Aerobic and Anaerobic Adaptations.docx

Aerobic and Anaerobic Adaptations ***5.1: Training and Changes in VO2max*** - VO2max: the measure of the maximal capacity of the body to transport and use oxygen during dynamic exercise using large muscle groups - It is defined by the Fick Equation: VO2max= max cardiac output X a-vO2...

Aerobic and Anaerobic Adaptations ***5.1: Training and Changes in VO2max*** - VO2max: the measure of the maximal capacity of the body to transport and use oxygen during dynamic exercise using large muscle groups - It is defined by the Fick Equation: VO2max= max cardiac output X a-vO2 difference - The primary difference in VO2max between people is stroke volume.   Training to increase VO2max - Training large muscle groups - Working out 3+ times per week, endurance based activity above 50% VO2 max - HIIT can increase VO2max as well.   Responses to increases in VO2max - 15-20% increase in gen pop. - Smaller increases will occur in those with an already high VO2max - Up to 50% increase in those with very very low VO2max - Short duration adaptations are likely due to increases in volume. Long duration responses are changes to stroke volume and a-vO2 differences.   Factors Influencing Stroke Volume - TPR (afterload), contractility and EDV (preload) - EDV is then made up of plasma volume, filling time and venous return, and ventricular volume. - So preload will increase and then afterload will decrease with changes. - There are improvements in a-vO2. there is a decrease in SNS vasoconstriction and there is better blood flow and means that filling time is expanded. This lets the body grab oxygen better due to increases in capillary density and the number of mitochondria.     ***5.2: Training and Changes in Fibre Type and Capillarity*** Fast to slow shift muscle fibre type - Reduction in fast fibres and increases in slow fibres - Magnitude of fibre type change determined by training factors and genetics. - This leads to enhanced diffusion of oxygen and better removal of wastes. - Endurance training is responsible for this shift. - Slow myosin isoforms have lower ATPase activity meaning they can perform more work with less ATP = better efficiency = better mechanical efficiency     ***5.3: Training and Changes in Fuel Utilisation*** Endurance Training Changes - Plasma glucose is the primary fuel for the nervous system. It\'s essential in maintaining base bodily functions and also supplies blood to the brain. - Increased transport of FFA into the muscle. This is due to increased capillary density in the muscle and an increase in fatty binding protein and fatty acid translocase (FAT). - High levels of carnitine palmitoyltransferase (CPT-1) and FAT works together to increase FFA entry into the mitochondria - Mitochondrial oxidation of FFA \> increased enzymes of B oxidation = increased rate of acetyl-CoA formation and high citrate level inhibits PFK and glycolysis. - These endurance trained adaptations means that plasma glucose is spared due to the body\'s adapted ability to use fat for fuel   ***5.4: Detraining following endurance training*** - Rapid decreases in VO2max. Approx 8% lost within 12 days, 20% after 84 days. - The decrease in VO2max as a result of detraining is caused by a decrease in maximal stroke volume and oxygen extraction (the reverse of what happened when we train) - Performance at submaximal intensities also declines quickly when in a state of detraining, due to a decrease in the number of mitochondria in muscle fibres. - Other decreases: max a-vO2 difference, mitochondria, oxidative capacity of muscle, type 2a fibres but an increase in type 2x fibres.   Retraining and VO2 max - Muscle mitochondria adapt quickly to training and will double within the first 5 weeks. - Mitochondrial adaptations lost quickly with detraining, 50% of that is lost in the first week and then the majority is lost within 2 weeks. It would take 3-4 weeks of training to regain what was lost. - Muscle memory is and isn\'t a thing. During retraining, because the mitochondrial developments are there, it means that the muscles will rapidly add the mitochondria when retraining.   ***5.5: Muscle Adaptations to Anaerobic Exercise*** - Anaerobic training intensities are ones done above VO2max and fuelled primarily by the ATP-PC and glycolysis systems. Adaptations from this system are different to that of endurance training. - 10-30 second effort, recruits both type 1 and 2 fibres, exercise lasting less than 10 seconds is fuelled by the ATP-PC system - Exercise that\'s 20-30 seconds, 80% of energy is needed anaerobically and the remaining 20% is aerobic. - Adaptations include: better buffering capacity, hypertrophy of type 2 fibres, elevates enzymes involved in both the ATP-PC system and glycolysis. - HIIT training greater than 30 seconds, promotes mitochondrial biogenesis. - 4 - 10 weeks of anaerobic training can increase the peak anaerobic capacity by 3-25% across individuals.     ***5.6: Training - Muscle and Systemic Physiology*** - Biochemical adaptations to training influence physical responses. Eg: changes to epinephrine/norepinephrine has an impact on HR and ventilation - Peripheral feedback from skeletal muscle to then go to the CNS: training leads to improved muscle homeostasis during exercise and reduced feedback from the muscle chemoreceptors to the CV control centre. Less feedback from the group 3 and 4 fibres of the CV centre means less work is required from the CNS = lower HR, ventilation, etc. - Central control of the physiological response to exercise: endurance exercise training reduces the feed forward output from the higher brain centres to the CV control centre during sub maximal exercise. When exercise adaptations occur there are improvements in muscle fibre oxidative capacity and reduced central command outflow during submax exercise