Chapter 13: The Physiology of Training Effect on VO2 MAX, Performance, Homeostasis and Strength EXERCISE PHYSIOLOGY Theory and Application to Fitness and Performance, 5th edition Scott K. Powers & Edward T. Howley Presentation revised and updated by TK Koesterer, Ph.D., ATC Humboldt State University

Objectives Explain the basic principles of training: overload and specificity Contrast cross-sectional with longitudinal research studies Indicate the typical change in VO2 MAX with endurance training programs, and the effect of the initial (pretraining) value on the magnitude of the increase State the VO2 MAX values for various sedentary, active and athletic populations State the formula VO2 MAX using HR, SV and a-v O2 difference; indicate which of the variables is most important in explaining the wide range of VO2 MAX values in the population

Objectives Discuss, using the variables identified in objective 5, how the increase in VO2 MAX comes about for the sedentary subject who participates in an endurance training program Define preload, afterload, and contractility, and discuss the role of each in the increase in the maximal SV that occurs with endurance training Describe the changes in muscle structure that are responsible for the increase in the maximal a-v O2 difference with endurance training Describe the underlying causes for the decrease in VO2 MAX that occurs with cessation of endurance training

Objectives Describe how the capillary and mitochondrial changes that occur in muscle as a result of an endurance training program are related to the following: a lower O2 deficit, and increased utilization of FFA and a sparing of blood glucose and muscle glycogen, a reduction in lactate and H+ formation, and an increase in lactate removal Discuss how changes in “central command” and “peripheral feedback” following an endurance training program can lower the HR, ventilation, and catecholamine responses to a submaximal exercise bout Contrast the role of neural adaptation with hypertorphy in the increase in strength that occurs with resistance training

Exercise A Challenge to Homeostasis Fig 13.1

Principles of Training Overload Training effect occurs when a system is exercised at a level beyond which it is normally accustomed Specificity Training effect is specific to the muscle fibers involved Type of exercise Reversibility Gains are lost when overload is removed

Research Designs to Study Training Cross-sectional studies Examine groups of differing physical activity at one time Record differences between groups Longitudinal studies Examine groups before and after training Record changes over time in the groups

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 VO2max = HRmax x SVmax x (a-vO2)max 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)  Plasma volume  Venous return  Ventricular volume  Afterload (TPR)  Arterial constriction  Maximal muscle blood flow with no change in mean arterial pressure  Contractility

Factors Increasing Stroke Volume Fig 13.2

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

Factors Causing Increased VO2max Fig 13.3

Detraining and VO2max Decrease in VO2max with cessation of training  SVmax  maximal a-vO2 difference Opposite of training effect Fig 13.4

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 Changes in Mitochondria 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

Training/Detraining Mitochondrial Changes Fig 13.5

Effect 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 Fig 13.6

Mitochondrial Number and ADP Concentration on VO2 [ADP] stimulates mitochondrial ATP production Increased mitochondrial number following training Lower [ADP] needed to increase ATP production and VO2

Mitochondrial Number and ADP Concentration on VO2 Fig 13.7

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

Effects of Endurance Training on O2 Deficit Fig 13.8

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

FFA Oxidation and Glucose-Sparing Fig 13.9

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 + NAD LDH

Mitochondrial and Biochemical Adaptations and Blood pH Fig 13.10

Blood Lactate Concentration Fig 13.11

Biochemical Adaptations and Lactate Removal Fig 13.13

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

One Leg Training Study Fig 13.14

Peripheral Control of Cardiorespiratory Responses Fig 13.15

Central Control of Cardiorespiratory Responses Fig 13.16

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 Fig 13.17