PHYL2730

PHYL2730

Fuel Production / Metabolism
1. Fats
  1. Fatty Acids
    1. Lipolysis
    2. Lipogenesis
2. Carbs
  1. Glucose
    1. Glycogenolysis (Glycogen stores to Glucose Pools)
    2. Glycogenesis (Glucose pools to Glycogen stores
    3. Gluconeogenesis
      1. During prolonged exercise- Liver producing glucose through the use of amino acids
    4. Stored in: Liver, Muscle (more in muscle than liver) and Body fluids (Narrow limits due to high reactivity)
3. Proteins
  1. Amino acids
Energy
1. Energy Balance
  1. Energy in (food) = Energy out (Work) + Energy out (heat) ± Energy stored (fat)
    1. Energy out (heat) = 60 - 70%
      1. Heat causes cardiovascular stress
2. Energy Systems
  1. Aerobic
    1. Substrates include: Glucose, Glycogen, Fat (Mainly), Amino Acids
      1. Fat needs to be burnt in oxygen
      2. Glycogen can be used anaerobically and aerobically
    2. The Oxidative System: Aerobic ATP production, Oxidative Phosporylation
      1. Oxidation of Fat: Breakdown of fat - Lipolysis
        FFA transported in the blood
        FFA activation (attached to CoA) - need ATP
        Beta Oxidation - converting fatty acids to Acetyl CoA
        Krebs Cycle
        Complete the oxidation of CHO, fats and proteins using NAD and FAD as hydrogen carriers
        Hydrogens removed for ETC
        ETC
        Citrate Synthase and Succinate Dehydrogenase are more active in endurance athletes
        Peripheral adaptations to training - in specific muscles trained
  2. Anaerobic
    1. Immediate Energy Source: ATP/ Pcr
      1. ATP
        ATP resting conc. doesn't change
        Rate of ATP resynthesis contributes to fatigue - Training improves rate
        Small amount of ATP maintained to avoid 0 ATP for energy pumps
      2. CP
        CP can be supplemented
        50% of people can supplement - good for resistance or high intensity exercise
        CP doesn't resynthesis until rest or low intensity exercise (Active recovery) - Aerobic process
        Used to maintain muscle ATP levels
    2. Non Oxidative Energy Source: The Glycolytic System
      1. Glycogenolysis
        Substrate: Glycogen
        Occurs in the cytosol/cytoplasm of the muscle cell
        Process involves series of enzymatically catalysed coupled reactions
      2. Glycolysis
        Breakdown of glucose to form Pyruvic acid + 2 ATP and Lactic Acid
        Lactic Acid
        Anaerobic Threshold
        Ventilation Threshold
        OPLA
        OBLA (Onset of Blood Lactate Accumulation)
        Lactate inflection point at 4mmol - Historically relevant
        Lactate Threshold
        Coincidence that ventilation threshold and lactate threshold match up
        Sped up by mass action
        Defined as; Production = Removal
        Highest sustainable work rate
        Accumulates first in muscle, then in blood
        Oxygen required for removal
        Reconverted to pyruvate → enters the TCA cycle → broken down into CO2 and Water
        Pyruvate
        Low intensity exercise
        Converted to Acetyl CoA → Mitochondria → Krebs Cycle
        High intensity exercise
        Large amount of pyruvate converted to lactic acid
3. Use of Energy Sources
  1. Rest: Primarily Fat
  2. Light - Moderate: High Fat use
  3. High Intensity (Sprint): 95% Glycogen contribution
  4. High Intensity (Endurance): Mainly glycogen but a small contribution of fat if oxygen is present
Muscle Fibre Type
1. Type 1 - Oxidative (Red Fibres)
  1. Aerobic Capacity
    1. Redness from Myoglobin
  2. Small Diameter
    1. Low force generation
    2. Small Mitochondria
      1. Only location where aerobic metabolism can occur
2. Type 2a - Fast Oxidative Glycolytic
  1. Endurance Training increases amount of these fibres
3. Type 2b - Fast Glycolytic
  1. Large diameter
  2. Fast to contract - Fatigue quickly
    1. Rely on anaerobic glycolysis - therefore accumulate lactic acid
  3. Sprint training doesn't allow the change from Type 2a → Type 2b due to limited recovery time
4. Recruitment Order: Type 1 → Type 2a → Type 2b
Oxygen Consumption
1. Fick Principle
  1. Product of Cardiac Output x (a-v) O2 diff
    1. (a-v)O2 diff → How much O2 a muscle has used (O2 going in - O2 leaving muscle
2. VO2 Max
  1. Test of central adaptation
    1. High VO2 = reduced risk of CVD
  2. EPO - Blood doping
    1. Death due to increased viscosity
  3. Decrease with age due to Max HR
3. RER - Respiratory Exchange Ratio
  1. CO2 produced and O2 Consumed
    1. Starts from 0.7 - 1.0
      1. At 1.0 (VO2 Max) Carbs are exclusively being burnt
      2. At rest 0.7 Fats are primarily being burnt
      3. 0.7 - 1.0 mixture of substrates being burnt
4. EPOC: Excess Post exercise Oxygen Consumption
  1. Excess caused by adrenaline circulating → driving up metabolic rate - removal of lactic acid
Responses to Training
1. Resting
  1. Increased Capillarisation
    1. Greater increase in Type 1 fibres - Aerobic metabolism
      1. Increased (a-v)O2 diff
  2. Increased Mitochondrial Density
    1. More efficient O2 use
  3. Decreased Heart Rate
  4. Increased Stroke Volume
  5. Glycogen super compensation. After exercise more receptive to taking up glucose due to enzyme - Glycogen-Synthase
  6. Increased blood volume
    1. Increased Plasma volume
      1. Decreased viscosity
        Prolonged period before heart stress
      2. Buffer against dehydration
      3. Dilutes catecholamine response - less mass action effect
        Delayed recruitment
  7. Increased RBC number
2. Exercising
  1. Adaptations
    1. Central
      1. VO2 Max
        Measure of endurance capacity
        Not a good predictor of performance - Plateaus as performance increases
    2. Peripheral
      1. Trained muscle has less blood submaximally, more blood maximally
        Less disruption to blood flow (submaximally)
      2. More effective O2 uptake
      3. Enzyme activity
        Less stress response (Less catecholamines)
        Increased heart filling time
        Increased SV
      4. Mitochondria measure of endurance capacity
        More closely related to performance
  2. Endurance training
    1. Capable of greater fat use
      1. Delayed stress response
        Delayed recruitment of Type 2b fibres
Cardiovascular System
1. Cardiovascular Disease
  1. Cholesterol
    1. LDL
      1. Prone to oxidation
        Leads to plaque build up (atherosclerosis)
      2. Increased by saturated fat consumption
    2. HDL
      1. Higher amount = low risk coronary heart disease
        High HDL has protective effect
        Removes cholesterol for disposal
        Exercise increases HDL conc
        Aerobic and endurance training increases HDL conc
        Resistance training seen to reduce total cholesterol
    3. Dietary prevention is fresh fruit and vege
  2. Triad
    1. Cerebrovascular Disease
      1. Haemorrhagic Stroke
        Bleeding in the brain
      2. Ischaemic stroke/ Cerebral Infarction (brain attack)
        Blockage of blood supply leading to death of that part of the brain
      3. Hypertension increases risk of stroke
        Risk can be reduced by exercise and changes in lifestyle factors
    2. Coronary Heart Disease
      1. Angina Pectoris
        Symptom of impaired oxygen to the heart - partial occulsion of blood and oxygen
      2. Myocardial Infarction
        Complete blockage leading to death of the heart (heart attack)
    3. Peripheral vascular Disease
      1. Peripheral Artery Disease
        Potential blockage of arteries of the lower limb - "Angina" of the lower limb
        Stiffness and pain during exercise - due to inability to supply O2 demand of lower limb muscles
        Management includes exercise, stop smoking, control of diabetes and hypertension
  3. Highly influenced by lifestyle factors
    1. Metabolic Syndrome: Collective group of risk factors - obesity, high blood pressure, diabetes, high cholesterol
      1. All these risk factors can be lowered by exercise
  4. RRP = HR x SBP
    1. Rate Pressure Product
      1. Estimate of how hard the heart is working
2. Cardiovascular Drift
  1. Increased heat = Increased stress response = Increased catecholamines
    1. Increased HR
  2. Q = increased HR x decreased SV
    1. Decreased blood volume due to decreased water = decreased venous return = increased heart rate = decreased SV
      1. Associated with increased temperature, increased hormone conc. and dehydration
        Intake of fluid or glucose intake can dampen effect
3. Cardiac Output
  1. Q = HR x SV
    1. Stroke Volume
      1. Frank Starling Mechanism
        The greater the distension (stretch), the greater the subsequent contraction
      2. Preload (amount of blood in the left ventricle) - increases the stretch
        The greater the pre-stretch, greater the force of contraction
    2. Heart Rate
      1. Declines with age
      2. 208 - (0.7 x age)
      3. Highly reproducible
      4. Strongly effected by sympathetic and parasympathetic activity
4. Main functions
  1. Deliver O2, nutrients
    1. Glucose, FFA... Substrates
  2. Remove CO2 and other metabolic end products
    1. Lactate, H ions
      1. Lactic acid → used as a fuel in other parts of the body
  3. Transports hormones and other molecules
  4. Temperature balance and fluid regulation
  5. Acid - Base balance (resting blood pH 7.4)
    1. Lactic acid accumulation = acidosis
  6. Immune Function
Endocrine Responses
1. Glucose / Insulin Response to Exercise
  1. High glucose and insulin conc. have an inflammatory response in blood vessels → Micro damage
    1. Spikes/ micro damage can be reduced by a low GI, high fibre diet
  2. Exercise provides glycaemic control
    1. Non insulin dependent glucose uptake
      1. Process of contraction → muscle permeability to glucose → GLUT4 receptors; Glucose uptake in absence of insulin
2. Insulin Antagonists
  1. Growth Hormone
  2. Cortisol
  3. Catecholamines (Noradrenaline/ Adrenaline
    1. Mass Action
      1. Occurs when rate of glycolysis is greater than the rate of the TCA cycle
        When out of sync the pyruvate is converted to lactic acid instead of going through the electron transport chain
        Lactic acid can still be produced in the presence of O2 due to the fast rate of the glycolytic pathway (out of sync)
      2. Seen in altitude training
      3. Can access glycogen of non exercising muscles
        Cori Cycle
        Blood Lactate → liver → Glyconeogenesis → Liver releases glucose into the blood
        Doesn't occur at a high enough rate to be sustainable
    2. Can cause vasoconstriction in some areas leading to increased lactate accumulation
    3. McArdles Paitents get catecholamine response but no mass action
    4. Curve similar to lactate threshold
  4. Glucagon
3. Types of Hormones
  1. Steroid
    1. Can enter the cell directly
      1. Lipid soluble
  2. Non Steroid
    1. Can't enter the cell; require second messenger

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	Created by suneater over 10 years ago