UNIT 4 ENHANCING PHYSICAL PERFORMANCE AOS 2 STRATEGIES FOR ENHANCING PHYSICAL PERFORMANCE
CH 11 TRAINING ADAPTATIONS
There are 2 types of Physiological responses to exercise:
1. Immediate short-term responses (acute responses) – last for the duration of the exercise and a short time afterwards. 2. Long-term responses (chronic adaptations) – the body adapts over time to an exercise program. Known as the training effect and will last until training ceases. Upon cessation, de-training (reversibility) will occur- revert back to pre- conditioned state. CHRONIC TRAINING ADAPTATIONS These depend on: The type of training undertaken. o Aerobic training – 6-12 weeks at systems and tissue level. The frequency, duration and intensity of the training. The individual’s capacity and hereditary factors.
SAID principle- Specific, Adaptation, Imposed, Demands “the particular activity we are involved in ill encourage our bodies to adapt in specific ways to meet that activity’s specific demands. Adaptation- long term physiological change in response to training loads that allows the body to meet new demands.
CHRONIC ADAPTATIONS TO AEROBIC/ENDURANCE TRAINING
A). CARDIOVASCULAR ADAPTATIONS to aerobic training -designed to bring about more efficient delivery of o2 to the working muscle. CV adaptations are good b/c they the risk of developing CV disease and other health related issues. -best developed through continuous, Fartlek and longer interval type training. Adaptations include: 1.Cardiac Hypertrophy; like skeletal muscle the heart will hypertrophy if exercised (enlarge). Left ventricle chamber will enlarge in volume and thus significantly SV. Aerobic. 2. capillarisation of heart; develops an increased coronary blood supply. 3. SV; Increased capillarisation, size and strength of the heart lead to an increased SV = a greater volume of blood is pumped out per beat. untrained athlete Trained athlete Rest SV= 70-80ml/beat Rest SV= 100ml/beat Max levels: SV = 110 ml/beat Max levels SV= 130ml/beat 4. Resting HR due to an increase in stroke volume the heart does not have to beat as frequently to supply the required blood flow. Rest 5l/min. Q = SV x HR (consider example p 268).
5. HR at Sub max levels due to the increased SV. Fig 11.8 p 267. more efficient heart
6.Improved HR recovery rates return to pre exercise levels earlier.
7. Q at Max workload; this is a result to the increase in SV and HR response to training. Fig 11.8 p 267 (more efficient heart)
8. Blood Pressure; aerobic exercise may lower BP and will prevent the development of high BP. Reduces the resistance of blood flow reducing the strain on the heart.
9. A-VO2 Diff’; better ability to absorb O2 from the bloodstream, lower concentration of O2 in venous blood. Ability to use more O2, due to myoglobin stores and number and size of mitochondria. 10. Blood Volume and Haemoglobin levels; up to 25% in blood volume, as a result RBC’s may increase and the haemoglobin content the O2 carrying capacity of the blood.
11. Capillarisation of the skeletal muscles; Capillaries supplying muscle fibre 5.9 trained / 4.4 untrained.
12. Changes to Cholesterol, Triglycerides, LDL and HDL Cholesterol, triglycerides and LDL. HDL
Complete Coursework 11.1 p 267 SUMMARY CV adaptations:
B) RESPIRATORY ADAPTATIONS to aerobic training 1. lung ventilation because of tidal volume and respiratory frequency. Pulmonary diffusion is also enhanced. 2. maximum oxygen uptake VO2max is increased due to Q, RBC numbers, a-VO2diff and in muscle capillarisation and a greater O2 extraction by muscles. Refer Fig 11.9 p 267 3.a higher lactate inflection point is developed:
C) MUSCLE TISSUE ADAPTATIONS to aerobic training
1. oxygen utilisation enhances the body’s ability to attract O2 into the muscle cells and then utilise it in ATP production via: in size and number of mitochondria. myoglobin stores.
2. muscular fuel stores storage of muscle glycogen, FFA and triglycerides and oxidative enzymes.
3. oxidation of glucose and fats metabolise these fuels more efficiently ‘glycogen sparing’. This can take place b/c oxidation of fats (due to storage of trig and FFA and more fat metabolising enzymes. A trained athlete relies less on glycogen as a fuel source- glycogen stores are not used as early in an exercise bout, delaying time to exhaustion due to glycogen depletion.
4. utilisation of the anaerobic glycolysis (lactic acid) system less reliance on anaerobic glycolysis to produce energy for ATP resynthesis until higher work intensity is reached. Enhanced capacity to the muscles to aerobically metabolise glucose and fats. This means that you work at higher intensities without exceeding LIP.
Muscle fibre type adaptations. Muscle fibres can be either: 1. Type 1 ST, 2.Type 2A FT oxidative OR 3. Type 2B FT glycolytic. Some research suggests that Type 2B FT glycolytic fibres can change towards Type 2 A oxidative with chronic endurance training. COMPLETE ACTIVITY 2 p 255 (LIU) CHRONIC ADAPTATIONS TO ANAEROBIC TRAINING
These adaptations are best developed through sprint training, short and fast interval training, plyometric, circuit and resistance training.
Adaptations include:
1. Muscle hypertrophy significant enlargement of muscle fibres (Type 2B FTF). cross sectional size of the muscle = strength. This is a result of size and number of myofibrils per muscle fibre and amounts of filaments. 2. muscular stores of ATP and PC and enzymes required to breakdown and resynthesise ATP due to muscle hypertrophy and results in an capacity of the ATP PC system = greater energy release and ATP restoration.
3. glycolytic capacity enhanced muscular storage of glycogen, thus LA system is also enhanced.
4. Cardiac hypertrophy in the thickness of the ventricular walls. There is no change in SV, just a more forceful contraction.
5. Other anaerobic training adaptations strength and size of connective tissues. motor unit recruitment = max contractions. nerve impulses. speed of contraction.
HANDOUT table 8.1 p 262/3 LIU Table 8.1 p 262/3