Anatomy and Physiology Assignment

Investigation into the Acute Physiological Responses to Exercise

Introduction:

The body is continually responding to the demands made upon it by the individual and by the environment, in order to maintain a stable internal environment known as homeostasis.

The body functions best when body fluids, temperatures, and the chemical constitution of blood are at specific levels. Any change in the body’s internal environment usually prompts an immediate response in an attempt to address the balance. The internal regulatory systems of the body cause the changes that we experience before, during and after exercise. Short term, or acute physiological responses occur as a result of increased stress on the normal resting functions of the body, such as breathing, heart rate and blood pressure.

This investigation aims to assess the consequences of exercise on oxygen uptake and heart rate of a specific subject, and to discuss how the homeostasis of the human body is affected by such changes.

Method

Have the subject complete a pre-test questionnaire.

Measure the subjects mass.

Measure resting blood pressure.

Fit a heart rate monitor and record resting heart rate.

Check that the ergometer and gas analysers have been calibrated.

Evacuate a ‘rack’ of Douglas bags.

Resting measurements should be taken with the subject seated on the bike or standing on the treadmill.

Have the subject place a mouthpiece and a nose clip on, and breathe quietly for one minute.

Open the valve on the first Douglas bag and collect expired air for six minutes.

Allow the subject to remove the mouthpiece.

Begin exercising the subject at an intensity they find easy (i.e. an unloaded basket) for four minutes. At two minutes and thirty seconds have the subject replace the nose clip and mouthpiece. Collect a one-minute expired air sample between three and four minutes. Record heart rate at the end of the fourth minute.

Method (continued)

The subject should continue to exercise at the next increment (0.3-0.5 kg added to the basket).

The subject should complete three exercise stages.

Analyse the contents of the Douglas bags and record the results.

Note the temperature of the expired air and barometric pressure.

Enter the data into the BBC computer and record the results.

Identify oxygen uptake from your data.

Perform the experiment on at least one subject, but do two if time allows.

Results:

(Graph 1)

(Graph 3)

Results:

Graph 1:

Information from this line graph shows a definite positive correlation between exercise intensity and heart rate. The graph shows that, as exercise intensity increases, there is also a marked, steady increase in the standard deviation of heart rate. Therefore the first noticeable acute physiological response to exercise, is that of increased heart rate.

Graph 2:

This graph quite simply shows the average mass among the subjects used in the laboratory investigation. This is important to give some sort of an understanding of how weight might influence the results achieved in the laboratory.

Graph 3

This is probably the most important graph and set of results, as they portray, very accurately, how the human body is adapting to physiological pressures, and what sort of response arises. The graph, as whole, looks at volume of air expired, volume of Oxygen uptake and also the volume of Carbon Dioxide output, and from this, the expiratory exchange ratio is calculated.

The findings show that, as exercise intensity increases, the body responds by increasing Oxygen uptake, Carbon Dioxide output, and the volume of air expired. Also, the Respiratory Exchange Ratio (RER) increases to cope with the demand of respiration and gaseous exchange between the blood and the tissues. It is possible to calculate from the RER the energy substrate used during the exercise. You can see from the table of data for graph 3, that the RER changed to adapt to each exercise intensity. At resting, RER was equal to a ratio of 0.70, increasing to a ratio of 0.98 during high intensity stage 3 exercise.

At rest, the average volume of expired air (VEstpd) was approximately 16.00 l/min, and as the exercise intensity progressed, the value increased to 50.30 l/min at stage 1 of exercise, at stage 2, the value was recorded as 64.86 l/min, this further increased to a value of 79.12 l/min. It is important to note the increase between each intensity for discussion later on.

The volume of Oxygen (O2) uptake between the same exercise intensities also increased, from 7 ml/kg/min to 45.05 ml/kg/min, similarly, the volume of Carbon Dioxide (CO2) output increased, although not in as great quantity as Oxygen uptake, but still quite important. Levels of CO2 output increased from 0.46 ml/kg/min, during rest, to 3.50 ml/kg/min, during stage 3 high intensity exercise.

Discussion:

During exercise blood flow needs to increase to meet the increasing demands for oxygen and energy substrate, as well as to remove waste products and toxins which build up as a biproduct of glucose breakdown for energy.

Even before you start to exercise, you will begin to experience an anticipatory rise in heart rate, caused due to the release of adrenaline and the impact of emotional excitement on the medulla of the brain.

The heart’s conduction system is composed of specialised cardiac muscle. This system includes the sinoatrial node and the atrioventricular node.

The sinoatrial (SA) node is a small mass of specialised muscle in the posterior wall of the right atrium. The SA node is known as the pacemaker of the heart because it automatically excites itself and starts each heart beat.

The SA node also consists of fibres, which fuse with the cardiac muscle fibres of the atrium; this allows muscle impulse to spread through the atria, producing atrial contraction. One group of atrial muscle fibres conducts the impulse directly to the atrioventricular (AV) node, located in the right atrium along the lower part of the septum. Here, transmission is delayed briefly. This delay allows the atria to complete their contraction before the ventricles begin to contract.

From the AV node the muscle impulse spreads into specialised muscle fibres that form the atrioventricular (AV) bundle. The AV bundle divides into right and left bundles, which extend into the right and left ventricles. Fibres of the AV bundle end on ordinary cardiac muscle within the myocardium, allowing the impulse to spread through the ordinary muscle fibres of the ventricles. The cardiac muscle fibres are joined together by intercalated discs; allowing impulses to spread rapidly from cell to cell.

The continual adjustment of heart rate is controlled by the sympathetic and parasympathetic nervous systems, these originate within the cardiovascular centre (CVC) in the medulla oblongata. It is also important to note that they work antagonistically. Under conditions of stress, sympathetic nerves can increase the contraction as much as 100%. Under more calm conditions, the vagus nerve, a parasympathetic nerve, slows the heart; the balance between the sympathetic and parasympathetic nerve stimulations determines the heart rate.

The endocrine system also helps regulate the heart rate. During stress, epinephrine and norepinephrine released from the adrenal medulla speed the heart rate. Increased body temperature, whether it results from strenuous exercise or fever, also increases heart rate. During vigorous exercise a normal heart can beat as many as 200 times per minute, increasing it’s output 4 to 5 times. The CVC responds to exercise by increasing the activity of the sympathetic nerve acting on the sinoatrial node of the heart, causing an increase in heart rate, it can therefore be assumed that exercise is closely related to an increase in heart rate.

As shown in graph 1, heart rate increased with increasing exercise intensities.

The CVC increases both heart rate and stroke volume in response to exercise. This may be facilitated by the release of adrenaline. As adrenaline increases heart rate and the strength of cardiovascular contraction, stroke volume of the heart is also increased. As blood carries oxygen, cardiac output will determine oxygen delivery and availability to the tissues of the body and as the demand for oxygen increases in response to exercise, therefore delivery must increase.

During exercise more blood is returned to the heart (venous return), due to increased blood flow around the body, this increased venous return then causes an increase in the preload of the ventricles, causing them to hold more blood, this combined with a greater strength of contraction, results in an increase in stroke volume. The raised heart rate and increased stroke volume causes an overall increase in cardiac output and blood pressure, allowing more oxygen to be delivered to the muscles, and also allowing the products of respiration to be removed. Vasoconstriction and vasodilation of arteries occur in a process of shifting and directing blood from non-vital areas to working muscles and lungs. During exercise, vasoconstriction occurs at arteries directed towards organs such as kidneys, intestines and the liver, meaning that blood flow is reduced to these areas, simply by reducing the cross-sectional area of the artery, this allows the blood to moved to somewhere else in the body. At the same time vasodilation occurs at arteries directed towards the working muscles and vital organs, here the cross-sectional area of the arteries increase, allowing more blood to flow through to the muscles and to other vital areas such as the lungs.

The basic rate and depth of respiration is controlled from the respiratory centre in the medulla of the brain. This centre is divided into three main areas:

The medullary rhythmicity area indicates the basic rate of respiration. There are two main types of neurons (inspiratory and expiratory) which carry impulses from this area to the muscles involved in respiration. During quiet respiration, both the inspiratory and expiratory neurons are inactive during expiration, this occurs passively due to the relaxation of the involved muscles and the elastic recoil of the lungs. However, during forced ventilation, the expiratory and inspiratory neurons become active, carrying impulses to the muscles of expiration and inspiration causing an increase in lung volume and minute ventilation (number of breaths per minute), expiration becomes an active process.
The pneumotaxic area has an inhibitory influence on inspiration. As the lungs fill with air, the pneumotaxic centre transmits inhibitory impulses to the inspiratory centre to stop its activity, allowing muscle relax and expiration to occur.

The apneustic area sends stimulatory messages to the inspiratory centre to prolong inspiration.

Other factors can modify the basic rhythm set by the respiratory centre:

The cerebral cortex can exert voluntary control over respiration, this is important as we can voluntarily stop breathing to prevent water or irritating gases entering our lungs.
Stretch receptors in the wall of the bronchi and bronchioles are stimulated when the lungs become over inflated; impulses are then sent to the inspiratory centre, which inhibit its activity and allow expiration to occur. This is also known as the Hering-Breuer reflex.

Chemoreceptors, which are sensitive to the concentration of hydrogen ions (H+), carbon dioxide (CO2) and oxygen (O2) in the blood are situated in the carotid arteries (carotid bodies) and the aortic arch (aortic bodies). Any increase in CO2 will cause an increase in H+, which will stimulate the Chemoreceptors to send impulses to the respiratory centre to increase the rate and depth of respiration. This will remove more CO2 until the levels are back to normal, in which the partial pressure of carbon dioxide (pCO2) is 40 mmHg. Low levels of CO2, below40 mmHg, will decrease respiratory stimulation and may result in a slow rate of respiration. The Chemoreceptors are also sensitive to decreases in the partial pressure of oxygen (pO2), but to only considerably large changes. The normal partial pressure of oxygen value is 105 mmHg, only when this decreases to 50 mmHg are the chemoreceptors stimulated.
Proprioceptors in the muscles and joints are thought to stimulate the respiratory centre to increase the rate and depth of breathing immediately upon commencing exercise, even before carbon dioxide and oxygen levels have changed, it is thought that proprioceptors detect changes in temperature as well as bodily movements associated with exercise.

At rest, the average volume of oxygen consumed (VO2) was 0.5 l/min, during maximal exercise this can increase to a value anywhere between 3-6 l/min, this is the maximum amount of oxygen a person can utilize, also known as VO2 MAX. VO2 MAX depends on the efficiency of the cardiovascular and respiratory systems.

The volume of expired air (VEstpd) has, at rest, changed from 16.00 l/min to 79.12 l/min at stage 3 intensity exercise. This acute response is directly associated to exercise, and as the intensity of the exercise increases, so to does the response.

Maximal exercise can cause O2 utilisation and CO2 production to increase some 20-fold, however, from our set of results the increase was not as significant due to a submaximal intensity. Never the less, the results were sufficient to prove that their increase was due to exercise. However, the exact mechanisms for the enhanced ventilation can not be associated with one factor alone, it is thought that the combined acute responses shown from the chemoreceptors, proprioceptors and the respiratory centre in the medulla of the brain, constitute the changes in lung ventilation.

It is commonly known that the cardiovascular and respiratory systems work together, ensuring that an adequate oxygen supply to the working muscles is maintained. The capacities at which these systems operate depend largely upon exercise intensity, duration and the type of activity being performed, whether it is aerobic or anaerobic activity.

By looking at the respiratory exchange rate (RER), it is possible to calculate the energy substrate used. An RER value of 0.7 to 0.8 indicates that the energy substrate used was lipids and fatty acids. The use of this substrate requires a lot of oxygen, it is usually only used when the body is in rest and can afford use a lot of oxygen. During physical stress or exercise, the body cannot afford enough oxygen for the use of this substrate, the RER value in this state is usually 0.9 to 1.0, indicating that the energy substrate used is now carbohydrate, this is more readily broken down than lipids or fats, allowing a quick and ready supply of energy.

The RER value is useful in determining the energy substrate used for individual sports events, this information can then be used to the advantage of the performer or athlete when preparing for events, especially the case for athletics or marathon running.

BIBLIOGRAPHY

Solomon, E. P., Schmidt, R., Adragna, P.J. (1990) Human Anatomy and Physiology, Harcourt Brace College publishers.

Tortora, G.J. (1996) Introduction to Anatomy and Physiology. Menlo Park, Ca: Benjamin Cummings.

McArdle, W.D., Katch, F.I., & Katch, V.L. (1997) Exercise Physiology. Philadelphia Pa: Williams & Wilkins.