents osteoporosis - Psychological health Improved self-image - Emergencies Endurance type 1 muscle fibre higher %, low type 2 % Power type 2 muscle fibre higher %, low type 1 % Best to have range of fibres, but affects type of sport you do Fibre type proportion related to type of activity (endurance/power) Winning not predicted by muscle fibres (can be small range difference) 80% outperform 85% Health Related (2) Lowering the risk of functional limitations - Maintaining or improving muscular strength later in life reduces the percentage of functional limitations over 50% for both men/woman Muscle strength across the lifespan (static, dynamic, pull strength and muscular endurance) Paediatric years childhood to young adult Elderly ** If you train as young adult, relatively maintain strength through old age** (does decrease) Decreasing muscle strength with aging Sarcopenia: loss of muscle mass and strength due to aging - 1-2% muscle mass per year past 50 yrs of age loss of strength varies/ may be greater Prevalence - Impacts 10-25% of the population under age 70 and 40% above age 80 - By 80 yrs a loss of 30-40% of muscle fivers (hypoplasia of muscles containing type II muscle fibers. Concerns - Risk of functional limitations ** Sarcopenia is a result of programmed cell death- apoptosis Characterized by: - DNA fragmentation - Nuclear condensation leading to formation of apoptotic bodies (engulfed by macrophages but do not induce an inflammatory response) - Cell shrinks when near apoptosis th January 6 Lecture Topic 4 continued DNA fragmentation - 2 main proteins DFF 40 (DNA fragmenting factor 40) degrades/fragments the DNA DFF 45 (DNA fragmenting factor 45) inhibits DFF40 DFF45 changed DFF40 active = DNA fragmentation - Casp-3 (Caspase 3) enzyme activated during apoptosis Nuclear condensation or Disassembly Uncondensed ring Necklace Collapse/ Disassembly Decreasing Muscle Strength with Aging Potential causes of Sarcopenia (still being identified) 1. Activation of apoptotic pathways caspases (enzymes that breakdown and degrade proteins and DNA) and AIF 2. Loss or hormonal adaptations (decrease in testosterone and growth hormone) 3. Loss of neurological influences (selective loss of type II motor units resulting in cluster of type I muscle fibre with age) Apoptotic pathways lead to programmed cell death Inactive Active Caspase-Dependent Processes Procaspases (inactive) Caspases (active) DNA / Protein Initiator caspases Effector Caspases Caspase -8, -10 Caspase -3 Caspase -9 Casepase -6,-7 Caspase -12 Activation: Increased [calcium] in muscle leaky sarcoplasmic reticulum ** Caspase -12 (perhaps -8,-10) Increased Reactive Oxygen Species (ROS) from mitochondria ** Caspase -8, -10 Released cytochrome c from a leaky mitochondria ** released cytochrome c Apaf1-ATP (Apoptosome) caspase -9 *** Bax and Bcl-2 regulate cytochrome-c release Activation of proteolytic pathways proteases (enzymes that breakdown and degrade proteins) 1. Caspase Dependent a) Ionic imbalance (accumulation of intracellular calcium, sodium; hydrogen; loss of potassium) 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) 2. Caspase- Independent a) Mitochondrial dysfunction- apoptosis-inducing factor (AIF) results in nuclear condensation and DNA fragmentation Impact of training (strength and endurance) on Apoptotic Pathways in the Elderly
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