Professional Documents
Culture Documents
KEY KNOWLEDGE: Chronic adaptations of the cardiovascular, respiratory and muscular systems to training. KEY SKILLS: Explain how chronic adaptations to the cardiovascular, respiratory and muscular systems lead to improved performance.
TRAINING METHODS plyometrics, resistance, interval, circuit, sprint, continuous, fartlek, flexibility
ADAPTATION a long-term physiological change in response to training that allows new demands to be met PLATEAU commonly occurs when the body adjusts to new loads and maintenance of existing conditions prevails HYPERTROPHY an increase in cell size that usually leads to increased tissue size as well
Principle of Adaptation
Training should be; Specific to their sport Specific to the desired outcome as a result of adaptations. Adaptations occur as a result of physical training principles. Stress on the body causes adaptations. A plateau occurs when the training load is not sufficient to cause stress. Aerobic and anaerobic training methods create different physiological adaptations.
Adaptations
These changes or adaptations in the body is specific to the training method/s applied Adaptation = a long-term physiological change in response to training loads that allows the body to meet new demands. If training load is insufficient to stress the body, no adaptations occur and a plateau will occur. Athletes train to adapt their bodies to a particular sport/activity.
Types of Adaptations
Adaptations can be classified as acute and chronic; Acute Immediate physiological response to exercise which last the duration of the exercise session. Type of training not important. Chronic Long-term adaptations to exercise.
Tidal volume
Oxidative enzymes
Ventilatory efficiency
Contractile proteins
Aerobic capacity
Triglyceride stores
CARDIOVASCULAR ADAPTATIONS
Changes that occur to the structure and function of the heart, blood vessels and the blood THE HEART (INCREASED LEFT VENTRICLE SIZE & VOLUME) The heart is a muscle, and like any other muscle, will become bigger and stronger due to training. The nature and degree of change is dependent upon the type of training. Aerobic training results in HYPERTROPHY (increase in size) of the heart specifically the LEFT VENTRICLE due to:
1. Increase size of the left ventricular cavity 2. Thickening of the left ventricular wall
UNTRAINED HEART
TRAINED HEART
Cardiac changes to VENTRICLE SIZE and THICKNESS resulting from different training regimes
Reference Aerobic training increases subject ventricle size and (no training effect) small increase to wall thickness
CORONARY ARTERIES
Note the extensive capillarisation about the two coronary arteries after a long term AEROBIC training program
A corresponding increase of haemoglobin* levels thus increasing the capacity to carry greater amounts of O2 to working muscles. More blood, greater SV More blood greater capacity to remove heat from the body
DECREASED BLOOD CHOLESTEROL, TRIGLYCERIDES AND LOW AND DENSITY LIPOPROTEINS Regular aerobic training may result in reduced blood cholesterol levels (triglycerides and low density lipoproteins* LDL), but may also result in increases in high density lipoproteins*HDL. BOTH training effects thought to reduce the chance of developing coronary heart disease.
Blood Pressure
Systolic Blood Pressure Pressure on the arteries following contraction of ventricles as blood is pumped out of the heart
Diastolic Blood Pressure Pressure in the arteries when the heart relaxes and ventricles fill with blood
The greatest changes occur with the systolic pressure. This is a direct result of: 1. Improved capillarisation 2.Improved elasticity of blood vessels 3.ed HDLs (high-density lipoproteins, breaking down fatty deposits/plaque built on inside of arterial walls)
People with high Blood pressure place a high stress on the cardiovascular system
Blood Vessels
capillary density to heart muscle blood flow (20%) away from organs to working muscles capillary density at muscles, mainly S/Twitch fibres
Blood
blood volume plasma levels red blood cell (RBC) count Haemoglobin blood pressure (rest & sub-max)
Typical metabolic and physiological values for healthy trained and untrained men
Variable Glycogen (nM) Mitochondria Volume (% muscle cell)
Resting ATP (mM) Resting PC (mM) Aerobic enzymesSuccinate dehydrogenase (mM) Max lactate (mM) Max stroke volume (mL) Max cardiac output (L/min) Resting heart rate (bpm) VO2 max (mL/kg/min) Blood volume (L)
Trained 120 8
6 18 15-20 150 180 30-40 40 65-80 6
% difference 41 272
100 64 133 36 50 75 -43 107 28
Aerobic training adaptations include increased capacities to use fat during exercise in preference to carbohydrate (glycogen sparing)
Energy from Carbohydrate (kcal) Before training
CARDIOVASCULAR ADAPTATIONS RESULTING FROM AEROBIC TRAINING, WHICH BRING ABOUT IMPROVED OXYGEN DELIVERY TO WORKING MUSCLES
Plasma volume
Ventricle size
Total blood volume Venous return Myocardial contractility Maximum stroke volume Maximum cardiac output
Haemoglobin
O2 O2
O2
Comparative average cardiac dimensions in normal subjects, college athletes and world-class athletes
Variable Normals College College swimmers runners Worldclass runners College wrestlers Worldclass shot putters
Left ventricle volume (mL) Stroke volume (mL) Left ventricle wall thickness (mm) Left ventricle mass (g)
CHRONIC RESPIRATORY ADAPTATIONS AS A RESULT OF AEROBIC TRAINING Aerobic Training vs. Respiratory Adaptations
lung / vital capacity: the volume of air that can be forcefully expired after maximum inspiration. Total lung capacity: The amount of air inside the lungs after a maximal inspiration tidal volume: the amount of air breathed in or out of the lungs per breath Alveolar capillirisation more capillares surrounding alveoli pulmonary diffusion: the amount of O2 and CO2 which moves between the capillaries and the alveoli (increases due to increased capilliarisation surrounding alveoli) ventilation (max intensity) primarily as a result of improved TV) ventilatory efficiency (the ease of O2 extraction of muscles responsible for breathing/once again a direct link to increases in capillirisation). ventilation (rest & sub-max) oxygen cost to ventilatory muscles (intercostals & diaphragm)
CHRONIC MUSCULAR ADAPTATIONS AS A RESULT OF AEROBIC TRAINING Aerobic Training vs. Muscular Adaptations
Aerobic training will bring about most specific and significant adaptations to slow
The increased arteriovenous oxygen difference results from: more blood being pumped to active muscles (especially slowtwitch fibres) muscle fibres being better able to extract transported oxygen as a results of increased mitochondria, more oxidative enzymes and increased myoglobin
More blood being pumped to active muscles (especially slow-twitch) Muscle fibres better at extracting and processing oxygen as a result of ed
Aerobic (Muscular)
Increased myoglobin stores. Increased muscular fuel stores ie.Glycogen, fatty acids, triglycerides and oxidative enzymes. Increased capillary density to slow twitch fibres. Increased use of fat at submaximal levels. Increased oxygen utilisation Increased size and number and density of mitochondria Increased stores and use of intramuscular triglycerides. Increased oxidation of glucose and fats Ability to metabolise and extract energy has improved. The body can therefore use glycogen sparing. Decreased use of lactic acid system Some muscle fibre adaptation.
Rapid aerobic training adaptations during initial stages of VO2 max, followed by smaller increases and plateaus over a two-year period
Elite
Months of training
Heart rate and oxygen consumption for endurancetrained athletes and sedentary college-aged students before and after 55 days of aerobic training
Sedentary college students Sedentary college students after 55 days of aerobic training
During exercise, more blood is sent to working muscles and less to other organs
Other organs
Aerobic training contributes to improved oxygen extraction from blood and increased a-VO2 diff.
Trained
Untrained
Components of the oxygen transport system at rest and during maximal exercise for trained and untrained subjects and endurance athletes
Condition
1 Untrained Rest
VO2 (mL/L)
Heart-rate (beats/min)
300
0.075
82
48.8
Maximal exercise
2 Trained Rest Maximal exercise 3 Endurance athlete Rest Maximal exercise
3100
300 3440 302 5570
0.112
0.105 0.126 0.122 0.189
200
58 192 50 190
138.0
49.3 140.5 49.5 155.0
Generalised potential increases in anaerobic energy metabolism of skeletal muscle with heavy training
100 90 80 70 60 50 40 30 20 10 0 Anaerobic enzymes PCr ATP Glycolytic capacity Glycogen
Anaerobic (Muscular)
Muscular Hypertrophy Enlargement of the fast twitch muscle fibres Increased muscular stores of ATP, PC, creatine and glycogen. Increased ATP-PC splitting and resynthesis of enzymes Increased glycolytic capacity Enhances lactic acid systems ability to use glycogen. Cardiac hypertrophy Increases contraction forces exerted by the left ventricle in the heart. Increased contractile proteins in muscles.
Increased myosin ATPase Molecule responsible for splitting ATP into ADP Increased muscle buffering capacity Muscles able to tolerate higher levels of fatiguing products Muscle hyperplasia Research in animals suggest that new muscle fibres may form under stress. Other Increase in strength of connective tissue, number of motor units, speed on nerve impulses and muscular contraction speed.
Fast-twitch
Type 11B Purely anaerobic white low low high low low high high high
Fast-twitch
Type 11A Partially aerobic White/red medium medium high medium medium Medium/low high Medium/low
Slow-twitch
Type 1 aerobic red high High Low High High low Low Low
Triglyceride stores
Fibre diameter Contraction speed
low
large high
Medium/low
intermediate moderate
High
Small slow
Force capacity
Fatigue resistance
high
low
intermediate
Medium/low
Low
high
Changes in physiological and metabolic functions with various durations of detraining in primarily aerobic trained athletes (averages in reported literature) Variable Short term (< three weeks of detraining) % decrease 20 8 9 17 Longer term ( 3 to 12 weeks of detraining) % decrease 35 20 25 29
VO2 max (mL/kg/min) Cardiac output (L/min) Stroke volume (mL) Capillary density (cap/mm)
Glycogen (mM)
Phosphocreatine (mM) Oxidative enzyme capacity Lactate threshold Muscle glycogen synthesis
24
15 29 7 29
50
27 32 18 40