Exercise Physiology

Maxwell Kruse 4/11/13 Bio 473 Section 008 TA: Nathan Garvin

Introduction During exercise, the rate and strength of skeletal muscle contractions are increased, which subsequently results in an elevated metabolism. Skeletal muscle contraction requires ATP to perpetuate the continued binding and unbinding of myosin-actin cross bridges. When exercise begins, muscle contraction is initially powered by the small amount of ATP stored in skeletal muscle fibers. These ATP reserves, however, can only sustain intense exercise for about 15 seconds. Thus, after a short time the bodys metabolism must increase to produce the additional ATP required for muscle contraction. Aerobic pathways produce ATP most efficiently, and are therefore the primary source of ATP during exercise. Consequently, aerobic exercise increases the bodys requirement for oxygen as well as its need to remove CO2, a waste product of the aerobic metabolism. The physiological response to exercise incorporates multiple body systems which act in coordination to meet these needs, as well as to maintain homeostasis of body temperature and blood pressure. During this experiment, three subjects were monitored as they ran on a treadmill in an attempt to analyze their physiological response to aerobic exercise. Exercise results in an increased rate and depth of breathing, which corresponds to enhanced oxygen delivery and CO2 removal from the bodys tissues. Immediately after exercise begins, ventilation rate increases. This occurs even before arterial PCO2 has increased or PO2 has decreased, due to feedforward responses from stretch sensitive proprioreceptors located in in skeletal muscles, joints, and tendons. These sensory neurons are stimulated by the increased movement associated with exercise, and signal to the motor cortex that this movement is occurring. The motor cortex subsequently relays these signals to the respiratory control center in the medulla, which then acts to elicit and immediate increase alveolar ventilation. With prolonged exercise, chemoreceptors act in coordination with proprioceptors to regulate hypernea, the hyperventilation that occurs with increased metabolism. Central chemoreceptors in the medulla monitor the pH of the cerebrospinal fluid, while peripheral carotid and aortic chemoreceptors monitor plasma PCO2, PO2, and pH. As oxygen consumption and CO2 production increase with increased aerobic metabolism, chemoreceptors sense these changes and signal to the respiratory control center to increase ventilation in order to prevent changes in the blood PCO2, PO2, and pH. These reflexes modulate alveolar ventilation to meet the increasing needs of exercising tissues as exercise intensity increases. It was therefore hypothesized that the oxygen consumption and CO2 clearance of each subject would increase immediately as the subjects began to exercise, and would continue to increase as the intensity of the exercise was

increased. It was also expected that O2 consumption and CO2 clearance would then decrease as the subjects recovered from exercise. In addition, it was expected that hemoglobin saturation would decrease slightly during exercise due to the increased rate of oxygen consumption by the exercising tissues. Cardiovascular function is altered in coordination with the respiratory system to deliver oxygenated blood to exercising tissues as well to increase venous return for CO2 removal. During exercise, mechanoreceptors and proprioceptors in the extremities send information of increased movement to the cardiovascular control center (CVCC) of the medulla. The CVCC reacts by inhibiting its parasympathetic output and increasing its sympathetic output. This increase in sympathetic activity increases heart rate and contractility, which ultimately results in an increased cardiac output to enhance delivery of oxygenated blood to exercising tissues, and removal of CO 2 waste. While this increase in sympathetic discharge by the CVCC causes vasoconstriction in most peripheral arterioles, blood flow to skeletal muscle actually increases with exercise. This is because the increased metabolism of the exercising muscle results in a local decrease in O2 concentrations and increases in CO2 concentrations, both of which act as paracrine vasodilators. The combination of generalized vasoconstriction of peripheral arterioles and local vasodilation in the arterioles within skeletal muscle functions to direct more blood flow towards the exercising tissues. Blood pressure also increases with exercise. The vasodilation that occurs in intramuscular arterioles exceeds the vasoconstriction caused by increased sympathetic output, resulting in a net decrease in peripheral resistance. However, this decrease in peripheral resistance is accompanied by a relatively large increase in cardiac output as previously described. Collectively, the increase in cardiac output and slight decrease in peripheral resistance bring about a slight increase in mean arterial blood pressure (MAP) during exercise (MAP = C.O. x peripheral resistance). Thus it was expected that heart rate and MAP would increase as the intensity of exercise increased. The increase in metabolism that occurs with exercise causes an increase in heat production raise body temperature ell above hich threatens to

. Sweating and dilation of cutaneous blood vessels are the primary responses

that resist changes in body temperature during exercise. Sweating acts to promote heat loss via evaporative cooling, and therefore resists increases in body temperature. Thermoreceptors in the hypothalamus and skin monitor body temperature, and control cutaneous blood flow via sympathetic pathways. When body temperature increases during exercise, the hypothalamus activates sympathetic cholinergic neurons that innervate cutaneous arterioles with

acetylcholine; this results in vasodilation of cutaneous arterioles. As a result, blood is able to flow closer to the skin, and heat can be lost to the environment. Although these processes are effective in preventing drastic deviations from a safe body temperature of strenuous e ercise enerally still results in an increase in temperature. For that

reason, body temperature was expected to increase for each subject during exercise. Studies such as this one that attempt to better understand the physiological processes involved with exercise provide valuable information that is applicable to a number of clinical settings. Measurements such as O2 consumption and MAP indicate an athletes level of physical fitness, and are used to track improvement throughout a trainin pro ram. Moreover stress tests are often carried out to measure the degree to which a person can exert themselves before risking cardiovascular failure. Information obtained with experiments that elucidate the normal mechanisms responsible for maintaining homeostasis during exercise, can also be used to understand how the body responds to patholo ical conditions. In conclusion the bodys ability to e ert itself durin e ercise depends on the integration of many different body systems. The study of exercise physiology is essential to understanding how these systems function, and can be used prevent disease, promote healthy behavior, and improve upon athletic performance. Methods Throughout this experiment, three subjects were monitored while resting, while running on a treadmill, and while recovering from e ercise. Prior to the e periment each subjects a e hei ht ei ht ender restin heart rate and

smokin habits ere recorded; this information as used to calculate each subjects e ercise heart rate (80% of their maximal heart rate). A heart rate monitor as used to measure the subjects heart rate. Heart rate, tidal volume, respiratory rate, concentration of O 2 in exhaled air, body temperature, hemoglobin saturation, and blood pressure were measured during this experiment. A spirometer was used to measure the subjects tidal volume, respiration rate was observed and counted, an oxygen analyzer was utilized to measure exhaled O 2 concentration, temperature was taken orally with a thermometer, and blood pressure was measured with a sphygmomanometer. A pulse o imeter as also used to measure the hemo lobin saturation of each subjects blood. Resting data for each of these measurements was collected twice prior to the beginning of the experiment, after subjects had been sitting for 0 minutes and then again after sitting for 3 minutes. These resting data served as controls.

Exercising data collection began 3 minutes after a subject had run at 5 mph, 0 degree incline. Exhaled O2 concentration, heart rate, and tidal volume were measured during the last 45 seconds of each 3-minute exercising period while subjects continued to run. The degree of incline was increased every three minutes after data collection as follows: 0 deg, 3 deg, 6 deg, 10 deg. Subjects exercised until their respective exercising heart rate was reached. At this point the exercise was terminated; the treadmill was stopped, and the hemoglobin, blood pressure, and body temperature data were collected immediately after subjects stopped running. After these final exercising data were collected, the subjects began to recover from exercise by walking at 2 mph on a 0 degree incline. After 3 minutes of walking at this pace, the treadmill was stopped and the first set of recovery data was taken while the subjects were sitting. The subjects then sat for 3 more minutes before the last set of recovery data was collected. After the experiment was completed, oxygen and MAP were calculated with the following equations: O2 consumption = (20.9% - % O2 of exhaled air) X tidal volume X resp. rate MAP = Diastolic Pressure + (1/3)(Systolic Pressure Diastolic Pressure)

Results Figure 1: The effect of exercise on heart rate over time

Heart Rate Vs. Time

250 Heart Rate (bpm) 200 150 100 50 0 0 5 10 15 20 25 Time (min) Figure 1 sho s ho each subjects heart rate as affected by varyin intensities of e ercise. Data collected at 0 and minutes represent the subjects restin heart rates. E ercisin heart rates are represented by the data bet een 6 and 15 minutes; the intensity of exercise was increased every 3 minutes throughout this 12 minute exercise period. The recovery heart rates were recorded at 18 and 21 minutes. The results of this e periment sho that each subjects heart rate increased as the intensity of exercise increased, as seen in Figure 1. The resting heart rates of the subjects ranged between 82 and 90 bpm. Subjects 1 and 3 both

exhibited rapid increases in heart rate from resting values to 156 bpm and 145 bpm respectively, after 3 minutes of running at 5 mph on a 0 degree incline. Subject 3, however, did not exhibit a noticeable increase in heart rate until 6 minutes of exercise were completed. After 6 minutes of exercise, the heart rates of all 3 subjects increased as exercise intensity increased (every 3 minutes treadmill incline was increased). Every subject reached or exceeded their respective exercising heart rate at minute 15 (after 12 minutes of exercise) while running at a 10 degree incline. At this maximal intensity exercise, heart rates were 193 bpm, 196 bpm, and 200 bpm, for subjects 1, 2, and 3 respectively. After exercising heart rate was reached, the exercising period was terminated and subjects began to recover by walking at 2 mph on a 0 degree incline. Heart rates decreased to 132 bpm, 159 bpm, and 129 bpm for subjects 1, 2, and 3 respectively during this recovery period. Heart rate then decreased again after minute 21 to rates between 109 and 134 bpm when subjects were allowed to recover while sitting for 3 minutes.

Figure 2: The effect of exercise on oxygen consumption over time

Oxygen Consumption vs. Time

Oxygen Consumption (l O2/min) 2.5 2 1.5 1 0.5 0 0 5 10 15 20 25 Time (min) Figure 2 depicts how O2 consumption changed with varying intensities of exercise. Resting O2 consumptions are represented by the data for minutes 0 and 3. Exercising O 2 consumptions are represented by the data collected between 6 and 15 minutes; the intensity of exercise was increased every three minutes for the entire 12 minute exercising period. O2 consumption data collected during minutes 18 and 21 represent recovery values for each subject. The data presented in Figure 2 indicates that for subjects 2 and 3 oxygen consumption increased with increasing intensity of exercise. This trend, however, was not seen for subject 1. Subjects 2 and 3 exhibited resting O2 consumptions that ranged from to 0.11-0.12 l O2/min and 0.04-0.17 l O2/min respectively, while subject 1 had a higher resting O2 consumption that ranged between 0.28-0.36 l O2/min. After exercising for 3 minutes at minimal intensity, the O2 consumption of subjects 2 and 3 increased to 1.01 l O2/min and 0.43 l O2/min respectively. Oxygen consumption continued to increase for subjects 2 and 3 as intensity of exercise was increased; subject 2 displayed a maximal O2 consumption of 1.66 l O2/min, and Subject 3 had a maximal consumption of 2.37 l O2/min. Although

Subject 1 had a higher resting O2 consumption, their exercising O2 consumptions were observed to be lower than subjects 2 and 3. Subject 1 exhibited a decrease in O2 consumption after exercise was initiated, and then showed only a small increase in O2 consumption as exercise intensity increased, reaching a maximal consumption rate of 0.49 l O2/min. Once the subjects were allowed to recover, all subjects exhibited a decrease in oxygen consumption while walking at 2 mph at a 0 deg incline. Subjects then displayed a small increase in oxygen consumption at minute 21, after sitting for 3 minutes.

Table 1: The effect of exercise on body temperature Body Time (min) 0 3 15 18 Activity Level Resting Resting After Exercise Recovery Subject 1 36.3 36.3 35.9 36.2 Subject 2 36.2 35.3 34.9 35.9 Subject 3 35.8 36.5 34.2 35.9 Average 36.1 36.0 35.0 36.0

21 Recovery 36.4 36.4 34.5 35.8 Table 1 displays body temperature results taken before exercise, after 12 minutes of exercise, and during recovery for all subjects as ell as an avera e of the subjects body temperature results . Body temperatures observed for minutes 0 and 3 represent resting values. The body temperature shown for minute 15 represents the body temperature measured after the 12 minute exercise period. Body temperatures shown for minutes 18 and 21 represent the body temperatures measured during recovery. As shown in Table 1, there was a slight decrease observed in body temperature after exercise for all three subjects. The average resting body temperature of the subjects was about 6 drop in avera e body temperature to recovery to about 6 . . After minutes of e ercise there as a sli ht

. Avera e body temperature of the three subjects then increased a ain after

verall ho ever body temperature remained relatively constant.

Table 2: The effect of exercise on hemoglobin saturation Hemoglobin Saturation (%) Time (min) 0 3 15 18 Activity Level Resting Resting After Exercise Recovery Subject 1 99 98 95 95 Subject 2 98 98 94 95 Subject 3 96 96 93 97 Average 97.7 97.3 94 95.7

21 Recovery 96 96 96 96 Table 2 shows how hemoglobin (Hb) saturation changed after exercise. The percent of Hb saturated with oxygen is shown while resting, immediately after 12 minutes of exercise, and during recovery for each subject. Average Hb saturation values of all three subjects are shown in addition to the individual Hb saturation values.

The results obtained with this experiment indicate that for all three subjects hemoglobin (Hb) saturation decreased after exercise; this is depicted in Table 2. The average resting Hb saturation ranged between 97.7% - 97.3%. Average Hb saturation decreased to 94% after exercise, and then increased again to about 95.7-96% during recovery. Table 3: The effect of exercise on blood pressure Mean Arterial Blood Pressure (mmHg) Time (min) 0 3 15 18 Activity Level Resting Resting After Exercise Recovery Subject 1 107 103 107 113 Subject 2 113 113 110 110 Subject 3 92 97 107 97 Average 104 104.3 108 106.7

21 Recovery 110 110 97 105.7 Table 3 shows how mean arterial blood pressure was affected by exercise. Mean arterial blood pressures are shown for each subject while resting, after exercise, and during recovery. Averages of these mean arterial blood pressures for the three subjects are also depicted. The data shown in Table 3 indicate that the average mean arterial blood pressures (MAP) of the subjects increased slightly after exercise. After exercise the average MAP increased from about 104 mmHg (resting) to 108 mmHg. The average MAP of the three subjects then decreased after recovering while walking to 106.7 mmHg, and then decreased again to 105.7 mmHg after recovering while sitting. The MAP values for the individual subjects, however, did not exhibit an obvious trend. Subject 1s MAP actually increased after recoverin from e ercise and Subject s MAP decreased after exercise when compared to the resting MAP. Overall, there was not a clear trend observed in the mean arterial blood pressures of each subject as activity levels changed. Discussion With this experiment three subjects were monitored while resting, throughout various intensities of exercise, and during recovery; measurements were taken throughout this experiment to assess ho the bodys physiolo y as affected by exercise. The data depicted in Figures 1 and 2 indicate that heart rate and oxygen consumption both increased with increasing exercise intensity, and then decreased again after recovery as expected. This is because as the intensity of exercise increased, aerobic metabolism increased thus increasin the bodys need for o y en. When the Subjects started to run on the treadmill, proprioreceptors throughout the body sensed an increase in movement of the limbs and sent this information to the medulla which subsequently initiated an increase in ventilation and heart rates. In addition, central and peripheral chemoreceptors that monitor changes in pH of the CSF and PO2, PCO2, and

pH of the plasma respectively, and acted to further increase ventilation to meet the requirements of the body as the exercise became more strenuous. This integration of the respiratory and cardiovascular systems allowed the Subjects to increase delivery of oxygenated blood to exercising tissues and remove CO 2 waste as their aerobic metabolism increased with increasing treadmill incline. Although all the data collected for heart rate appeared to be strong, the data obtained for oxygen consumption did not appear to be accurate for Subject 1. Subject 1 showed an initial decrease in O2 consumption after the first 3 minutes of exercise, and then showed only a very slight increase in O 2 consumption for the remainder of the exercising period. These unexpected results are likely due to the fact that there was difficulty recording Subject s respiratory rate durin e ercise. In addition the spirometer was found to be leaking during data collection for Subject 1. Both of these errors would decrease the accuracy of the O 2 consumption calculation and could cause the apparent decrease in O2 consumption observed here. Therefore, the O2 consumption data for Subject 1 should be ignored. The data obtained for O2 consumption otherwise appeared strong however, and agreed with the initial hypothesis. It was hypothesized that Hb saturation of the blood would decrease after exercise due to the increased oxygen consumption of the exercising tissue, and then increase again during recovery. As seen in Table 2, the data obtained with this experiment support that hypothesis, and therefore appear to be strong. As aerobic metabolism increases to meet the energy needs of exercising tissue, tissue PO2 is reduced and the partial pressure gradient for diffusion of oxygen from blood to muscle is increased. Thus, more O2 is released from Hb during exercise, resulting in a reduced Hb saturation. Although the majority of the data for O2 consumption, heart rate, and Hb saturation were as expected, the data collected for body temperature and mean arterial pressure (MAP) were not. During exercise, much of the energy produced by the increased metabolism is lost as heat. Although sweating and increased cutaneous blood flow act as thermoregulatory responses to prevent major increases in body temperature during exercise, body temperature is known to typically increase during strenuous exercise. The data presented in Table 1 however, indicate that body temperature decreased after exercise for all three subjects, and consequently did not support the initial hypothesis. Although this may be due to the fact that the thermoregulatory response of the body was so strong that it actually decreased core body temperature, this is unlikely. The unexpected results obtained for body temperature after exercise are likely due to the fact that the temperature was taken orally. The increased air flow through the oral cavity

caused by hypernea after exercise may have increased the rate of evaporative cooling and convection in the mouth, leading to a reduced and inaccurate body temperature reading. It is also possible that blood flow was directed away from the mouth and towards exercising tissues, which would decrease the amount of heat released from the blood by convention to the oral cavity. The results obtained for body temperature after exercise could be made more accurate by measuring body temperature using a different type of thermometer such as a skin thermometer, or by measuring temperature of the underarm or anus rather than in the mouth. The increase in heart rate that occurs with exercise was expected to cause an increase in MAP. However, MAP was only expected to increase slightly after exercise because local changes in the microenvironment of exercising tissue act as paracrine signals triggering vasodilation of intramuscular arterioles; this functions to allow for hyperemia in the exercising muscle, but also functions to reduce the MAP raising effects of an increased heart rate. Although a slight increase in MAP was seen after exercise when the blood pressures of all 3 subjects were averaged, the MAP data for each individual subject did not follow any obvious trend; the MAP for subject 1 actually increased during recovery, and the MAP for subject 2 decreased after exercise. The data collected for MAP therefore did not appear to be strong. Due to the fact that subjects were breathing heavily and there was a significant amount of people talking while blood pressures were taken, it was difficult to obtain accurate blood pressure measurements. This reduced the accuracy of the MAP data, which could contribute to why these data did not provide strong support for the initial hypothesis. Perhaps taking blood pressure in a more quiet room or using measuring MAP electronically would have improved the accuracy of the results. Although unexpected data were obtained for temperature, O2 consumption for Subject 1, and MAP, these unexpected results were likely due to minor sources of error. Ultimately, this experiment was successful in analyzing the human bodys physiolo ical response during exercise of varying intensity. The data obtained here could be applied to a clinical settin to assess the fitness levels of each of the subjects. For e ample the fact that Subject 3 had the greatest O2 consumption at exercising heart rate, may indicate that this subject had the greatest capacity for endurance exercise. In addition, the novel finding that oral temperature decreased during exercise, may prove to have physiological significance; perhaps more heat was lost in the mouth in order to warm the increased volume of air that was inspired. Further research should be done to investigate this question, and additional trials of this same experiment could be conducted to improve the accuracy of the results.

10

References Biol. 473 E ercise Physiology Lab Manual, PSU, Bio 473 Laboratory Sp 2013. Biol. 4 Writin Guidelines for E ercise Physiolo y Reprot PSU, Bio 473 Laboratory Sp 2013.

Silverthorn, Dee Unglaub. "15 Blood Flow and the Control of Blood Pressure." Human Physiology An Integrated Approach - 6E. 6 ed. Glenview, IL: Pearson, 2013. 509-543. Print. Silverthorn, Dee Unglaub. "25 Exercise." Human Physiology An Integrated Approach - 6E. 6 ed. Glenview, IL: Pearson, 2013. 836-846. Print.

11