VO2 During Exercise - KINE 3800 Fall 2024 Lecture Notes PDF

VO2 as a measure of energy expenditure during exercise Lectures: Week 8 KINE 3800: APPLIED HUMAN MOVEMENT INSTRUCTOR: DR. CHRISTOPHER PERRY Key concepts for week 8 lab: cycle ergometer tests to predict VO2max Understand the relationship between exercise intensity and oxygen consumption (VO2)...

VO2 as a measure of energy expenditure during exercise Lectures: Week 8 KINE 3800: APPLIED HUMAN MOVEMENT INSTRUCTOR: DR. CHRISTOPHER PERRY Key concepts for week 8 lab: cycle ergometer tests to predict VO2max Understand the relationship between exercise intensity and oxygen consumption (VO2) Understand the relationship between heart rate and VO2 across exercise intensities Apply this knowledge through predictive exercise tests to predict VO2max based on heart rate and exercise intensity relationships Understand the effects of exercise training on aerobic metabolism during exercise  Relationship between work rate and VO2 for cycling Fig 1.6 Access the text alternative for slide images. © McGraw Hill, LLC 3  Cascade of Oxygen and carbon dioxide between the atmosphere and muscles Fig 9.2 Access the text alternative for slide images © McGraw Hill, LLC; modified by C. Perry for KINE 3800 4 Cardiac output (Q) The amount of blood pumped by the heart each minute Product of heart rate and stroke volume Heart rate  Number of beats per minute Stroke volume  Amount of blood ejected in each beat Q = HR × SV on training state and sex Depends 5 Changes in arterial-mixed venous O2 content during exercise Arteriovenous difference (a-vO2 difference) Amount of O2 that is taken up from 100 ml blood Increases during exercise due to higher O2 uptake in tissues  Used for oxidative ATP production Fick equation Relationship between cardiac output (Q), a-vO2 difference, and VO2 VO2 = Q x a – vO2 difference 6  Changes in cardiovascular variables during exercise Fig 9.24 Access the text alternative for slide images. © McGraw Hill, LLC; modified by C. Perry for KINE 3800 7  Changes in cardiovascular variables during exercise Fig 9.24 Access the text alternative for slide images. © McGraw Hill, LLC, modified by C. Perry for KINE 3800 8  Changes in cardiovascular variables during exercise Fig 9.24 Access the text alternative for slide images. © McGraw Hill, LLC, modified by C. Perry for KINE 3800 9  Astrand-Rhyming cycle ergometer test for predicting VO2max From: Åstrand, P.O., and I. Rhyming. 1954. A nomogram for calculation of aerobic capacity (physical fitness) from pulse rate during submaximal work. Journal of Applied Physiology 7:218–221. 10  Direct measures (non-predictive) tests: How do you verify that VO2 max has been reached during an incremental exercise test? Verification of VO2 max-key points Gold Standard for verification of VO2 max is a plateau in O2 consumption with increase in work rate Most subjects do not achieve a plateau in O2 consumption during an incremental exercise test If a plateau in O2 consumption is not achieved, what secondary criteria can confirm VO2 max has been achieved? Suggested criteria include: Reaching age-predicted max heart rate (+/− 10 beats/min) Achieving blood lactate concentration of 8 mM or higher Attaining a respiratory exchange ratio of 1.15 or higher Research reveals that these criteria do not always “prove” that VO2 max has been reached  ‘VO2peak’ is often used as a preferred term © McGraw Hill, LLC, modified by C. Perry for KINE 3800 11 Sources of error in predictive tests Individual differences in HR vs VO2 Technical errors (can you identify possibilities?) Differences in efficiency 12 Efficiency during exercise Energy expenditure can be estimated during many types of physical activity Examples include: Running Walking Stationary cycling The relationship between exercise intensity and energy expenditure (VO2) differs between types of exercise 13  Relationship between walking or running speed and VO2 Fig 1.5 Access the text alternative for slide images. © McGraw Hill, LLC 14 Exercise efficiency Exercise efficiency = ratio of work output to energy input A more efficient individual uses less energy to perform the same amount of work  Several methods to compute exercise efficiency-common and simple method is net efficiency 15 Calculation of net efficiency Net Efficiency defined Ratio of work output divided by energy expended above rest Work output % Net efficiency  100 Energy expended (above rest) Most Net efficiency of cycle ergometry often ranges from 15 to 27% 16  Factors that impact efficiency Exercise intensity Curvilinear relationship between work rate and energy expenditure Therefore, efficiency decreases at high exercise intensities because of the higher energy cost of very heavy exercise Speed of movement There is an optimum speed of movement and deviation away from optimum speed reduces efficiency Muscle fiber type Slow muscle fibers (type 1) are more efficient in using ATP compared to fast muscle fibers (type 2) slow-twitch muscle fibers, which move more slowly but help to keep you moving longer. fast-twitch muscle fibers, which help you move faster, but for shorter period more force less oxidate more prone to fatigue type 2 uses more ATP. 17  Relationship between energy expenditure and work rate Energy expenditure Work rate Fig 1.8 Access the text alternative for slide images. © McGraw Hill, LLC 18  Effect of speed of movement on net efficiency Fig 1.8 Access the text alternative for slide images. © McGraw Hill, LLC 19 Effects of exercise training on aerobic metabolism during exercise Understand the relationship between exercise intensity and oxygen consumption (VO2) Understand the relationship between heart rate and VO2 across exercise intensities Apply this knowledge through predictive exercise tests to predict VO2max based on heart rate and exercise intensity relationships Understand the effects of exercise training on aerobic metabolism during exercise  Principles of training Overload Training effect occurs when a physiological system is exercised at a level beyond which it is normally accustomed Specificity Training effect is specific to:  Muscle fibers recruited during exercise  Energy system involved (aerobic vs. anaerobic)  Velocity of contraction  Type of contraction (eccentric, concentric, isometric) Reversibility Gains are lost when training ceases © McGraw Hill, LLC 21  Endurance training and VO2 max Training to increase VO2 max Large muscle groups, dynamic activity 20–60 min, ≥3 times/week, ≥50% VO2 max Increases in VO2 max with endurance training Average = 15 to 20% increase Smaller increases in individuals with high initial VO2 max  Individuals with high may require higher exercise training intensities (>70% VO 2 max) to obtain improvements Up to 50% in those with low initial VO2 max © McGraw Hill, LLC 22  Impact of genetics on VO2 max and exercise training response Heritability (genetics) Determines approximately 50% of VO2 max in sedentary adults Genetics also plays key role in determining the training response Average improvement in VO2 max is 15 to 20% Low responders improve VO2 max by 2 to 3% High responders can improve VO2 max by approximately 50% with rigorous training Large variations in training adaptations reveal that heritability of training adaptations is approximately 47% See A Closer Look 13.1 for details © McGraw Hill, LLC 23  See a Closer Look 13.1 for details on the role that genetics plays in athletic performance Access the text alternative for slide images © McGraw Hill, LLC 24  Why does training improve VO2 max? VO2max is defined by the Fick equation VO2max = maximal cardiac output X a-vO2 diff Differences in VO2 max between individuals Primarily due to differences in SV max Exercise-induced improvements in VO2 max Short duration training (approximately 4 months); Increase in stroke volume is dominant factor in increasing VO2max Longer duration training (approximately 28 months); Both stroke volume and a-vO2 increase to improve VO2max © McGraw Hill, LLC 25 Effects of endurance training on performance and homeostasis The ability to perform prolonged, submaximal exercise is dependent on the ability to maintain homeostasis Endurance exercise training results in numerous adaptations in muscle fibers that assist in maintaining homeostasis Shift in muscle fiber type (fast-to-slow) and increased number of capillaries Increased mitochondrial volume Training-induced changes in fuel utilization Increased antioxidant capacity Improved acid-base regulation 26 Endurance training promotes a fast-to-slow shift( the percentage) in muscle fiber type and increased capillarization Fast-to-slow shift in muscle fiber type Reduction in fast fibers and increase in number of slow fibers Magnitude of fiber type change determined by duration of training, type of training, and genetics Increased number of capillaries surrounding muscle fibers Enhanced diffusion of oxygen Improved removal of wastes 27 Endurance training increases mitochondrial volume and turnover in skeletal muscle Endurance training increases the volume of both subsarcolemmal and intermyofibrillar mitochondria in muscle fibers Results in improved oxidative capacity and ability to utilize fat as fuel Training also increases mitochondrial turnover (i.e., breakdown of damaged mitochondria and replacement with healthy mitochondria) Breakdown of damaged mitochondrial is termed “mitophagy” See A Closer Look 13.2 for details 28 Endurance training increases mitochondrial volume and turnover in skeletal muscle- See Closer Look 13.2 for details Access the text alternative for slide images. 29  Endurance training-induced changes in VO2 max Fig 13.1 Access the text alternative for slide images. © McGraw Hill, LLC 30 Accessibility Content: Text Alternatives for Images 31 Relationship between work rate and VO2 for cycling - Text Alternative Return to parent-slide containing images. The x-axis represents the cycle ergometer work rate expressed as watts, with values ranging from 0 through 250 in increments of 50. The y-axis represents energy expenditure expressed in terms of oxygen consumption in units of milliliters per kilogram per minute, with values ranging from 0 through 40 in increments of 5. The curve is a linear slope that rises smoothly from 50 to 200 along the x-axis, reaching a peak value of 35 on the y-axis. There are the following points (coordinates) on the linear slope, (50, 15), (100, 23), (150, 30), and (200, 37). Return to parent-slide containing im ages. 32 Changes in cardiovascular variables during exercise - Text Alternative Return to parent-slide containing images. The five factors represented are blood pressure, stroke volume, cardiac output, heart rate, and the arterial– mixed venous oxygen difference. The x-axis is the same for all five graphs, and it represents the percent VO2 max with values ranging from 0 through 100 in increments of 25. The y-axis of graph one represents blood pressure in millimeters of mercury with values ranging from 80 through 240 in increments of 40. The curve for diastolic is a flat line at 80 on the y-axis. The curve for systolic is a rising straight line from 120 at 25 to 200 at 100. A dotted line drawn parallel to the systolic line and joining the start of the diastolic line is labeled mean. The y-axis of graph two represents stroke volume in milliliters per beat with values ranging from 80 through 140 in increments of 20. The curve of the graph rises from 80 at 25 to 120 at 50, and it remains steady until 100. The peak point of the graph is labeled as approximately 40 percent VO2 max. The y-axis of graph three represents cardiac output in liters per minute with values ranging from 5 through 25 in increments of 5. The curve of the graph rises from 10 at 25 to 15 at 50. Then it rises to 20 at 100. The y-axis of graph four represents heart rate in beats per minute with values ranging from 50 through 200 in increments of 50. The curve of the graph is a rising straight line from 100 at 25 to 200 at 100. The y-axis of graph five represents the arteriovenous O2 difference with the values 6, 12, and 18. The curve of the graph rises from 9 at 25 to 15 at 50. Then it rises to 18 at 100. Return to parent-slide containing im ages. 33 Relationship between walking or running speed and VO2 - Text Alternative Return to parent-slide containing images. The x-axis represents walking or running speed expressed as meters per minute, with values ranging from 0 through 250 in increments of 50. The y-axis represents energy expenditure expressed in terms of oxygen consumption in units of a liter per minute and milliliters per kilogram per minute, with values ranging from 0 through 60 in increments of 10 (with interval units). Walking has a small linear curve that rises from 50 to 100, reaching a peak value of 10. The expression VO2 equals 0.1 times x plus 3.5 (milliliters per minute per kilogram) is given beside this line. Running has a long linear curve that rises steeply from 150 to 250, reaching a peak value of 50. The expression VO2 equals 0.2 times x plus 3.5 (milliliters per minute per kilogram) is given besides this line. Return to parent-slide containing im ages. 34 Relationship between energy expenditure and work rate - Text Alternative Return to parent-slide containing images. The x-axis represents the work rate expressed as watts, with values ranging from 0 through 350 in increments of 50. The y-axis represents energy expenditure expressed in terms of kilojoules, with values ranging from 20 through 80 in increments of 10. A dotted linear curve and a curvilinear curve both rise from 50 to 300 on the x-axis, with the curvilinear curve reaching a peak value of 80 on the y-axis. There are the following points (coordinates) on the curvilinear curve, (50, 22), (100, 28), (150, 38), (200, 50), (250, 64), and (300, 78). Return to parent-slide containing im ages. 35 See a Closer Look 13.1 for details on the role that genetics plays in athletic performance - Text Alternative Return to parent-slide containing images. The header of the table shows a magnifying glass. The table shows the following data: The highly popular book by Malcolm Gladwell, “Outliers: the story of Success,” examined factors that contribute to high levels of both athletic and career success. The book asserted that to become an elite athlete, all that is required is 10,000 hours of practice. Unfortunately, this is a myth. While the quality of coaching, long hours of training, and nutritional support contribute to athletic success, many other factors also play key roles in athletic achievement. For example, depending on the sport, world-class athletes have a narrow range of physiological, morphological (e.g., body size), biomechanical, and psychological traits (51); this observation suggests that world-class athletes share similar genetic components. Indeed, studies confirm that genetics plays a major role in determining athletic success (51). In this Closer Look feature, we consider two examples where genetics plays a key role in becoming an elite athlete. First, let’s consider the impact that genetics play in basketball where being tall is a major advantage. It is well- established that body height has a strong heritability component. For instance, it is estimated that 65% to 80% of body height is determined by height-enhancing genes (51). Therefore, inheriting the appropriate “height genes” from tall parents is important if someone is to become a highly successful basketball player (51). Further, genetics play an important role in determining whether an individual becomes an elite endurance athlete. Although several factors contribute to achievement in endurance sports, one of the key elements that determine success in endurance events is a high V̇ O2 max. Therefore, it is not surprising that world-class endurance athletes possess a high V̇ O2 max. Let’s discuss the genetic contribution to V̇ O2 max in both untrained people and individuals following endurance exercise training. As discussed in the text, research reveals that genetics explain approximately 50% of the variation in V̇ O2 max between sedentary individuals. Therefore, people who start with a high V̇ O2 max before beginning a training program are in a good position to achieve early success in endurance sports (51). Why does genetics play a key role in determining the V̇ O2 max in untrained individuals? At least two factors are involved. First, the fiber type composition of skeletal muscle fibers is important. For example, having a high percentage of type 1 (slow) muscle fibers is a major advantage for endurance athletes because competitive endurance events impose a high aerobic metabolic demand on the muscle (51). In this regard, about 45% of the variability in the amount of type 1 fibers in skeletal muscles are genetically determined (51). Second, genetics play an important role in determining both heart size and maximal cardiac output (2). As you will learn later in this chapter, two factors that define V̇ O2 max are maximal cardiac output and the ability of the exercising muscle to take up and utilize oxygen to produce ATP. Collectively, these two physiological components interact to explain the large influence that genes have on V̇ O2 max in untrained people. Genes also play a key role in determining physiological adaptations to training. Indeed, studies show that heritability accounts for about 50% of the variability in the response to endurance exercise training (47). Specifically, while the average training-induced improvement in V̇ O2 max is 15% to 20%, some individuals are “low responders” to exercise training and achieve only a 2% to 3% improvement in V̇ O2 max. In contrast, “high responders” to endurance training can increase their “untrained” V̇ O2 max by 40% to 50%. These large genetically controlled variations in the training response confirm that becoming a champion endurance athlete requires that you are a “high responder” to training (5–8, 47). Although the complete details of how genes regulate training adaptation remain unclear, a total of 97 genes are known to contribute to the genetic differences in the training improvement of V̇ O2 max (53,61). In summary, having a high V̇ O2 max is essential to achieve world-class performances in endurance races. Research indicates that genetics plays an important role in determining both the V̇ O2 max of sedentary individuals and the trainability of individuals in response to an exercise training program. It follows that, to become a world-class endurance athlete, an individual must possess a high V̇ O2 max in the untrained state and the person must also be a high responder to endurance training. Together, these research findings confirm that without a rich genetic endowment, world-class performance in endurance events is not possible (51). See Bouchard (2019), Sarzynski and Bouchard (2020), Ross et al. (2019), and Williams et al. (2017) in the Suggested Readings to learn more about the impact of genetics on V̇ O2 max and the training adaptations to exercise. Return to parent-slide containing images. 37 Endurance training increases mitochondrial volume and turnover in skeletal muscle-See Closer Look 13.2 for details - Text Alternative Return to parent-slide containing images. The header of the table shows a magnifying glass. The table shows the following data: As discussed in the text, both endurance exercise training (i.e., continuous submaximal exercise) and high-intensity interval training promote the synthesis of new mitochondria (called mitochondrial biogenesis), resulting in an increased volume of both subsarcolemmal and intermyofibrillar mitochondria in the trained muscle fibers. Research reveals that the exercise-induced increase in mitochondrial volume is primarily due to increased mitochondrial size and not an increased number of mitochondria (35). This exercise-induced increase in mitochondrial volume in muscle fibers results in an improved oxidative capacity and increased ability to use fat as a fuel source. This improved ability to metabolize fat as a fuel during exercise is advantageous because it spares carbohydrates and prevents depletion of the limited carbohydrate stores in both muscle and liver (35). In addition to promoting mitochondrial biogenesis, endurance exercise training also increases the removal of damaged mitochondria. Specifically, endurance exercise training promotes the breakdown and removal of “old” and damaged mitochondria; these damaged mitochondria are replaced with “new” and healthy mitochondria that are larger. The process of removal and replacement of muscle mitochondria is commonly referred to as mitochondrial turnover. The removal of damaged mitochondria occurs via a process called mitophagy. In short, mitophagy is the selective removal of “old” and damaged mitochondria by lysosomes. The result of exercise-induced increases in mitochondrial turnover is that the muscle mitochondrial population in trained individuals is larger and healthier than the mitochondrial population found in muscle fibers of untrained individuals. As mentioned earlier, this increase in the volume of healthy mitochondria results in an improved oxidative capacity and the increased ability of the muscle fibers to metabolize fats. For more details about exercise and mitochondria, see Memme et al. (2021) in the suggested readings. Return to parent-slide containing images. 38 Endurance training-induced changes in VO2 max - Text Alternative Return to parent-slide containing images. A bar graph shows percent improvement on the y-axis with values ranging from 0 through 45 in increments of 5. The bar graphs are shown for max cardiac output, max a-vO2 difference, and VO2 max. At 4 months, max cardiac output reaches 10 percent, the max a-vO2 difference is at 1 percent, and VO2 max reaches 26 percent. At 32 months, max cardiac output reaches 15 percent, max a-vO2 difference reaches 25 percent, and VO2 max reaches 41 percent. Return to parent-slide containing images. 39