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Transcript of The Physiology of Training Effect on VO 2max, Performance, Homeostasis, and Strength Powers, Chapter...
The Physiology of Training
Effect on VO2max, Performance, Homeostasis, and Strength
Powers, Chapter 13
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
Endurance Training and VO2max
• Training to increase VO2max
– Large muscle groups, dynamic activity– 20-60 min, 3-5 times/week, 50-85% VO2max
• Expected increases in VO2max
– 15% (average) - 40% (strenuous or prolonged training)
– Greater increase in highly deconditioned or diseased subjects
• Genetic predisposition – Accounts for 40%-66% VO2max
Calculation of VO2max
• Product of maximal cardiac output (Q) and arteriovenous difference (a-vO2)
• Improvements in VO2max – 50% due to SV
– 50% due to a-vO2
• Differences in VO2max in normal subjects
– Due to differences in SVmax
VO2max = HRmax x SVmax x (a-vO2)max
Stroke Volume and Increased VO2max
• Increased SVmax
– 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
6Figure 12-11
Factors Increasing Stroke Volume
a-vO2 Difference and Increased VO2max
• Improved ability of the muscle to extract oxygen from the blood– Muscle blood flow– Capillary density– Mitochondial number
• Increased a-vO2 difference accounts for 50% of increased VO2max
Summary of Factors Causing Increased VO2max
Detraining and VO2max
• Decrease in VO2max with cessation of training– SVmax , maximal
a-vO2 difference
• Opposite of training effect
Endurance Training: Effects on Performance
• Improved performance following endurance training
• Structural and biochemical changes in muscle– Mitochondrial number, Enzyme activity– Capillary density
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
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
Time-course of Training/Detraining Mitochondrial Changes
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)
Changes in CS Activity Due to Different Training Programs
Influence of Mitochondrial Number on ADP Concentration and VO2
• [ADP] stimulates mitochondrial ATP production
• Increased mitochondrial number following training– Lower [ADP] needed to
increase ATP production and VO2
Biochemical Adaptations and Oxygen Deficit
• Oxygen deficit is lower following training– Same VO2 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
Endurance Training Reduces the O2 Deficit at the Onset of Work
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
Biochemical Changes, FFA Oxidation, and Glucose-Sparing
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 + NADH lactate + NADLDH
Mitochondrial and Biochemical Adaptations and Blood pH
Biochemical Adaptations and Lactate Removal
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
Link Between Muscle and Systemic Physiology: One Leg Training Study
Peripheral Control of Cardiorespiratory Responses to Exercise
Central Control of Cardiorespiratory Responses to Exercise
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
Neural and Muscular Adaptations to Resistance Training