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York University
Kinesiology & Health Science
KINE 1020

th 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 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)  Caspase’s (active)  DNA / Protein Initiator caspases Effector Caspase’s 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  Improved calcium handling – therefore not as much accumulation  Improve mitochondrial function  Increased Bcl-2/ Bax ration (therefore less cytoch-c leakage)  Decreased Apaf-1  Reduced AIF January 9th Lecture - Topic 5 Muscle diseases: definitions and types Any disorder or disease that affects the human muscle system: a) Primary muscle disease – the pathology originates with the muscle (internal membranes/metabolic) disorders b) Secondary muscle disease – the pathology originates in other systems: - Nerve  neuromuscular disease/disorder - Bone/Joint  musculoskeletal disease/disorder - Inflammatory system  inflammatory muscle diseases/disorders - Immune system  autoimmune muscle diseases/disorders ** Examples** a) Primary muscle diseases; McArdle’s disease, Forbe’s disease b) Secondary muscle diseases - Neuromuscular disease/disorder Parkinson’s disease; muscular dystrophy - Inflammatory muscle disease/disorder  Dermatomyositis - Autoimmune muscle diseases/disorders  Multiple Sclerosis; Myositis, Muscle Rheumatism **Symptoms** 1. Muscle atrophy (decrease size) AND muscle weakness 2. Pain – defects in cardio/inflammatory systems 3. Tetany – involuntary contractions for arms/legs due to change in calcium levels 4. Twitching – single motor unit firing due to loss of nerve cells 5. Muscular hypertrophy and accompanying increase in stiffness (Myotonia congenita); increase size due to more fat in muscle (form of muscular dystrophy) 6. Biochemical parameters - Reduced muscle glycogen; mitochondrial oxidative potential - Increased myoglobin, acid maltase; CK 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/examples of muscle diseases/disorders. Classifications a) Upper motor neuron disease b) Lower motor neuron disease c) N-M junction disease Muscle weakness results from a chain of events that begins with a: a) Nerve impulse traveling in the upper motor neuron from the cerebral cortex in the brain to the spinal cord. b) The nerve impulse then travels in the lower motor neuron from the spinal cord to the neuromuscular junction; c) Acetylcholine is release and diffuses across the neuromuscular junction, stimulation acetylcholine receptors to depolarize the muscle membrane. d) The result is the contraction of the muscle fibre (actin/myosin)  Contraction depends on the integrity of each of these parts; disease or disorder in any part causes muscle weakness. Classifications (In detail) Upper motor neuron disease (cerebral cortex  spinal cord) Muscle weakness typical of upper motor neuron disease includes: a) CV- stroke producing weakness of one side of the body. The arm is typically flexed, leg extended and limbs have increased tone. Some movement may be preserved, although the use of the hand is particularly limited. b) With upper motor neuron disease the muscle bulk is usually well preserved (different than lower motor neuron) c) Other causes of upper motor neuron disorder include tumours and spinal cord injury. Lower motor neuron disease – flaccid muscle weakness 1. Spinal cord – muscle wasting is prominent  shrinkage and eventual death of neurons  denervation of muscle a) Motor neurons lying in the spinal cord  most common amyotrophic lateral sclerosis (ALS) and Lou Gehrig disease b) Generally between 50 and 70 years of age and have upper and lower motor neuron weakness – paralysis progresses rapidly, and death within 3 years c) Infant amyotrophic lateral sclerosis is fatal within one year d) No causes is yet known for any of these diseases and no cure available 2. Peripheral nerves diseases (peripheral neuropathies or polyneuropathies)  Symptoms usually being in the hands and feet and progress toward the body  Also associated with sensory disturbances a) Peripheral neuropathies – degeneration of the axons (core of nerve fibres)  Axons can regenerate but only at a rate of one to two millimetres per day. - After injury to a nerve at the elbow, the hand will not recover for 6-9 months.  Damage to blood vessels (physical and/or chemical) tend to cause axonal types of neuropathy. b) Myelin sheath – peripheral neuropathy caused by degeneration of the myelin sheaths (covering of axons) demyelinating neuropathies  Symptoms are similar to axonal neuropathies but since axon remains intact, muscles rarely atrophy.  Recovery from demyelinating neuropathies can be rapid  Other causes of peripheral neuropathy include diabetes, mellitus nerve trauma, inherited factors and chronic renal failure. c) N-M (neuromuscular) Junction disease  These diseases 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 propagate and action potential in the muscle fibre.  Diseases of neuromuscular transmission may be acquired or inherited and may be the result of autoimmune disorders, such as myasthenia gravis congenital disorders; toxis such as those present in botulism. The 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 (pelvic/shoulder) are involved. There is a progressive loss of muscle size/strength which is caused by loss of muscle proteins later changing to muscle fibre death and tissue death. Tests for muscular dystrophies include a) Measurement of the activity of creatine kinase in the blood b) Analysis of a muscle biopsy (Structural) c) Recordings from an electromyography frequently establish that the muscle weakness is due to primary degeneration of the muscles Nine types of muscular dystrophy Steinert’s disease or myotonic muscular dystrophy:  Type of muscular dystrophy which is most common in adults  Muscles remain in spasms or become stiffened after a slight use or exercise  Lower temperature increases these symptoms  ** Affects both males and females** Duchenne Muscular Dystrophy (Most common)  Type more common in children and only affects males between 2-6 yrs of age  Decreases in the mass of muscle is progressive and in most cases, children are wheelchair ridden by the start of 10 yrs.  Usually do not survive more than 20 years. Becker muscular dystrophy  Similar to duchenne but symptoms are milder and can appear till 25 yrs of age  Affected people can live and enjoy life and also able to walk but have heart problems  ** Only present in males** Emery – Dreifuss  Type which affects from childhood to teen years  **Only affects males**  Affects muscles of pectoral region to upper arms and lower parts of legs  Patients have extreme heart problems that are fatal Limb-Girdle  Type which affects teenage to adult  ** affects both males/females**  Starts from hip (pelvic girdle) and then goes to shoulder (pectoral girdle)  Arms and legs later affected  Sufferers are unable to walk and most patients live past mid adulthood. Fascioscapulohumeral Muscular Dystrophy  Affects muscles of the face, scapula, humerus  ** affects both males/females**  50% of sufferers able to walk throughout their life  Almost all patients live a normal life span Oculophyrangeal Muscular Dystrophy  Affects primarily eyes/throat region  Occurs around 40 yrs of age  Symptoms include weakness of eyes and facial muscles which cause swallowing problems. ** < 5%**  This type predisposes the patients to pneumonia and choking Muscle diseases: Myasthenia gravis  Failure in the transmission of nerve impulses to the muscles  Persistent muscular weakness and tendency to be easily fatigued Symptoms: weakness in face/limbs, double vision, difficult swallowing, fatigue during exercise Controlled by:  Treatment with high doses of corticosteroids (depress the immune response)  Anticholinesterase medications (Stimulate transmission of nerve impulses) Muscle diseases: Myotonic Diseases  Myotonia (difficulty in relaxing/slow relaxing) a muscle after contraction Causes:  Continual electrical activity of the sarcolemme  Multiple firing of the nerve is most common form - Problem lies in abnormal ion channels or ion pumps in the sarcolemma  Delayed disengagement of the thick/thin filaments of myosin and actin  Physical inactivity and cold enhance condition Muscle diseases and disorder: Fibromyalgia  Common syndrome which person has long-term body wide pain  Tenderness in joints, muscles and tendons  Linked to chronic fatigue, sleep problems, depression, headaches, anxiety Causes (Unknown but 4 possible causes) a) Physical/emotional trauma b) Abnormal pain response – EEG  areas in brain that are responsible for pain react differently in patients c) Sleep disturbances d) Infection (virus) but none identified  ** Common among woman ages 20-50 ** Symptoms Pain symptoms (range from mild – severe) a) Painful areas are called tender points and spread out from those areas - Tender points found in soft tissue of neck, shoulders, chest, lower back, hips, shins b) Pain may feel like a deep ache or shooting/burning pain c) Joints are not affected (although pain feels like it is coming from joints) - People wake up with body aches/stiffness - Pain gets worse in day/night Tests to diagnose Fibromyalgia  3 months of widespread pain in at least 11 of 18 areas Treatment  Goal to relieve pain a) Physical therapy b) Exercise/fitness program Stress-relief methods (light massage and relaxation techniques) January 11 Lecture Topic 6 Skeletal Muscle: Adaptations, Strength training and conditioning Outline  Muscular adaptations - Acute  injury and damage - Chronic  fibre transitions, hypertrophy - Timing  Principles of strength training  Program design characteristics Acute Changes – associated with Skeletal muscle fatigue a) Inability to maintain the required power output (decline in force/velocity) [ Edwards 1980’s] b) Condition which there is a loss in the capacity for developing force/velocity of muscle - Resulting from muscle activating under a demand/load (reversible by rest) - [NIH – respiratory muscle 1990] c) Inability to maintain the required power output (related to decline in force, velocity and power)  which is reversible Acute Changes – Characteristics of fatigue: Eccentric Contractions  As force decreases, # of fibres (vice-versa) [Linear Co-relation; 0.89]  ** This led researches to implicate proteases: calcium activated neutral protease – calpain  Decreased strength/power output  Muscle damage (injury)  Delayed onset muscle soreness (DOMS)  Restricted range of motion (ROM)  Increased blood proteins Fatigue – Possible sites/causes Central 1) Planning of voluntary movement 2) Motor cortex and supraspinal outputs 3) Upper motor neurons 4) Lower motor neurons Peripheral 5) Neuro-muscular (NM) junction and sarcolemma 6) Sarcoplasmic reticulum (Ca ions movements) 7) Action-myosin interactions 8) Metabolic supply (all 3 systems) and accumulation Neuro-muscular (NM) junction and Sarcolemma: High intensity contractile activity A. Neuromuscular junction: - No evidence that N-M blockage is a problem - Neither is the release/uptake of acetylcholine a problem B. Sarcolemma and t-tubule systems: - Action potential propagation is changed a) Fatigue is associated with +10mV change in membrane potential; resting membrane electrical potential goes from -80 to -70 mV with heavy exercise b) Fatigue associated with a drop in the amplitude of the action potential (peak of excitation); therefore not sufficient to activate channels in T-tubule system - Caused by K+ ions leaking out of muscle cell and Na+ ions leaking in c) Na+ and K+ pump has been suggested (ATP decreases or ROS [reactive oxygen species] increases) ** Resting Membrane potential changes and Peak action potential changes (decreases)** Sarcoplasmic Reticulum (Ca ion movements) Fatigue with heavy exercise associated with  Reduction in SR [calcium] as a result of decreased SR Ca2+ ATPase pump  (SERCA) and/pr because more calcium remains bound in SR (linked to phosphate) a) Reduced SERCA activity due to - Lower [ATP] - Inefficient or leaking (because of action of ROS) b) Increased bindings due to: - Increase inorganic phosphate which comes from increasing muscle contractions Fatigue with heavy exercise associated with:  End result less calcium for release upon stimulation/excitation and conversely more calcium remains in the cytoplasm with heavy exercise (fatigue) Muscle weakness and Low Frequency Fatigue (LFF)  Ca ions release channel (Ryanodine receptor –RyR) does not release sufficient calcium th January 16 Lecture Action- Myosin – Contractile Protein Interactions Fatigue with heavy exercise associated with a) Increasing inorganic phosphate (Pi) - Delays detachment phase of A-M cross-bridges b) Increasing hydrogen ions levels will decrease the pH - Heavy exercise from ~7.2 to ~6.8 (more acidity) - Myosin ATPase activity is reduced at lower pH Fatigue with heavy exercise associated with: a) Loss of contractile protein(s) - ~60% reduction in each of myofibrillar proteins troponin –I, tropomyosin b) Loss of cytoskeletal (Structural) proteins - ~50% loss of alpha-actinin (z-line) - ~80% loss of desmin (myofibril-linking protein) Cause – Myofibril prtein losses a result of increased protease activity - Calcium activated neutral protease – Calpain (CANP1; CAPN2) Metabolic Supply (3 systems) and accumulation Fatigue with heavy exercise associated with: a) Phosphagen sources  Reduced levels or lower supply of creatine phosphate (CP) or phosphocreatine (PCr) - Can be ~80% depleted b) Anaerobic Glycolysis  Lower supply – reduced glycogen concentrations  Build up/accumulation of intracellular muscle lactate (vs., lactic acid) c) Aerobic – oxidative phosphorylation  Accumulation or increased ROS Overview of Acute Impact of fatigue with Heavy Strength/Resistance Exercise Summary of Fatigue Factors Chronic Impact of Fatigue with Heavy Strength/Resistance Exercise Resistance training  Muscle hypertrophy Muscle Remodelling Endurance training  Mitochondrial biogenesis Muscular Adaptations to Strength/Resistance Training Muscular Adaptations – remodelling a) Muscle Fibre Transitions b) Muscle Hypertrophy c) Timing of Muscular Adaptations Muscular Adaptations – Remodelling  Formation of new muscle fibres is critical to normal muscle function – “turnover” - Number and type of muscle fibres genetically determined - Replace old fibres with new fibres  Formation of new muscle fibres is called myogenesis - Satellite cell  Myoblast  Myotube  Muscle - Activators include myoD and myogenin - Inhibitors include myostatin Stimulation of myogenesis with training?  Resistance training - Increases myoD and myogenein (stimulates myogenesis) expression (peak ~36 hrs) - Reduces myostatin  Endurance training - Modest impact on regulators of myogenesis Muscular adaptations – muscle fibre transitions (indentified through MHC) – Myosin heavy Chain Transformations 1) MHC – Time 1 / 2 is ~ 30 hrs 2) MHC changes after 2-3 workouts 3) More oxidative Conversions (?) Muscular Adaptations – Hypertrophy  Increase in size of muscle (also muscle fibre) with strength/resistance/anaerobic training  Increase in muscle fibre size due to more protein as a result of increased protein synthesis  Therefore hypertrophy resulting from training is a result of protein degradation and protein synthesis Muscular adaptations – Hypertrophy  Cycles of degradation (PD) and synthesis (PS) are critical for hypertrophy (and transitions)  PD – peak at end of exercise and slows down in recovery lasting ~ 24 hrs  PS – little increase immediately after exercise and reaches peak ~ 36-48 hrs of recovery - Factors promoting PS  Are there muscle fibre specific adaptations Resistance training  Both types increase (Type II > I)  3-6 months - Increased Type II ~35%, Increased Type I ~ 20%  Athletes vs. untrained - Type II ~132% then UT, Type I > ~ 60% then UT Factors Promoting protein synthesis (3 factors) 1) Intensity and volume of the workload - Principles of strength/resistance training a) Contraction type – eccentric > concentric  Leading to increased organelle disassembly (sacromere), protein targeting (E3- ligases)  cell “clean up” b) Tension – greater tension > membrane disruption results in  Release of growth factors (calcinerurin)  Increase in signalling pathways for gene transcription and PS c) Metabolic stress – greater anaerobic contribution to energy (ATP) production  greater growth hormone response; Associated with - High tension ; restricted or occluded blow flow - Moderate loading, high volumes and short rest intervals 2) Nutrient intake a) Water (cellular hydration) is associated with decreased protein degradation and increased protein synthesis - Creatine loading  results in cellular hydration b) Carbohydrates – increasing intake  insulin - Strength athletes – 55% - 65% CHO or 6g /day c) Protein (amino acids) – 9 essential increased in diet (intake) or supplementation - Diet recommend range of 1.7 to 2.2g/kg - Supplementation  brain-chained amino acids; whey protein - Type - Timing 3) Hormonal environment a) Androgenic – testosterone b) Anabolic – steroids; testosterone esters; growth hormone; testosterone enhancers (banned substances) Muscular adaptations – Hypertrophy Structural changes 1.) Increased # of myofibrils 2.) Increased density of the sodium-potassium pump; sarcoplasmic reticulum and t-tubule 3.) Results in an improved calcium handling (important for power/speed activity) 4.) Hyperplasia (increase in muscle fibre number) Timing of muscular and neural changes Principles of Strength or Resistance Training – Conditioning (New Topic) Strength/Resistance Training: Principles of Program Design  Progression (habituation) is a long term goal of all programs - No training/workout equals no benefits  Ten Success factors 10 Success factors  Muscle action(s) - Exercise Selection  Repetitions - Exercise Order  Set - Rest periods/intervals  Volume - Repetition Velocity  Intensity - Frequency Muscle Action(s)  ECC > CON – both are considered dynamic actions with constant external resistance (isoinertial) results in variable force production throughout the ROM  ISOM (isometric) – no movement with constant external resistance  ISOK (Isokinetic) – variable external resistance  force production across the ROM constant Repetition  Complete movement cycle  (moving weight up and down) Set  A specified group or number of repetitions Volume  Total amount of work performed during a workout Intensity  Magnitude of loading (weight lifted) – related to RM (max weight lifted in 1 effort) 1RM or 90% of 1RM Frequency  Number of training sessions per day or week Exercise Selection  A selected group exercise to be performed in a session or training program Exercise Order  Sequence of exercises Rest periods/Intervals  Amount of rest taken between sets, reps and/or exercises Repetition velocity  Velocity at which reps are performed 5 basic principles – generic to all programs 1) Progressive overload 2) Specificity 3) Variation 4) Individualization 5) Reversibility January 23 Cardiorespiratory System and Metabolism (New Topic) Human respiratory System Upper tract  Nasal/mouth (warms and moistens air)  Cilia are hair like projections and line the primary bronchus to remove debris from lungs - push substances and mucus up until the epiglottis so it can be swallowed  Primary bronchus Lower tract  Larynx, Trachea  Right/left bronchus  bronchioles  clusters of alveoli Conductive zone (NO gas exchange) Mouth nose  trachea  larynx  Bronchi  bronchioles  humidifies/warms/filters air Respiratory zone (gas exchange OCCURS) Bronchioles  alveoli - Alveoli connected to blood vessels to get O2 into blood Inspiration vs. Respiration Inspiration  External intercostals muscles (down/contract)  Diaphragm (down)  Lungs expand Expiration  External intercostals muscles (up/relax)  Diaphragm (up)  Lungs deflate Lung Function Tests  Spirometer (measures volume of air you can breathe in and out)  Tidal volume (inhale/exhale per regular breathe)  Max inhale/exhale  Vital capacity  Total lung capacity (everything in lung)  Residual capacity/volume (air left over after exhaling) Lung Numbers  Tidal Numbers = 500ml (males/females)  Total Lung Capacity = 6000 ml (male) , 4200 ml (female) ** Minute Ventilation (rest) = Breathing frequency (breath/min) x Tidal volume (L) = 12-15 (breath/min) x 0.5 (L) = 6.0 – 7.5 L /min The Heart  SA (Sinoatrial) node = pacemaker Why we need atria?  Atrial walls are thing so blood can easily return to heart  Atria contractions “overfill” the ventricles  slightly stretched, better contraction/ejection - (Frank-sterling mechanism  Elastic recoil)  ** Note: ventricle walls are much thicker to generate blood pressure necessary to distribute blood around the body. The path of blood flow Right side (deoxygenated) lungs Left side (oxygenated)  body Normal resting values Heart Rate (HR) 50-80 bpm Stroke Volume (SV) 60-80 ml/beat Elite values Heart Rate (HR) 30-40 bpm Stroke Volume (SV) 90-110 ml/beat  Cardiac Output (Q) = HR x SV  Average Blood volume = 5L Anatomy of respiratory System (Dead air space and gas exchange) Composition of Air ** Dead space is why Artificial Respiration (AR) works** Inhaled Air  78% nitrogen  21% oxygen  0.03% CO2  0.97% other Exhaled Air  78% nitrogen  17% oxygen  3.3% CO2  1.97% other How does oxygen travel in the blood?  Carries 98.5% of all O2  Holds up to 4 O2 molecules  Also carries other gasses (CO2, CO, NO, etc.)  Oxygen diffuses to de-attach/attach from/to blood cells - Transit time (time for diffusion to occur) What happens with exercise?  Oxygen intake reaches a steady state to meet the energy demands using aerobic metabolism  Process takes time  “Extra energy?” What is a MET (Metabolic Equivalent)  1 MET = 3.5 ml O2/kg/min  Amount of energy you use at rest  Marker of exercise intensity January 25 Cardiorespiratory System and metabolism (continued) What happens with exercise? Fick’s Equation VO2 = HR x SV x (CaO2 – CvO2)  Heart rate (HR), Stroke Volume (SV). and Oxygen Extraction all increase Exercise and Heart Rate  Heart rate: Vagal (Parasympathetic) withdrawal (sudden increase in HR due to quick change from resting to active)  ~100-110 bpm (quick) - Sympathetic activation  HRmax (slower)  Age-predicted heart rate maximum = 220 – age - Usually accurate within 10-15 beats per min  Used to predict exercise intensity; much easier than measuring oxygen uptake (VO2) Exercise and Stroke Volume  Stroke volume: increases with exercise - Greater contractility - Reduced peripheral resistance (vasodialation)  Increased ejection fraction (heart empties more) - Elite athletes have higher stroke volumes Exercise and Oxygen Extraction Theory 1) Deliver same, extract greater proportion 2) Deliver more, extract same proportion 3) Deliver more, extract greater proportion (correct)  Delivery is a function of [Hb] (haemoglobin –unchanged/decreases) + blood delivery (increases due to Q)  Extraction is related to diffusion gradient, diffusion area and barriers to diffusion What limits Maximal Exercise? VO2 = HR x SV x (CaO2 – CvO2) Would we increase VO2 max if we could make: 1.) The heart beat faster (NO, SV goes down) 2.) The heart beat more blood per beat (YES, increase SV, exercise  bigger heart) 3.) Delivery more O2 (YES, exercise help increase [Hb], O2 delivery - Blood doping works 4.) The muscles take up more of the oxygen that is delivered to it (UNLIKELY) Q limits Maximal Exercise (Cardiovascular Drift) th January 27 Lecture Cardiorespiratory System and Metabolism What causes the differences in VO2 max (Untrained vs. Trained) Untrained advantages in: Transit time, CaO2 (%) Elite advantages in: SV, Minute ventilation, Breathing frequency, Tidal volume, [Hb], Diffusion gradient, diffusion area, a-vO2 (5) Neutral in: HR and Blood Volume How is VO2 measured?  Spirometer  Douglas bags ** VO2 max important for doing different activities** Energy Transfer Systems and Exercise || Energy System During Exercise Immediate Energy Sources; Anaerobic – Alactic System  ATP = adenosine Triphosphate (7.3 – 11 kcal) ATPase ATP ADP + Pi + Energy (2-3 sec Creatine Kinease PCr + ADP ATP + Cr (6-8 sec)  ATPase get rid of phosphate so ADP + Pi + energy left - Phosphate replaced by Phospho-creatine (PCr) - PCr decreases gradually, so does ATP  exhaustion Energy Systems for Exercise Glycolysis – Anaerobic  Glycolysis does not require oxygen (anaerobic)  ATP – PCr and Glycolysis provide the energy for ~2min of all-out activity  ** Net production of 2 ATP** + H Pyruvate Metabolism Anaerobic  Without oxygen present, pyruvate produced by Glycolysis becomes lactate (lactic acid)  Lactate can be transported by blood to liver and used in gluconeogenesis (produce glucose)  Too much lactate forms lactic acid and lowers the pH impairing enzyme activity The oxidative System  The oxidative system uses oxygen to generate energy  Oxidative production of ATP occurs in mitochondria  Can yield more energy than anaerobic systems  Slow to turn on  Primary method of energy production during endurance events -Rate  Slower but produces much more (38 ATP) Common criteria used to document successful VO2 max Test  Primary Criteria - Plateau in VO2 despite increasing work rate  Plateau in oxygen uptake  Secondary Criteria - HR > 90% of age predicted max - Blood Lactate > or = 8 mmol/L - RPE (ratings of perceived exertions) [BORG scale; 6-20] > or = 17 - RER > or = 1.10 th January 30 Cardiorespiratory System and Metabolism Respiratory Exchange Ratio (RER) ** Measurable** RER = VCO2 Expired/ VCO2 Consumed  Indicates type of substrate being metabolized (0.7 [fat] to 1.0 [carbs]) Respiratory Quotient (RQ) **Theory** What happens during maximal exercise?  RER goes up with exercise due to increased CO2 production relative to oxygen consumption  Related to buffering of lactic acid How do we counteract too much lactic acid?  Bicarbonate (released from kidneys) helps to buffer the acid. What is Tvent?  Ventilatory Threshold: is the point in which the ventilation increases disproportionately to the oxygen uptake Why should I care about Tvent? st February 1 Lecture Cardiorespiratory System and Metabolism (review questions on slide) Cardiorespiratory Fitness Training (FITT) 1.) Frequency of Training  Optimal 3-5 days a week  No benefits < 2 days  Benefits will plateau at 5 days 2.) Intensity of Training  Lower intensity will only increase fitness in individuals who are unfit  Lower intensity = longer duration vs. Higher intensity = shorter duration  Higher intensity prone to injury & over training 3.) Time (duration) of exercise  20-60 minutes of continuous or intermittent (e.g. 10 min bouts) aerobic activity a day  Lower intensity exercise (40-65% VO2 max) should be conducted over longer period of time (> 30 mins) 4.) Type (mode) of training  Any activity that uses large muscle groups, is rhythmic and aerobic in nature, and can be maintained continuously. How much can I improve my VO2 max?  Studies > 5 months - Moderate intensity 3-5 days a week  20-25% Improvement  Substantial inter-individual differences (-5 to 60%) WHY?  We don’t know. - Not related to age, sex, race or initial fitness level. GENES? Effect of Volume and Intensity on Maximal Oxygen Uptake  More you exercise, more VO2 increases as you get older  After training, heart rate increases  means you’ve worked harder February 6 Lecture Cardiorespiratory System Training Endurance Strategies  Carb loading  Fat loading  PCr  Sodium Bicarbonate Inventory of Fuel Supply  Carbohydrates - Muscle glycogen 350g (1400 kcal) - Liver glycogen 60g (240 kcal) - Plasma glucose 10g (40 kcal)  Protein - Whole body (24,000 kcal)  Fat - Muscle 500g (3850 kcal) - Adipose tissue 14kg (107,800 kcal) CHO loading – classic  Do exercise, then slow it down as race time gets close (see graph) - ** problem** Exercise with 0 carbs, get very moody CHO loading – Modified ** Similar results but no grumpiness **  Preferred Carb loading and Performance  No benefit for events less than 90 min  Extra water weight  Bloating Events longer than 90 minutes  Postpone time to fatigue by 20%  Improves time to go a set distance by 2-3% ** Carb loading changes fuel during exercise**  Non carb loaded uses more fat  Loaded carb uses less fat Replenishment of Glycogen  General recommendation - Beginning immediately post exercise (golden hour) - Continue until 500g ingested or a large high-carb meal is consumed - Moderate to high glycemic index CHO are more effect in regenerating glycogen stores than low GI - Glycogen stores replenish at a rate of about 5% to 7% per hour High-fat diet and performance  >30% fat  Many studies use >50% Theory  Use more fat and spare glycogen Acute effects of a high-fat diet  Lower muscle and liver glycogen stores  Lower whole-body CHO oxidation  Increased rating of perceived exertion ** Need to train at high fat diets!!** Which is better? (depends)  Time to exhaustion High Carb  Time trials High Carb = High Fat - Greatest benefit of High carb diet in untrained - High fat diets better tolerated in trained athletes - ** More well trained, the better** Creatine Supplementation  Found in dietary meat  90% stored in skeletal muscle (60% as PCr)  70% of people will increase creatine stores with supplementation (20g/day) **Muscles can hold only certain amount of creatine** **Creatine increases water intake**  gained weight = water  Aid in high intensity activities < 30 secs - Power/strength (5-15%) - Single (1-5%) and repetitive (5-15%) sprint performance - Jumping, cycling, but not running  NO help for endurance events Sodium Bicarbonate Ingestion  Help with buffering acid  0.3-0.5 g/kg/BM  Improve mean power by 2% in high-intensity races  Large variation ** Risk: GI discomfort** Caffeine and Aerobic exercise  Helps with endurance events  Improves endurance time trials 10-15%  May also help with power and resistance training (60-180 sec)  BANNED substance ** 1 cup of coffee, enough for ergogenic aid** Detraining on VO2 max  After you stop training, VO2 max drops severely (lose it in half the time)  Happens faster for elite athletes  SV and Q max also decreases th February 8
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