Physiological Adjustments To Exercise Lecture 2 PDF

Prof. K.C. Kregel Exercise Physiology Lecture 2 MECHANISMS OF HEALTH AND DISEASE Physiological Adjustments to Exercise Lecture 2 Kevin C. Kregel, Ph.D. Professor, Depart...

Prof. K.C. Kregel Exercise Physiology Lecture 2 MECHANISMS OF HEALTH AND DISEASE Physiological Adjustments to Exercise Lecture 2 Kevin C. Kregel, Ph.D. Professor, Department of Health & Human Physiology Executive Vice President and Provost The University of Iowa e-mail: [email protected] Ph: 319-335-3565 Learning Objectives 1. Understand the broad array of cardiovascular system adjustments that are associated with an increase in exercise intensity. Understand the exercise-intensity dependent pattern of redistribution of cardiac output away from visceral regions to active skeletal muscle. 2. Understand how the type of exercise being performed (e.g., dynamic vs. isometric) can impact the blood pressure response to exercise. 3. Understand how exercise performance can be impacted by parameters such as oxygen carrying-capacity, red blood cell number, and hemoglobin concentration. 4. Understand various pulmonary responses to aerobic exercise (e.g., ventilation, tidal volume, and respiratory rate). 5. Understand the metabolic changes that occur with increasing intensity of aerobic exercise and appreciate how these responses are reflected in changes in respiratory and blood gas parameters. Key Terms Cardiac output Mean arterial pressure Stroke volume Dynamic exercise Heart rate Isometric exercise Arteriovenous oxygen difference Hemoglobinopathies Splanchnic blood flow Erythropoietin Cutaneous blood flow Minute ventilation Skeletal muscle blood flow Tidal volume Blood pressure Respiratory rate Total peripheral resistance Pg. 1 Prof. K.C. Kregel Exercise Physiology Lecture 2 IV. CARDIOVASCULAR RESPONSES A. Central Circulatory Responses 1. Cardiac Output (CO): During exercise, CO increases with O2 uptake in a relatively sedentary individual from a resting value of 4- 6 liters/min to 25-30 liters/min (Fig. 8). Highly trained endurance athletes may have CO's of 35 to 40 liters/min. With training, the relationship between oxygen uptake and CO is not altered (i.e., for a given work load, CO is unchanged). However, maximal oxygen uptake and maximal CO are increased with aerobic training. The factors responsible for the increase in CO during exercise include the integrated effects of tachycardia, sympathetic stimulation, and the operation of the Frank-Starling mechanism. Fig. 8. Cardiac output response to increasing levels of exercise in untrained and trained individuals. 2. Stroke Volume (SV): SV is the amount of blood ejected by the heart per beat. SV is governed by: (a) venous return, (b) distensibility of the ventricles, and (c) contractile force in relation to aortic pressure. The change in SV from rest to exercise depends upon body position. Moving from a supine to a standing or sitting position is accompanied by a diminution in end-diastolic size of the heart and a decrease in SV. Exercise responses: SV increases rapidly at the onset of exercise and then reaches a plateau that is maintained throughout the exercise period (Fig. 9). Pg. 2 Prof. K.C. Kregel Exercise Physiology Lecture 2 Fig. 9. Stroke volume response to changes in posture and increasing levels of exercise in untrained and trained individuals. Training effect: aerobically trained individuals have a higher SV at rest and at any absolute submaximal exercise level (Fig. 9). 3. Heart Rate (HR): HR increases linearly with workload (Fig. 10). Hot environments, emotional factors, nervousness and apprehension may affect it both at rest and during light to moderate work. During maximal work, HR is remarkably similar under various conditions with a standard deviation of only ± a few beats/min. With habitual training, heart rate at rest and during a given bout of submaximal work is lower than in the untrained subject. The mechanisms responsible for these training effects are assumed to involve an increased centrogenic vagal cholinergic drive combined with a reduction in sympathetic activity. Note also that maximal HR is similar in sedentary and aerobically trained individuals (there is some evidence for a decline of a few beats/min in trained). Fig. 10. Heart rate response to increasing levels of exercise in untrained and trained individuals. Pg. 3 Prof. K.C. Kregel Exercise Physiology Lecture 2 4. Relationship between CO, SV, and HR: CO (L/min) = SV (mL/beat) x HR (beats/min) There is a linear increase in CO as a function of oxygen consumption (VO2) with aerobic exercise (see Fig. 8), and this response is mediated by increases in both HR and SV. Example for sedentary young individual: Rest: 5.25 L/min = 75 mL/beat x 70 beats/min Exercise: 24.0 L/min = 120 mL/beat x 200 beats/min 5. Cardiovascular Drift: During prolonged aerobic exercise at a constant submaximal workload (steady-state), there is a gradual increase in HR and decrease in SV, while cardiac output stays constant (see Fig. 11). The mechanism driving this response involves a decrease in blood volume (due to sweating and fluid shift from plasma to tissues), followed by an increase in skin blood flow (to aid thermoregulation). This redistribution of cardiac output generates a decrease in central venous cardiac filling pressure (preload) that reduces stroke volume. Note that there is a compensatory increase in HR (baroreceptor-mediated) to maintain cardiac output. Panel B: Separate experiments were performed in endurance-trained cyclists. The protocol involved cycling at 62-65% of VO2max in a 35°C environment for 120 min. Subjects became dehydrated and hyperthermic (they lost 4.9% of their body weight over the 120-min exercise bout). Note the declines in cardiac output, stroke volume, and skin blood flow as a function of exercise duration. Pg. 4 Prof. K.C. Kregel Exercise Physiology Lecture 2 Note that the Y-axis values are % change and not absolute values. Fig. 11. Changes in cardiovascular parameters during prolonged submaximal exercise (Modified from Coyle and Gonzalez-Alonso, 2001). Pg. 5 Prof. K.C. Kregel Exercise Physiology Lecture 2 B. Partitioning of Cardiac Output during Exercise 1. Overview of cardiac output redistribution with exercise. With increasing intensity of exercise (i.e., increasing VO2), there is an increase in sympathetic-mediated vasoconstriction to kidneys, splanchnic regions, and inactive muscle. This results in increases vascular muscle resistance, which diverts blood away from these areas and redistributes it to active muscle (Fig. 12). Fig. 12. Redistribution of cardiac output at rest and different levels of exercise up to VO2 max in a healthy young man. (Modified from L.B. Rowell, Human Circulation, Oxford University Press, 1986). 2. Splanchnic and Renal Blood Flows (SBF, RBF): a) The splanchnic and renal vascular beds each receive about 25% of the CO at rest, yet extract only 15-20% of the available oxygen. b) These regions are regarded as major sites for redistribution of oxygen and regulation of blood pressure. Blood flow to each declines during exercise in proportion to the intensity of the work performed, as represented by the declining portion of cardiac output going to the region in Fig. 12. 3. Cutaneous Blood Flow a) The distribution of CO to the skin may also be a function of percent max VO2. Skin blood flow initially decreases during exercise and then increases as body temperature rises with increments in the duration and intensity of exercise. Skin blood flow finally decreases when the skin vessels constrict as total body oxygen consumption nears maximal values (Fig. 12). Pg. 6 Prof. K.C. Kregel Exercise Physiology Lecture 2 b) Blood pools in the skin during heat exposure (and during exercise in the heat), thus reducing venous return and central blood volume (the volume of blood in the lungs and heart). 4. Cerebral Blood Flow: is unchanged during exercise. 5. Skeletal Muscle Blood Flow (MBF): a) The major circulatory adjustment to prolonged exercise occurs in the vasculature of active muscles. Local formation of vasoactive metabolites dilates the resistance vessels in the active skeletal muscle beds, and this dilation progresses with increasing intensity of exercise (see Fig. 12). b) Maximal muscle blood flow increases with training. C. Blood Pressure 1. Relationship between CO, total peripheral resistance (TPR), and mean arterial blood pressure (MAP): MAP = CO x TPR Note that systolic blood pressure (SBP) increases progressively with workload in a subject going from rest to maximal exercise. SBP increases can be in the range of 60-80 mmHg. At the same time, diastolic BP will remain relatively unchanged or even fall slightly from resting levels (due in part to a decline in TPR – see below). As a result, there is only a modest increase in MAP over the course of a maximal exercise test. 2. TPR: As noted above, CO increases in relation to increases in workload (or VO2). There is an abrupt and profound fall in TPR at the onset of exercise, and there is a progressive decline in TPR with increases exercise intensity. As a result, MAP rises slightly with increasing exercise intensity (Fig. 13). Fig. 13. Blood pressure responses to increasing intensities of aerobic exercise. Pg. 7 Prof. K.C. Kregel Exercise Physiology Lecture 2 3. Type of Exercise impacts BP responses a) Dynamic (or rhythmic) exercise: The larger the activated muscle mass with dynamic exercise, the more pronounced is the vasodilatation of the resistance vessels. The result is a lower peripheral resistance, which contributes to a lower mean blood pressure. b) Isometric exercise: Isometric contractions can cause far greater increases in arterial BP than does dynamic exercise. The rate of rise of arterial BP is proportional to the isometric contraction force expressed as percent of maximal voluntary contraction (%MVC) (Fig. 14A). In addition, the larger the mass of contracting muscle, the greater the pressor (i.e., increase in BP) response (Fig. 14B) Fig. 14. A) Blood pressure responses to increasing levels of handgrip exercise (isometric), represented as a percent of maximal voluntary handgrip (MVC). B) Blood pressure responses to different levels of isometric contraction (i.e., different amounts of muscle mass) as a function of duration of contraction. 4. Effects of Training a) Aerobic Training: Arterial blood pressure responses during an aerobic exercise bout are similar in trained and untrained subjects. However, resting blood pressure is generally lower in endurance-trained individuals (especially in those who are Pg. 8 Prof. K.C. Kregel Exercise Physiology Lecture 2 borderline or moderately hypertensive before training). These reductions occur in both systolic and diastolic blood pressure. b) Resistance Training: Although large increases in blood pressure are produced during lifting of heavy weights, resistance training does not result in elevations of resting blood pressure. If fact, mild reductions in resting systolic and diastolic blood pressure have been observed. D. SUMMARY: Cardiovascular responses during exercise (Fig. 15 below): Fig. 15. Effect of different levels of Heart rate exercise on several (beats/min) cardiovascular responses (modified from Berne et al.). Stroke Volume (ml) Over progressively increasing workloads: Cardiac linear increase in Output (L/min) HR SV increases and then plateaus Arterial pressure linear increase in (mmHg) CO small linear increase Total peripheral in MAP resistance (mm Hg/ml/min) decline in TPR linear increase in O2 consumption VO2 (ml/min) linear increase in a-v Arteriovenous O2 difference oxygen difference (ml/dl) Work (kg-m/min) Pg. 9 Prof. K.C. Kregel Exercise Physiology Lecture 2 E. Blood Volume 1. Total Blood Volume. Endurance training increases total blood volume, and the effect is dependent on the intensity of training. This increased blood volume results primarily from an increase in plasma volume (PV), but there is also an increase in the volume of red blood cells (RBCs). 2. PV. The increase in PV with aerobic training is thought to result from two mechanisms. First, exercise increases the levels of plasma proteins such as albumin, which produces an increase in the blood's osmotic pressure; the result is that more fluid is retained in the blood. Second, exercise increases the release of antidiuretic hormone and aldosterone (hormones that cause the reabsorption of water and sodium in the kidneys), which contributes to an increase in plasma volume. 3. RBCs and Hemoglobin (Hb). RBCs transport oxygen, which is primarily bound to Hb. An increase in RBC volume with endurance training also contributes to the overall increase in blood volume (although this is an inconsistent finding). While the actual number of RBCs may increase (along with Hb concentration), the hematocrit (ratio of RBC volume to total blood volume) may actually decrease. Interestingly, a trained individual’s hematocrit can decrease to such an extent that the athlete appears to be anemic. F. O2 Carrying Capacity and Performance Impact 1. Overview. Both the total amount (absolute values) of Hb and the total number of RBCs are typically elevated in highly trained athletes. Importantly, these changes increase oxygen carrying capacity in the blood, enhance the delivery of oxygen to active muscles, and contribute to an increase in maximal oxygen consumption and aerobic capacity. 2. Oxygen Extraction during Exercise: Oxygen extraction is the amount of oxygen removed from the blood by tissues as blood passes through the tissue. Therefore, a-vO2 difference represents the arterial concentration of oxygen minus the venous concentration of oxygen (in mL/100 mL blood). The governing equation, known as the Fick equation, is: VO2 = CO x a-vO2 difference Pg. 10 Prof. K.C. Kregel Exercise Physiology Lecture 2 3. Key point: a-vO2 difference increases with exercise intensity (see Fig. 16). At any given absolute workload, a-vO2 difference does not change in trained vs. untrained subjects. Fig. 16. a-vO2 difference values in response to increasing levels of exercise. 4. Erythropoietin (EPO): EPO is a glycoprotein that controls erythropoiesis (RBC production). EPO is produced primarily by interstitial fibroblasts in the kidney in response to reduced oxygen pressure in arterial plasma and regulates RBC production within the marrow of the long bones. 5. Medical uses of EPO (recombinant human EPO; rHuEpo): effective treatment for combatting anemia from conditions such as various hemoglobinopathies, chronic kidney disease, inflammatory bowel diseases (e.g., Crohn’s), and chemotherapy. 6. EPO as an ergogenic aid: EPO use can enhance performance in endurance sports. Pg. 11 Prof. K.C. Kregel Exercise Physiology Lecture 2 Scientific data: EPO treatment (e.g., weeks) increases RBC number/mass and Hb concentration. These changes result in increased oxygen transport capacity in the blood, which is the primary reason for an accompanying increase in VO2max*. *Note 1: These increases can be on the order of 8-10% in healthy subjects or endurance-trained recreational athletes. However, there is no evidence of improved performance in elite athletes (see Heuberger et al., Br J Clin Pharmacol 2013). *Note 2: Performance gains at submaximal exercise intensities have also been noted, with improvements of more than 50% in ‘time to exhaustion’ (with a standardized exercise test). Pg. 12 Prof. K.C. Kregel Exercise Physiology Lecture 2 V. Respiratory function A. Ventilatory responses to exercise: VE = minute ventilation VT = tidal volume fb = frequency of breathing (or respiratory rate) VE = VT x fb (L/min) (L/b) (breaths/min) 1. Example At rest: 12 br/min x 0.5 L/br = 6 L/min Maximal exercise: 60 br/min x 2.5 L/br = 150 L/min 2. Relevant points: The relationship between VE and VO2 (or work rate) has two components. These are a linear rise followed by a curvilinear, accelerated increase in response to exercise work rates greater than than 65 to 75% of VO2 max (Fig. 19). Fig. 19. Relationship between increasing oxygen uptake (VO2) with aerobic exercise and minute ventilation (VE). Pg. 13 Prof. K.C. Kregel Exercise Physiology Lecture 2 B. Changes in VT and fb with exercise (Fig. 20): 1. Both increase linearly until heavy exercise 2. At heavy exercise intensities, VT plateaus and the increase in VE is met by a greater increase in respiratory rate (fb). Fig. 20. Changes in tidal volume (VT) and frequency of breathing (fb) as a function of increasing exercise intensity. C. Impact of aerobic training on VE responses (Fig. 21 below): 1. trained subjects have lower VE at a given submax VO2 2. A higher VE max is attained in trained subjects. Fig. 21. Relationship between increasing oxygen uptake (VO2) with aerobic exercise and minute ventilation (VE) in trained (T) and untrained (UT) subjects. D. Depth vs. rate of breathing: Breathing styles during aerobic exercise will vary; however, in trained individuals exercising at moderate intensities, most of the increase in VE will be due to an increase in VT (because of small increases in fb) Pg. 14 Prof. K.C. Kregel Exercise Physiology Lecture 2 E. Does VE limit work capacity? If you were to plot the increases in VO2 and VE during a progressive exercise test to maximal workloads, VO2 will reach a plateau (i.e., VO2 max). If exercise continues for a few additional minutes, VO2 remains constant but VE continues to rise due to the progressively increasing stimulus of anaerobic metabolites (primarily lactate). key point from these observations is that pulmonary ventilation does not limit maximal oxygen uptake. F. Ventilatory adjustments during exercise: There are several metabolic changes that occur during progressive increases in exercise intensity (Fig. 22). Note the changes in pattern in some of the variables, including blood gas concentrations, at the dark vertical line in the figure, which represents a stage termed the "anaerobic threshold" or "lactate inflection point." This inflection point typically occurs at VO2 max levels of 65 to 75% of VO2 max, and is postulated to be linked to the developing lactic acidosis at higher work loads as anaerobic glycolysis takes over more of the muscle energy supply. Fig. 22. Changes in respiratory “anaerobic threshold” and blood gas parameters with increasing intensity of exercise to VO2 max. VCO2 is the volume of expired CO2; PaO2 is the partial pressure of oxygen in arterial blood; P2CO2 is the partial pressure of carbon dioxide in arterial blood (modified from Berne et al.). VO2 (L/min) Pg. 15