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ADAPTATIONS RESULTANT INCREASE / DECREASE NET EFFECT RESPIRATORY SYSTEM Respiratory muscles become stronger Increase in active alveoli surface area ADAPTATIONS Increase in: Efficiency of mechanics of breathing Maximum exercise lung volumes (minute ventilation) Maximal breathing rate Respiratory fatigue resistance Increase in: External respiration / diffusion a-VO2 difference (less O2 exhaled = more used) RESULTANT INCREASE / DECREASE Increased VO2 max NET EFFECT CARDIO-VASCULAR SYSTEM: HEART Hypertrophy Increase in: volume EDV (filling capacity) ventricular stretch and recoil force of ventricular contraction stroke volume (SV) HR recovery after exercise Decrease in: Resting HR (bradycardia) Increased blood flow Increased maximal cardiac output Increased O2 transport ADAPTATIONS RESULTANT INCREASE / DECREASE NET EFFECT VASCULAR SYSTEM Increased elasticity of arterial walls Increased number of RBC’s and increased plasma volume Increased capillarisation of alveoli and Type 1 muscle fibre tissues Increase in: Vascular shunt efficiency, to redistribute blood from organs to active muscles BP regulation Increase in: Gaseous exchange / O2 transport Venous return Stroke volume and cardiac output Increase in: Surface area a-VO2 difference speed for diffusion removal of CO2 and LA during OBLA Increased circulatory efficiency Improved O2 and CO2 transport ADAPTATIONS RESULTANT INCREASE / DECREASE NET EFFECT MUSCULO-SKELETAL SYSTEM Increased Type 1 and 2a hypertrophy / efficiency Increased muscle capillarisation Increased Type 2a fibre ability to work aerobically Increased myoglobin stores Increased aerobic enzymes Increased number of mitochondria Decrease in: energy costs Increase in: O2 and CO2 transport / diffusion Increase in: Fibre type percentage working aerobically Increase in: O2 storage and transport to mitochondria Improved: Reliance on metabolism of FAT instead of glycogen Improved: Utilisation of O2 Increased maximal capacity of muscle fibres to generate ATP aerobically