the physiology of training
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Powers, Chapter 13. The Physiology of Training. Effect on VO 2max , Performance, Homeostasis, and Strength. 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 - PowerPoint PPT PresentationTRANSCRIPT
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