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The Physiology of Training Effect on VO 2max, Performance, Homeostasis, and Strength Powers, Chapter 13.

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Presentation on theme: "The Physiology of Training Effect on VO 2max, Performance, Homeostasis, and Strength Powers, Chapter 13."— Presentation transcript:

1 The Physiology of Training Effect on VO 2max, Performance, Homeostasis, and Strength Powers, Chapter 13

2 Principles of Training Overload 足夠的負荷 – Training effect occurs when a system is exercised at a level beyond which it is normally accustomed Specificity 專一性 – Training effect is specific to the muscle fibers involved – Type of exercise Reversibility 回復性 – Gains are lost when overload is removed

3 Endurance Training and VO 2max Training to increase VO 2max – Large muscle groups, dynamic activity – 20-60 min, 3-5 times/week, 50-85% VO 2max Expected increases in VO 2max – 15% (average) - 40% (strenuous or prolonged training) – Greater increase in highly deconditioned or diseased subjects Genetic predisposition – Accounts for 40%-66% VO 2max

4 Calculation of VO 2max Product of maximal cardiac output (Q) and arteriovenous difference (a-vO 2 ) Improvements in VO 2max – 50% due to  SV – 50% due to  a-vO 2 Differences in VO 2max in normal subjects – Due to differences in SV max VO 2max = HR max x SV max x (a-vO 2 ) max

5 Stroke Volume and Increased VO 2max Increased SV max –  Preload (EDV, end diastolic volume)  Plasma volume  Venous return  Ventricular volume –  Afterload (TPR, total peripheral resistance)  Arterial constriction  Maximal muscle blood flow with no change in mean arterial pressure –  Contractility 收縮能力

6 6 Figure 12-11

7 Factors Increasing Stroke Volume

8 a-vO 2 Difference and Increased VO 2max Improved ability of the muscle to extract oxygen from the blood –  Muscle blood flow –  Capillary density –  Mitochondial number Increased a-vO 2 difference accounts for 50% of increased VO 2max

9 Summary of Factors Causing Increased VO 2max

10 Detraining and VO 2max Decrease in VO 2max with cessation of training –  SV max,  maximal a-vO 2 difference Opposite of training effect

11 Endurance Training: Effects on Performance Improved performance following endurance training Structural and biochemical changes in muscle –  Mitochondrial number,  Enzyme activity –  Capillary density

12 Structural and Biochemical Adaptations to Endurance Training  Mitochondrial number   Oxidative enzymes – Krebs cycle (citrate synthase) – Fatty acid (  -oxidation) cycle – Electron transport chain  NADH shuttling system Change in type of LDH Adaptations quickly lost with detraining

13 Detraining: Time Course of Changes in Mitochondrial Number About 50% of the increase in mitochondrial content was lost after one week of detraining All of the adaptations were lost after five weeks of detraining It took four weeks of retraining to regain the adaptations lost in the first week of detraining

14 Time-course of Training/Detraining Mitochondrial Changes

15 Effect of Exercise Intensity and Duration on Mitochondrial Enzymes Citrate synthase (CS) – Marker of mitochondrial oxidative capacity Light to moderate exercise training – Increased CS in high oxidative fibers (Type I and IIa) Strenuous exercise training – Increased CS in low oxidative fibers (Type IIb)

16 Changes in CS Activity Due to Different Training Programs

17 Influence of Mitochondrial Number on ADP Concentration and VO 2 [ADP] stimulates mitochondrial ATP production Increased mitochondrial number following training – Lower [ADP] needed to increase ATP production and VO 2

18 Biochemical Adaptations and Oxygen Deficit Oxygen deficit is lower following training – Same VO 2 at lower [ADP] – Energy requirement can be met by oxidative ATP production at the onset of exercise Results in less lactic acid formation and less PC depletion

19 Endurance Training Reduces the O 2 Deficit at the Onset of Work

20 Biochemical Changes and FFA Oxidation Increased mitochondrial number and capillary density – Increased capacity to transport FFA from plasma to cytoplasm to mitochondria Increased enzymes of  -oxidation – Increased rate of acetyl CoA formation Increased FFA oxidation – Spares muscle glycogen and blood glucose

21 Biochemical Changes, FFA Oxidation, and Glucose-Sparing

22 Blood Lactate Concentration Balance between lactate production and removal Lactate production during exercise – NADH, pyruvate, and LDH in the cytoplasm Blood pH affected by blood lactate concentration pyruvate + NADHlactate + NAD LDH

23 Mitochondrial and Biochemical Adaptations and Blood pH

24 Biochemical Adaptations and Lactate Removal

25 Links Between Muscle and Systemic Physiology Biochemical adaptations to training influence the physiological response to exercise – Sympathetic nervous system (  E/NE) – Cardiorespiratory system (  HR,  ventilation) Due to: – Reduction in “feedback” from muscle chemoreceptors – Reduced number of motor units recruited Demonstrated in one leg training studies

26 Link Between Muscle and Systemic Physiology: One Leg Training Study

27 Peripheral Control of Cardiorespiratory Responses to Exercise

28 Central Control of Cardiorespiratory Responses to Exercise

29 Physiological Effects of Strength Training Strength training results in increased muscle size and strength Neural factors – Increased ability to activate motor units – Strength gains in initial 8-20 weeks Muscular enlargement – Mainly due enlargement of fibers (hypertrophy) – Long-term strength training

30 Neural and Muscular Adaptations to Resistance Training


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