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 Presentation

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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

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