The heart is an organ which pumps blood, which in turns carries oxygen and nutrients to the cells of the body and transports away the waste products such as carbon dioxide, lactic acid etc.
Cardiac Output
CO is defined as the volume of blood pumped by the heart in one minute, and is expressed in liters per minute or milliliters per minute. CO is the product of heart rate times stroke volume (the amount of blood pumped with each beat of the heart). For example if HR equals 72 beats per minute and stroke volume equals 70 ml of blood, then the CO is equal to 5,040 ml/min or 5.04 lts./min (72x70). CO can also be calculated from the amount of oxygen consumed per minute and the amount of oxygen taken up by the blood as it flows through the lungs. These relationships can be expressed by the Fick principle as follows:
For example if the oxygen content of the venous blood entering the lings is 16 volumes percent, that of the arterial blood leaving the lungs is 20 volumes percent and the oxygen consumption of the body 200 ml per minute, the amount of oxygen used per minute equals the amount of oxygen taken up by the lungs per minute. From the above data it can be seen that each 100 ml of blood flowing through the lungs picks up 4 ml of oxygen. Since the total amount of oxygen absorbed into the blood from the lungs each minute is 200 ml, then a total of fifty 100 ml portions of blood must flow through the lungs each minute to absorb this amount of oxygen. Thus the cardiac output is
The blood samples to measure the oxygen content by the Fick's procedure is taken by Cardiac catheterization and the oxygen consumption rate is measure by a respirometer apparatus.
Another method used to measure CO is the dye dilution method. Other methods include the carbon dioxide rebreathing test and radioisotope test.
It should be pointed out that Fick technique is considered most accurate to measure the CO under resting or steady state conditions of exercise, while CO in rapid changing conditions the dye dilution technique is more accurate.
Cardiac Output during rest
At rest in the supine position, the normal cardiac output in adults is approximately 5 liters per minute. This is generally achieved with a heart rate of 70beats per min for the untrained and 45 beats per min for endurance trained person. Since the trained person’s cardiac output at rest is also about 5 lits, then the decrease in heart rate must be offset by an increased in stroke volume if the cardiac output formula, the calculated stroke volume for the untrained person would be around 71.4 ml of blood per beat, whereas the stroke volume for the untrained person would be about 111.1 ml per beat.
Cardiac Output during exercise
During exercise upto 40 to 60 percent of maximal capacity, cardiac output in trained athletes may be increased to 40 lts per min. At this level of work, it is known that this 5-7 fold increase in cardiac output is due to increases in both heart rate and stroke volume. At levels beyond 40 to 60 percent of maximum, increases in cardiac output are mainly a function of heart rate increases. At the same time, it should be emphasized that since heart rate in strenuous exercise increases approximately the same in both athletes and non athletes, the greater changes in cardiac output attained by the trained athletes is due to their greater ability for increasing the stroke volume of the heart. This is more than double the size of the stroke volume for untrained subjects. Again substituting the heart rate values in the cardiac output formula, the calculated stroke values for the untrained person would be around 100 ml of blood per beat, whereas the stroke volume for the trained person would be approximately 200 ml per beat.
The regulation of cardiac output involves the regulation of heart rate and stroke volume.
Heart rate
The impulse that causes the heart to contract rhythmically originates within the heart muscle itself, in the right atrium known as the pacemaker or S-A node. Unlike skeletal muscles, the heart muscle possesses autorhythmicity. However both the nervous and chemical factors are involved in the regulation of the heart rate during rest and exercise.
The autonomic nervous system which supplies the parasympathetic or vagus nerves and the sympathetic nervous system or the accelerator nerves to the S-A node plays an important role in regulating heart rate.
Stimulation of the parasympathetic fibers cause the release of acetylcholine (Ach) from their ends, which slows the rate of impulse formation in the S-A node and also slows the rate of conduction through the A-V bundle which slows the impulse into the ventricles. Such impulses are cardio-inhibitory and the final result is a slower heart rate.
Stimulation of the sympathetic fibers causes the release of norepinephrine from their ends. The norepinephrine speeds up both the S-A node rates and the conduction rates. Such impulses are called cardio-acceleratory which results in a faster and stronger heart rate.
This different effect of the two nerves is referred to as reciprocal innervation of the heart muscle.
The nerves controlling the heart arise from specific areas of the medulla of the brain called cardio-inhibitory and cardio-acceleratory centers, the control of the heart rate is predominantly through reflexes.
The cardio-acceleratory centers are affected by several afferent stimulation sources which are referred to as pressor. They are
(i) proprioceptive reflexes originating in the working muscles and joints to contribute to increases in heart rate.
(ii) impulses arising in the chemoreceptors of the carotid body and the aortic body as a result of decreased pH or increased carbon dioxide results in an increased heart rate.
(iii) impulses arising in the adrenal medulla cause a discharge of norepinephrine and epinephrine hormones into the blood stream and an increase in heart rate.
The cardio inhibitory or depressor afferent sources are from the activity of the stretch receptors in the carotid sinus and the aortic arch. The activities from these receptors tend to slow the heart rate down.
Two other factors that are important are an increase in body temperature and a fall in the blood oxygen content, also play a large role in the increased heart rate.
Heart Rate Response to Exercise
Heart rate increases linearly with increasing oxygen consumption in both the trained and untrained individuals. During exercise the heart rate of a well trained person is consistently lower at any given workload or Vo2 than that of the untrained person
Endurance training also tends to lower maximal HR from about 200 to around 185 to 190 beats per minute. That this rate tends to lower with exercise means that since training also increases work capacity (and max Vo2), maximal HR in trained individuals are obtained at relatively higher workloads and Vo2 levels than in untrained subjects.
Endurance training also tends to lower the resting heart rate (bradycardia). For example the resting HR in highly trained athletes may be as low or lower that 40 to 45 beats per minute. On the other hand in healthy untrained subjects, the resting rates may be high as 90 to 100 beats per minute. Thus the trained is generally categorized as having a lower resting HR and the untrained as having a higher resting heart rate.
The highest attainable HR during performance of strenuous work not only depends upon the state of conditioning but also on age. For instance the maximum HR at the age of 20 is about 200 which is reduced to approximately 155 at the age of 70. This is one of the biological changes which comes with old age.
The type of exercise also influences the increase in HR. For example, the greatest acceleration of the heart occurs in speed exercises like sprint running, whereas the smallest increase takes place in strength exercises such as weight training and throwing. In distance running the increase in HR is somewhere between sprint and strength activities.
Besides exercise and training, other factors which affect the HR are Posture, Sex, Age and Emotion and Environmental factors.
Stroke Volume (SV)
Stroke Volume response to exercise
The following graph clearly indicates that Stroke volume increases progressively from rest to moderate work and then it levels off at about 30 to 40 percent of the maximum aerobic power. The dynamics of adjustment are the same in the trained and the untrained person. However the trained person operates at a higher level.
The trained athletes have a greater capacity for not only pumping more blood by the heart per beat, but they also have a greater capacity for extracting more oxygen from the blood into the muscle tissues than sedentary subjects.
The following figure illustrates the relationship between CO, SV and HR as a function of oxygen uptake. It shows that once SV reaches its maximum level (which is usually at a workload of 30 to 40 percent of maximum aerobic power, or at a heart rate of 110 to 120 beats per minute), any additional increases in CO are obtained only through increases in HR.
It should be noted that during maximum work when the HR may reach values as high as 200 beats per minute, the SV is generally at its maximum, which means that the time available for filling of the ventricles at heart rates up to 200 is sufficient to allow maximal stroke volumes.
At rest and in supine position the stroke volume of an adult untrained man is around 70 to 100 ml per beat depending on body size, while the maximal values may range between 100 to 120 ml per beat.
In trained adult men, the resting SV are around 100 to 120 ml per beat whereas maximal values may come up to 150 to 200 ml per beat.
Hence a relatively slow HR and a relatively large SV is characteristic of a trained person and denotes an efficient circulatory system.
In women due to the smaller size of the heart, their SV is usually 25% lower.
When assuming a sitting or standing position, since under the influence of gravity blood normally pools in the lower portions of the body, resulting in a drop in venous return to the heart, this may result in about 30% reduction in SV.
There is a definite relationship between maximum aerobic work and CO and that SV to a large extent limits CO. Since nearly everyone has about the same maximum HR levels, it is generally agreed among exercise physiologists that SV is the difference between an individual with a large cardiac output and one with only a normal output.
Cardiac Output
CO is defined as the volume of blood pumped by the heart in one minute, and is expressed in liters per minute or milliliters per minute. CO is the product of heart rate times stroke volume (the amount of blood pumped with each beat of the heart). For example if HR equals 72 beats per minute and stroke volume equals 70 ml of blood, then the CO is equal to 5,040 ml/min or 5.04 lts./min (72x70). CO can also be calculated from the amount of oxygen consumed per minute and the amount of oxygen taken up by the blood as it flows through the lungs. These relationships can be expressed by the Fick principle as follows:
For example if the oxygen content of the venous blood entering the lings is 16 volumes percent, that of the arterial blood leaving the lungs is 20 volumes percent and the oxygen consumption of the body 200 ml per minute, the amount of oxygen used per minute equals the amount of oxygen taken up by the lungs per minute. From the above data it can be seen that each 100 ml of blood flowing through the lungs picks up 4 ml of oxygen. Since the total amount of oxygen absorbed into the blood from the lungs each minute is 200 ml, then a total of fifty 100 ml portions of blood must flow through the lungs each minute to absorb this amount of oxygen. Thus the cardiac output is
The blood samples to measure the oxygen content by the Fick's procedure is taken by Cardiac catheterization and the oxygen consumption rate is measure by a respirometer apparatus.
Another method used to measure CO is the dye dilution method. Other methods include the carbon dioxide rebreathing test and radioisotope test.
It should be pointed out that Fick technique is considered most accurate to measure the CO under resting or steady state conditions of exercise, while CO in rapid changing conditions the dye dilution technique is more accurate.
Cardiac Output during rest
At rest in the supine position, the normal cardiac output in adults is approximately 5 liters per minute. This is generally achieved with a heart rate of 70beats per min for the untrained and 45 beats per min for endurance trained person. Since the trained person’s cardiac output at rest is also about 5 lits, then the decrease in heart rate must be offset by an increased in stroke volume if the cardiac output formula, the calculated stroke volume for the untrained person would be around 71.4 ml of blood per beat, whereas the stroke volume for the untrained person would be about 111.1 ml per beat.
Cardiac Output during exercise
During exercise upto 40 to 60 percent of maximal capacity, cardiac output in trained athletes may be increased to 40 lts per min. At this level of work, it is known that this 5-7 fold increase in cardiac output is due to increases in both heart rate and stroke volume. At levels beyond 40 to 60 percent of maximum, increases in cardiac output are mainly a function of heart rate increases. At the same time, it should be emphasized that since heart rate in strenuous exercise increases approximately the same in both athletes and non athletes, the greater changes in cardiac output attained by the trained athletes is due to their greater ability for increasing the stroke volume of the heart. This is more than double the size of the stroke volume for untrained subjects. Again substituting the heart rate values in the cardiac output formula, the calculated stroke values for the untrained person would be around 100 ml of blood per beat, whereas the stroke volume for the trained person would be approximately 200 ml per beat.
The regulation of cardiac output involves the regulation of heart rate and stroke volume.
Heart rate
The impulse that causes the heart to contract rhythmically originates within the heart muscle itself, in the right atrium known as the pacemaker or S-A node. Unlike skeletal muscles, the heart muscle possesses autorhythmicity. However both the nervous and chemical factors are involved in the regulation of the heart rate during rest and exercise.
The autonomic nervous system which supplies the parasympathetic or vagus nerves and the sympathetic nervous system or the accelerator nerves to the S-A node plays an important role in regulating heart rate.
Stimulation of the parasympathetic fibers cause the release of acetylcholine (Ach) from their ends, which slows the rate of impulse formation in the S-A node and also slows the rate of conduction through the A-V bundle which slows the impulse into the ventricles. Such impulses are cardio-inhibitory and the final result is a slower heart rate.
Stimulation of the sympathetic fibers causes the release of norepinephrine from their ends. The norepinephrine speeds up both the S-A node rates and the conduction rates. Such impulses are called cardio-acceleratory which results in a faster and stronger heart rate.
This different effect of the two nerves is referred to as reciprocal innervation of the heart muscle.
The nerves controlling the heart arise from specific areas of the medulla of the brain called cardio-inhibitory and cardio-acceleratory centers, the control of the heart rate is predominantly through reflexes.
The cardio-acceleratory centers are affected by several afferent stimulation sources which are referred to as pressor. They are
(i) proprioceptive reflexes originating in the working muscles and joints to contribute to increases in heart rate.
(ii) impulses arising in the chemoreceptors of the carotid body and the aortic body as a result of decreased pH or increased carbon dioxide results in an increased heart rate.
(iii) impulses arising in the adrenal medulla cause a discharge of norepinephrine and epinephrine hormones into the blood stream and an increase in heart rate.
The cardio inhibitory or depressor afferent sources are from the activity of the stretch receptors in the carotid sinus and the aortic arch. The activities from these receptors tend to slow the heart rate down.
Two other factors that are important are an increase in body temperature and a fall in the blood oxygen content, also play a large role in the increased heart rate.
Heart Rate Response to Exercise
Heart rate increases linearly with increasing oxygen consumption in both the trained and untrained individuals. During exercise the heart rate of a well trained person is consistently lower at any given workload or Vo2 than that of the untrained person
Endurance training also tends to lower maximal HR from about 200 to around 185 to 190 beats per minute. That this rate tends to lower with exercise means that since training also increases work capacity (and max Vo2), maximal HR in trained individuals are obtained at relatively higher workloads and Vo2 levels than in untrained subjects.
Endurance training also tends to lower the resting heart rate (bradycardia). For example the resting HR in highly trained athletes may be as low or lower that 40 to 45 beats per minute. On the other hand in healthy untrained subjects, the resting rates may be high as 90 to 100 beats per minute. Thus the trained is generally categorized as having a lower resting HR and the untrained as having a higher resting heart rate.
The highest attainable HR during performance of strenuous work not only depends upon the state of conditioning but also on age. For instance the maximum HR at the age of 20 is about 200 which is reduced to approximately 155 at the age of 70. This is one of the biological changes which comes with old age.
The type of exercise also influences the increase in HR. For example, the greatest acceleration of the heart occurs in speed exercises like sprint running, whereas the smallest increase takes place in strength exercises such as weight training and throwing. In distance running the increase in HR is somewhere between sprint and strength activities.
Besides exercise and training, other factors which affect the HR are Posture, Sex, Age and Emotion and Environmental factors.
Stroke Volume (SV)
Stroke Volume response to exercise
The following graph clearly indicates that Stroke volume increases progressively from rest to moderate work and then it levels off at about 30 to 40 percent of the maximum aerobic power. The dynamics of adjustment are the same in the trained and the untrained person. However the trained person operates at a higher level.
The trained athletes have a greater capacity for not only pumping more blood by the heart per beat, but they also have a greater capacity for extracting more oxygen from the blood into the muscle tissues than sedentary subjects.
The following figure illustrates the relationship between CO, SV and HR as a function of oxygen uptake. It shows that once SV reaches its maximum level (which is usually at a workload of 30 to 40 percent of maximum aerobic power, or at a heart rate of 110 to 120 beats per minute), any additional increases in CO are obtained only through increases in HR.
It should be noted that during maximum work when the HR may reach values as high as 200 beats per minute, the SV is generally at its maximum, which means that the time available for filling of the ventricles at heart rates up to 200 is sufficient to allow maximal stroke volumes.
At rest and in supine position the stroke volume of an adult untrained man is around 70 to 100 ml per beat depending on body size, while the maximal values may range between 100 to 120 ml per beat.
In trained adult men, the resting SV are around 100 to 120 ml per beat whereas maximal values may come up to 150 to 200 ml per beat.
Hence a relatively slow HR and a relatively large SV is characteristic of a trained person and denotes an efficient circulatory system.
In women due to the smaller size of the heart, their SV is usually 25% lower.
When assuming a sitting or standing position, since under the influence of gravity blood normally pools in the lower portions of the body, resulting in a drop in venous return to the heart, this may result in about 30% reduction in SV.
There is a definite relationship between maximum aerobic work and CO and that SV to a large extent limits CO. Since nearly everyone has about the same maximum HR levels, it is generally agreed among exercise physiologists that SV is the difference between an individual with a large cardiac output and one with only a normal output.
