The Physiology of Training: Effect on VO2 Max, Performance, Homeostasis, and Strength

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 typical VO2 max values for various sedentary, active, and athletic populations. State the formula for VO2 max using heart rate, stroke volume, and the a-vO2 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 stroke volume that occurs with endurance training. Describe the changes in muscle structure that are responsible for the increase in the maximal a-vO2 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 adaptations to submaximal exercise: a. a lower O2 deficit b. an increased utilization of FFA and a sparing of blood glucose and muscle glycogen c. a reduction in lactate and H+ formation d. an increase in lactate removal Discuss how changes in “central command” and “peripheral feedback” following an endurance training program can lower the heart rate, ventilation, and catecholamine responses to a submaximal exercise bout. Contrast the role of neural adaptations with hypertrophy in the increase in strength that occurs with resistance training.

Outline Principles of Training Detraining and VO2 Max Overload Specificity Research Designs to Study Training Endurance Training and VO2 Max Training Programs and Changes in VO2 Max VO2 Max: Cardiac Output and the Arteriovenous O2 Difference Stroke Volume Arteriovenous O2 Difference Detraining and VO2 Max Endurance Training: Effects on Performance and Homeostasis Biochemical Adaptations and the Oxygen Deficit Biochemical Adaptations and the Plasma Glucose Concentration Biochemical Adaptations and Blood pH Biochemical Adaptations and Lactate Removal Endurance Training: Links Between Muscle and Systemic Physiology Peripheral Feedback Central Command Physiological Effects of Strength Training Physiological Mechanisms Causing Increased Strength Neural Factors Muscular Enlargement Concurrent Strength and Endurance Training

Exercise: A Challenge to Homeostasis Introduction Exercise: A Challenge to Homeostasis Figure 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: Muscle fibers involved Energy system involved (aerobic vs. anaerobic) Velocity of contraction Type of contraction (eccentric, concentric, isometric) Reversibility Gains are lost when overload is removed

Principles of Training In Summary The principle of overload states that for a training effect to occur, a system or tissue must be challenged with an intensity, duration, or frequency of exercise to which it is unaccustomed. Over time the tissue or system adapts to this load. The reversibility principle is a corollary to the overload principle. The principle of specificity indicates that the training effect is limited to the muscle fibers involved in the activity. In addition, the muscle fiber adapts specifically to the type of activity: mitochondrial and capillary adaptations to endurance training, and contractile protein adaptations to resistive weight training.

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

Research Designs to Study Training In Summary Cross-sectional training studies contrast the physiological responses of groups differing in habitual physical activity (e.g., sedentary individuals versus runners). Longitudinal training studies examine the changes taking place over the course of a training program.

Endurance Training and VO2 Max Training to increase VO2 max Large muscle groups, dynamic activity 20–60 min, 3–5 times/week, 50–85% VO2 max Expected increases in VO2 max Average = 15% 2–3% in those with high initial VO2 max Requires intensity of 95–100% VO2 max 30–50% in those with low initial VO2 max Training intensity of 40–70% VO2 max Genetic predisposition Accounts for 40%–66% VO2 max Prerequisite for VO2 max of 60–80 ml•kg–1•min–1

Range of VO2 Max Values in the Population Endurance Training and VO2 Max Range of VO2 Max Values in the Population

A Closer Look 13.1 The HERITAGE Family Study Endurance Training and VO2 Max A Closer Look 13.1 The HERITAGE Family Study Designed to study the role of genotype in cardiovascular, metabolic, and hormonal responses to exercise and training Some results: Heritability of VO2 max is ~50% Maternal contribution is ~30% Large variation in change in VO2 max with training Average improvement 15–20% Ranged from slight decrease to 1 L/min increase Heritability of change in VO2 max is 47% Difference genes for sedentary VO2 max and change in VO2 max with training

Endurance Training and VO2 Max In Summary Endurance training programs that increase VO2 max involve a large muscle mass in dynamic activity for twenty to sixty minutes per session, three to five times per week, at an intensity of 50% to 85% VO2 max. Although VO2 max increases an average of about 15% as a result of an endurance training program, the largest increases are associated with deconditioned or patient populations having very low pretraining VO2 max values. Genetic predisposition accounts for 40% to 60% of one’s VO2 max value. Very strenuous and/or prolonged training can increase VO2 max in normal sedentary individuals by more than 40%.

VO2 Max: Cardiac Output and the Arteriovenous Difference Calculation of VO2 Max Product of maximal cardiac output and arteriovenous difference Differences in VO2 max in different populations Primarily due to differences in SV max Improvements in VO2 max 50% due to SV 50% due to a-vO2 VO2 max = HR max x SV max x (a-vO2) max

Differences in VO2 Max Values Among Populations VO2 Max: Cardiac Output and the Arteriovenous Difference Differences in VO2 Max Values Among Populations

Changes in VO2 Max with Training VO2 Max: Cardiac Output and the Arteriovenous Difference Changes in VO2 Max with Training

VO2 Max: Cardiac Output and the Arteriovenous Difference In Summary In young sedentary subjects, approximately 50% of the increase in VO2 max due to training is related to an increase in maximal stroke volume (maximal heart rate remains the same), and 50% is due to an increase in the a-vO2 difference. The large differences in VO2 max in the normal population (2 versus 6 liters/min) are due to differences in maximal stroke volume.

Stroke Volume Increased maximal stroke volume  Preload (EDV) VO2 Max: Cardiac Output and the Arteriovenous Difference Stroke Volume Increased maximal stroke volume  Preload (EDV)  Plasma volume  Venous return  Ventricular volume  Afterload (TPR)  Arterial constriction  Maximal muscle blood flow with no change in mean arterial pressure  Contractility Changes occur rapidly 11% increase in plasma volume with six days of training

Factors Increasing Stroke Volume VO2 Max: Cardiac Output and the Arteriovenous Difference Factors Increasing Stroke Volume Figure 13.2

Endurance Training and VO2 Max A Closer Look 13.2 Why Do Some Individuals Have High VO2 Max Values Without Training? Some individuals have very high VO2 max values with no history of training VO2 max = 65.3 ml•kg–1•min–1 Compared to 46.3 ml•kg–1•min–1 in sedentary with low VO2 max Higher VO2 max due to: Higher maximal cardiac output, stroke volume, and lower total peripheral resistance No difference in a-vO2 difference or maximal heart rate Higher stroke volume linked to: Higher blood volume and red cell volume

Arteriovenous O2 Difference VO2 Max: Cardiac Output and the Arteriovenous Difference Arteriovenous O2 Difference a-vO2 max  Muscle blood flow  SNS vasoconstriction Improved ability of the muscle to extract oxygen from the blood  Capillary density  Mitochondial number

Factors Causing Increased VO2 Max VO2 Max: Cardiac Output and the Arteriovenous Difference Factors Causing Increased VO2 Max Figure 13.3

VO2 Max: Cardiac Output and the Arteriovenous Difference In Summary The training-induced increase in maximal stroke volume is due to both an increase in preload and a decrease in afterload. a. The increased preload is primarily due to an increase in end diastolic ventricular volume and the associated increase in plasma volume. b. The decreased afterload is due to a decrease in the arteriolar constriction in the trained muscles, increasing maximal muscle blood flow with no change in the mean arterial blood pressure.

VO2 Max: Cardiac Output and the Arteriovenous Difference In Summary In young sedentary subjects, 50% of the increase in VO2 max is due to an increase in the systemic a-vO2 difference. The increased a-vO2 difference is due to an increase in the capillary density of the trained muscles that is needed to accept the increase in maximal muscle blood flow. The greater capillary density allows for a sufficiently slow red blood cell transit time through the muscle, providing enough time for oxygen diffusion, which is facilitated by the increase in the number of mitochondria.

Detraining and VO2 Max Decrease in VO2 max with cessation of training  SV max Rapid loss of plasma volume  Maximal a-vO2 difference  Mitochondria  Oxidative capacity of muscle  Type IIa fibers and  type IIx fibers Initial decrease (12 days) due to  SV max Later decrease due to  a-vO2 max

Detraining and Changes in VO2 Max and Cardiovascular Variables Detraining and VO2 Max Detraining and Changes in VO2 Max and Cardiovascular Variables Figure 13.4

Detraining and VO2 Max In Summary The decrease in VO2 max with cessation of training is due to both a decrease in maximal stroke volume and a decrease in oxygen extraction, the reverse of what happens with training.

Effects of Endurance Training on Performance Endurance Training: Effects on Performance and Homeostasis Effects of Endurance Training on Performance Maintenance of homeostasis More rapid transition from rest to steady-state Reduced reliance on glycogen stores Cardiovascular and thermoregulatory adaptations Neural and hormonal adaptations Initial changes in performance Structural and biochemical changes in muscle  Mitochondrial number  Capillary density

Structural and Biochemical Adaptations to Endurance Training Endurance Training: Effects on Performance and Homeostasis Structural and Biochemical Adaptations to Endurance Training Increased capillary density Increased number of mitochondria Increase in oxidative enzymes Krebs cycle (citrate synthase) Fatty acid (-oxidation) cycle Electron transport chain Increased NADH shuttling system NADH from cytoplasm to mitochondria Change in type of LDH

Changes in Oxidative Enzymes with Training Endurance Training: Effects on Performance and Homeostasis Changes in Oxidative Enzymes with Training

Time Course of Training/Detraining Mitochondrial Changes Endurance Training: Effects on Performance and Homeostasis Time Course of Training/Detraining Mitochondrial Changes Training Mitochondria double with five weeks of training Detraining 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 Endurance Training: Effects on Performance and Homeostasis Time Course of Training/Detraining Mitochondrial Changes Figure 13.5

Endurance Training: Effects on Performance and Homeostasis A Closer Look 13.3 Role of Exercise Intensity and Duration on Mitochondrial Adaptations Citrate synthase (CS) Marker of mitochondrial oxidative capacity Effect of exercise intensity 55%, 65%, or 75% VO2 max Increased CS in oxidative (IIa) fibers with all training intensities Effect of exercise duration 30, 60, or 90 minutes No difference between durations on CS activity in IIa fibers Increase in CS activity in IIx fibers with higher-intensity, longer-duration training

Changes in Citrate Synthase Activity with Exercise Endurance Training: Effects on Performance and Homeostasis Changes in Citrate Synthase Activity with Exercise Figure 13.6

Biochemical Adaptations and the Oxygen Deficit Endurance Training: Effects on Performance and Homeostasis Biochemical Adaptations and the Oxygen Deficit [ADP] stimulates mitochondrial ATP production Increased mitochondrial number following training Lower [ADP] needed to increase ATP production and VO2 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 Faster rise in VO2 curve, and steady state is reached earlier Results in less lactic acid formation and less PC depletion

Mitochondrial Number and ADP Concentration Needed to Increase VO2 Endurance Training: Effects on Performance and Homeostasis Mitochondrial Number and ADP Concentration Needed to Increase VO2 Figure 13.7

Endurance Training Reduces the O2 Deficit Endurance Training: Effects on Performance and Homeostasis Endurance Training Reduces the O2 Deficit Figure 13.8

Biochemical Adaptations and the Plasma Glucose Concentration Endurance Training: Effects on Performance and Homeostasis Biochemical Adaptations and the Plasma Glucose Concentration Increased utilization of fat and sparing of plasma glucose and muscle glycogen Transport of FFA into the muscle Increased capillary density Increased fatty acid binding protein and fatty acid translocase Transport of FFA from the cytoplasm to the mitochondria Increased mitochondrial number Higher levels of CPT I and FAT Mitochondrial oxidation of FFA Increased enzymes of -oxidation Increased rate of acetyl-CoA formation High citrate level inhibits PFK and glycolysis

Endurance Training: Effects on Performance and Homeostasis Effect of Mitochondria and Capillaries on Free-Fatty Acid and Glucose Utilization Figure 13.9

Endurance Training: Effects on Performance and Homeostasis In Summary The combination of the increase in the density of capillaries and the number of mitochondria per muscle fiber increases the capacity to transport FFA from the plasma  cytoplasm  mitochondria. The increase in the enzymes of the fatty acid cycle increases the rate of formation of acetyl-CoA from FFA for oxidation in the Krebs cycle. This increase in fat oxidation in endurance-trained muscle spares both muscle glycogen and plasma glucose, the latter being a focal point of homeostatic regulatory mechanisms. These points are summarized in Figure 13.9.

Biochemical Adaptations and Blood pH Lactate production during exercise Increased mitochondrial number Less carbohydrate utilization = less pyruvate formed Increased NADH shuttles Less NADH available for lactic acid formation Change in LDH type Heart form (H4) has lower affinity for pyruvate = less lactic acid formation pyruvate + NADH lactate + NAD LDH M4  M3H  M2H2  MH3  H4

Mitochondrial and Biochemical Adaptations and Blood pH Figure 13.10

Biochemical Adaptations and Lactate Removal Biochemical Adaptations and Blood pH Biochemical Adaptations and Lactate Removal Lactate removal By nonworking muscle, liver, and kidneys Gluconeogenesis in liver Increased capillary density Muscle can extract same O2 with lower blood flow Redistribution of blood flow to liver and kidney Increased lactate removal

Redistribution of Blood Flow and Lactate Removal Biochemical Adaptations and Blood pH Redistribution of Blood Flow and Lactate Removal Figure 13.13

Biochemical Adaptations and Blood pH In Summary Mitochondrial adaptations to endurance training include an increase in the enzymes involved in oxidative metabolism: Krebs cycle, fatty-acid (-oxidation) cycle, and the electron transport chain. Those mitochondrial adaptations result in the following: a. a smaller O2 deficit due to a more rapid increase in oxygen uptake at the onset of work b. an increase in fat metabolism that spares muscle glycogen and blood glucose c. a reduction in lactate and H+ formation that helps to maintain the pH of the blood d. an increase in lactate removal

A Closer Look 13.4 Exercise and Resistance to Infection J-shaped relationship between amount and intensity of exercise and risk of URTI Marathon run alters immune system Elevated neutrophils, reduced lymphocytes and natural killer cells Decreases in NK and T-cell function Decreases in nasal neutrophil activity Decreases in nasal and salivary IgA concentrations Increases in pro-inflammatory cytokines “Open window” hypothesis Immune suppression following marathon increases risk of infection

J-Shaped Relationship Between Exercise and URTI Exercise and Resistance to Infection J-Shaped Relationship Between Exercise and URTI Figure 13.11

The “Open Window” Theory Exercise and Resistance to Infection The “Open Window” Theory Figure 13.12

Links Between Muscle and Systemic Physiology Endurance Training: Links Between Muscle and Systemic Physiology 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 Lack of transfer of training effect to untrained leg

Lack of Transfer of Training Effect Endurance Training: Links Between Muscle and Systemic Physiology Lack of Transfer of Training Effect Figure 13.14

Peripheral and Central Control of Cardiorespiratory Responses Endurance Training: Links Between Muscle and Systemic Physiology Peripheral and Central Control of Cardiorespiratory Responses Peripheral feedback from working muscles Group III and group IV nerve fibers Responsive to tension, temperature, and chemical changes Feed into cardiovascular control center Central Command Motor cortex, cerebellum, basal ganglia Recruitment of muscle fibers Stimulates cardiorespiratory control center

Peripheral Control of Heart Rate, Ventilation, and Blood Flow Endurance Training: Links Between Muscle and Systemic Physiology Peripheral Control of Heart Rate, Ventilation, and Blood Flow Figure 13.15

Central Control of Cardiorespiratory Responses Endurance Training: Links Between Muscle and Systemic Physiology Central Control of Cardiorespiratory Responses Figure 13.16

Endurance Training: Links Between Muscle and Systemic Physiology In Summary The biochemical changes in muscle due to endurance training influence the physiological responses to exercise. The reduction in “feedback” from chemoreceptors in the trained muscle and a reduction in the need to recruit motor units to accomplish a work task results in reduced sympathetic nervous system, heart rate, and ventilation responses in submaximal exercise.

Physiological Effects of Strength Training Muscular strength Maximal force a muscle or muscle group can generate 1 repetition maximum (1-RM) Muscular endurance Ability to make repeated contractions against a submaximal load Strength training Percent gain inversely proportional to initial strength Genetic limitation to gains in strength High-resistance (2–10 RM) training Gains in strength Low-resistance training (20+ RM) Gains in endurance

A Closer Look 13.5 Aging, Strength, and Training Physiological Effects of Strength Training A Closer Look 13.5 Aging, Strength, and Training Decline in strength after age 50 Loss of muscle mass (sarcopenia) Loss of both type I and II fibers Atrophy of type II fibers Loss of intramuscular fat and connective tissue Loss of motor units Reorganization of motor units Progressive resistance training Causes muscle hypertrophy and strength gains Important for activities of daily living, balance, and reduced risk of falls

Physiological Mechanisms Causing Increased Strength Strength training results in increased muscle size and strength Initial 8–20 weeks Neural adaptations Long-term training (20+ weeks) Muscle hypertrophy High-intensity training can result in hypertrophy with 10 sessions

Neural and Muscular Adaptations to Resistance Training Physiological Mechanisms Causing Increased Strength Neural and Muscular Adaptations to Resistance Training Figure 13.17

Neural Factors Early gains in strength Initial 8–20 weeks Adaptations Physiological Mechanisms Causing Increased Strength Neural Factors Early gains in strength Initial 8–20 weeks Adaptations Improved ability to recruit motor units Learning Coordination

Muscular Enlargement Hypertrophy Physiological Mechanisms Causing Increased Strength Muscular Enlargement Hypertrophy Enlargement of both type I and II fibers Low-intensity (high RM), high-volume training results in smaller type II fibers Heavy resistance (low RM) results in larger type II fibers No increase in capillary density Hyperplasia Increase in muscle fiber number Mainly seen in long-term strength training Not as much evidence as muscle hypertrophy

The Winning Edge 13.1 Periodization of Strength Training Physiological Mechanisms Causing Increased Strength The Winning Edge 13.1 Periodization of Strength Training Traditional training programs Variations in intensity (RM), sets, and repetitions Periodization Also includes variation of: Rest periods, type of exercise, number of training sessions, and training volume Develop workouts to achieve optimal gains in: Strength, power, motor performance, and/or hypertrophy Linear and undulating programs Variations in volume/intensity over time More effective than non-periodized training for improving strength and endurance

Concurrent Strength and Endurance Training Physiological Mechanisms Causing Increased Strength Concurrent Strength and Endurance Training Potential for interference of adaptations Endurance training increases mitochondial protein Strength training increases contractile protein Depends on intensity, volume, and frequency of training Studies show conflicting results

Physiological Mechanisms Causing Increased Strength In Summary Increases in strength due to short-term (eight to twenty weeks) training are the results of neural adaptations, while gains in strength in long-term training programs are due to an increase in the size of the muscle. There is evidence both for and against the proposition that the physiological effects of strength training interfere with the physiological effects of endurance training.

Study Questions Define the following principles of training: overload and specificity. Give one example each of a cross-sectional study and a longitudinal study. What are the typical VO2 max values for young men and women? Cardiac patients? Given the formula for VO2 max using heart rate, stroke volume, and the a-vO2 difference, which variable is most important in explaining the differences in VO2 max in different populations? Give a quantitative example. Describe how the increase in VO2 max comes about for the sedentary subject who undertakes an endurance training program. Explain the importance of preload, afterload, and contractility in the increase of the maximal stroke volume that occurs with endurance training.

Study Questions What are the most important changes in muscle structure that are responsible for the increase in the maximal a-vO2 difference that occurs with endurance training? What causes the VO2 max to decrease following termination of an endurance training program? Describe how the capillary and mitochondrial changes that occur in muscle as a result of an endurance training program are related to the following adaptations to submaximal exercise: a. a lower O2 deficit b. an increase utilization of FFA and sparing of blood glucose and muscle glycogen c. a reduction in lactate and H+ formation that helps to maintain the pH of the blood d. an increase in lactate removal

Study Questions Define central command and peripheral feedback and explain how changes in muscle as a result of endurance training can be responsible for the lower heart rate, ventilation, and catecholamine response to a submaximal exercise bout. In short-term training programs, what neural factors may be responsible for the increase in strength? Contrast hyperplasia with hypertrophy, and explain the role of each in the increase in muscle size that occurs with long-term strength training. Does strength training interfere with the physiological effects of endurance training?