Give an account of the Sympathetic Nervous System and Intrinsic Essay

Topic: Give an account of the Sympathetic Nervous System and Intrinsic (auto-regulation) in Redirecting blood to Exercising Tissues

Description: Preferred language style: English (U.S.)

We Will Write a Custom Essay Specifically
For You For Only $13.90/page!


order now

As per the Topic and subject matter.  No deviation. Must be authentic.

Exercises seem to be a challenge to the circulatory system.  The skeletal muscles require large amounts of blood supply that have to be increased ruing physical activity.  In athletes who have well-trained, the cardiac output has to rise to 6 to 7 times that of normal, whereas in non-athletes it increases to 4 to 5 times that of normal (Guyton, 2006).

            At rest, two to four ml of blood flows through every 100 grams skeletal muscle on an average, every minute (Ganong, 2003).  In strenuous exercises (only in athletes who have well-trained) the blood flow can rise to 15 to 25 times that of normal to about 50 to 80 ml per minute for 100 grams of skeletal muscles, every minute (Guyton, 2006).

            A graph demonstrating the flow of blood through the calf muscles before exercises, during and after the exercises is demonstrated.  Strong leg exercises were performed for about six minutes.  The exercises that were performed were strenuous in nature.  As the muscular contractions were increased, the blood flow at that point of time decreased.  Usually, when muscles contract to more than 10 % of their maximal contraction capacity, they begin to exert some amount of pressure on the arteries that supply the blood.  The blood flow is completely ceased when the muscles contract to more than 70 % its maximum contraction capability.  When the contractions were reduced, the blood flow increased at that point of time.  Hence, in between the contractions of muscles, the blood flow was increased (Ganong, 2003).  This rhythmic cycle continued during the period exercises were performed.  After the exercises were completed, the blood flow in the arteries stayed high for a few minutes and then returned to normal.  Severe uncontrollable contractions of the muscles are known as ‘tetanic contractions’ (Guyton, 2006).  Some studies have even demonstrated that blood flow to the muscles may even rise before the exercises are performed suggesting a neural control mechanism (Ganong, 2003).  The blood flow to the active muscle groups during exercises can be accurately measured with Xenon washout technique with portable using light-weight CdTe(Cl) detectors.  Noninvasive techniques such as plethysmography and Doppler do not seem to be effective in measure the blood flow during exercises.  These techniques can only be used to determine the blood flow during rest.

            The capillaries that supply the muscles at rest have little or no blood supply.  They begin to open up during exercises.  As the capillaries open up, the nutrients and the oxygen have to diffuse to a shorter distance in order to reach the muscle cells and tissue requiring oxygen and nutrients (Guyton, 2006).  The capillary surface areas in fact increase to two to three times that of normal (Guyton, 2006).  The number of open capillaries increase to about 10 to a 100 times that of normal.  Once the capillaries open up, the lumen for blood flow increases, and the speed at which it flow reduces (Ganong, 2003).

            Blood flow control during exercises of the skeletal muscles occurs through local and neural mechanism.  Studies conducted in laboratory animals in which sympathectomy (removal of the sympathetic nerve or the sympathetic ganglion) was performed, demonstrated that the blood flow to the skeletal muscle groups during rest was twice that of normal animlas.  There was almost no difference between the increase in the blood flow in animals in whom sympathectomy was conducted and normal animals, once exercises were begun.  Thus local factors also play an important role in increasing the blood flow to the active skeletal muscles (Ganong, 2003).

Local – There is a deficiency of oxygen in the muscle and hence the blood supply is increased.  This is one of the main reasons for an increase in the blood flow.  The chemicals produced due to a shortage of oxygen in the tissues may activate certain receptors present in the arterioles leading to dilation.  As the arterioles open up, there is an increased blood flow, followed by a rise in the supply of oxygen to the tissues.  The oxygen concentration in the tissues slowly begins to rise.  The vasodilatation also takes place because the arteriole wall muscles cannot contract without a normal concentration of oxygen.  Some of the substance that causes vasodilatations includes adenosine.  Sometimes the muscles arterioles are not affected by the presence of adenosine, and in such circumstances other vasodilators act such as potassium ions, ATP molecules, lactic acid and carbon dioxide (Guyton, 2006).  The potassium ions present in the active muscles also initiate vasodilatation in the active muscle groups initially.  Studies have shown that in individuals having a deficiency of potassium, the blood flow may not increase to a higher level.  Exercises also cause a local rise in the temperature of the area leading to some amount of vasodilatation (Ganong, 2003).

Nerve control – The skeletal muscles are supplied by sympathetic nerve tract that bring about vasoconstriction.  These nerve fibers release a neurotransmitter known as ‘nor-epinephrine’ at the nerve endings.  These neurotransmitters can reduce the blood flow during rest to half or one-third that of normal.  Vasoconstriction helps to maintain circulation and the arterial pressure during periods of physical stress.  The adrenal glands release large quantities of nor-epinephrine along with epinephrine into the blood whenever physical activity is increased.  They act on the blood vessels of the muscles to cause vasoconstriction.  Epinephrine, on the other hand, is responsible for causing vasodilatation as a greater number of beta-adrenergic receptors are present in the vessels, are activated.  Nor-epinephrine, activates the alpha-adrenergic receptors.  During exercise, the adrenal glands release both epinephrine and nor-epinephrine causing selective vasoconstriction and vasodilatation (Guyton, 2006).

            During exercises three major events take place:-

1.      The sympathetic nervous system is stimulated throughout the body.

2.      The arterial pressure is increased.

3.      The cardiac output is increased.

Signals are sent from the brain to the muscles during exercises to bring about muscle contractions.  The vasomotor center present in the lateral medulla also sends sympathetic signals throughout the body (Guyton, 2006).  The brain (cerebral cortex0 to be precise), give rise to certain cholinergic sympathetic nerve fibers that are a part of the vasodilator system.  They enter and pass through the several parts of the brain including the medulla oblongata, and also relay in the mesencephlon and the hypothalamus.  The sympathetic nerve contains preganglionic nerve fibers, post-ganglionic nerve fibers and the ganglion.  The preganglionic nerve fibers which are sympathetic stimulate the postganglionic nerve fibers present in the skeletal muscles.  Acetylcholine is utilized as a neurotransmitter by these nerve fibers.  Once, stimulated, the arteries and the arterioles in the skeletal muscles get dilated.  However, some of the muscle groups present may consume lower amounts of oxygen because the blood may have to be diverted through various access routes present in these tissues, rather than capillaries solely.  Once the sympathetic nervous system brings about activation of vasodilatation in the active muscle groups, the adrenal glands automatically produce greater amounts of epinephrine and nor-epinephrine.  The effect of epinephrine seems to support vasodilatations of the arteries and arterioles that supply blood to the active muscle groups.  Some studies have demonstrated that stimulation of vasodilatation of the skeletal muscles may in fact even develop before the exercises are performed.  This does not seem to be a steady practical observation (Ganong, 2003).  However, several studies exist to show that in active muscles groups sympathetic nerve activity is increased (Rowell, 1997).

According to Khan Et al (2000), neural control of the increased blood flow has been explained by two different theories.  In the first theory, known as ‘central command’, the central motor areas release certain signals which increase the sympathetic stimulation of blood flow during exercises.  In the second theory, various local receptors (by chemical and mechanical means) in the muscles are stimulated, and as a response (reflex action), the blood flow to the active group of muscles are increased.

Once, the sympathetic activity rises, the parasympathetic signals sent to the heart get obstructed.  The following events follow:-

·               The heart rate is increased and the force of contractions of the cardiac muscles is also increased de o the sympathetic stimulation and obstruction of the parasympathetic waves.

·               All the arterioles in the peripheral tissues (except those of the active muscle group) are contracted.  Hence, with the simultaneous effect on the heart, the blood flow is increased to all the active muscles, but decreased to the non-active muscle groups.  This acts as a compensatory mechanism and is known as ‘lending’ the blood (2 liters of additional blood flow to the muscles belonging to the active group per minute).  However, the blood supply to the brain and the heart are not decreased during exercises.  This is mainly because these vital organs have very poor vasoconstrictor effect.

·               The muscles present in the walls of the veins get contracted so that the systemic filling pressure can be increased.  Hence, the venous return to the heart is increased and the cardiac output also gets elevated (Guyton, 2006).

Increase in the arterial pressure occurs due to sympathetic stimulation.  Due to multiple factors, that is vasoconstriction of the arterioles and arteries that supply the non-active muscles; increased cardiac output of the heart; and increase in the mean systemic filling pressure following venous contraction, the arterial pressure rises.  It can be increased between 20 mm Hg to 80 mm Hg, varying based on the degree or intensity of the physical activity.  Vasoconstriction of a few non-active arteries can cause the rise in the arterial pressure to 170 mm of Hg.  When the individual exercises only a few groups of muscles, the arterial pressure is bound to rise to a higher level (170 mm of Hg) such as climbing a ladder and simultaneously placing a nail in the wall.  However, during whole body exercises, such as swimming or jogging, the arterial pressure increased to a lower level (that is 20 to 30 mm of Hg) (Guyton, 2006).  Recent studies have shown that in order to increase the arterial pressure, increased sympathetic activity may result in limitations of the blood flow to the active muscles (Thomas, 2004).

Studies conducted in the laboratory have demonstrated that when the muscles are activated without a rise in the arterial pressure, the blood flow does not increase to more than eight times that of normal.  However, studies conducted in marathon runners demonstrate that the blood flow can be increased to about 20 times that of normal.  This extra blood flow may be brought about by an increase in the arterial blood pressure (Guyton, 2006).

The cardiac output increases in the same way depending on the intensity of the physical activity.  It is very important that the cardiac muscles have adequate strength and are conditioned to provide an increased cardiac output to supply nutrients and oxygen to the skeletal muscles (Guyton, 2006).

References:

Bonnelykke S. V., Wroblewski, H., Galatius, S., Haunso, S., & Kastrup, J. (2000). “Assessment of continuous skeletal muscle blood flow during exercise in humans.” Microvasc Res, 59(2), 301-309. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10684736&query_hl=2&itool=pubmed_DocSum

Chatterjee, C. C. (1994). Human Physiology, (1oth Ed, Vol. 2). Calcutta: Medical Allied Agency.

Ganong, W. F. (2003). Review of Medical Physiology, (23rd ed). St. Louis: McGraw-Hill.

Guyton, A. C. (2006). Textbook of Medical Physiology, (11th Ed). Philadelphia: Saunders.

Khan, M.H., & Sinoway, L. I. (2000). “Muscle reflex control of sympathetic nerve activity in heart failure: the role of exercise conditioning.” Heart Fail Rev, 5(1), 87-100.  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16228918&query_hl=2&itool=pubmed_docsum

Michikami, D., Kamiya, A., Qi, F., Niimi, Y., Iwase, S., & Mano, T. (2000). “Arm elevation enhances muscle sympathetic nerve activity during static exercise.” Environ Med, 44(1), 46-48. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12296369&query_hl=2&itool=pubmed_DocSum

Rowell, L. B. (1997). “Neural control of muscle blood flow: importance during dynamic exercise.” Clin Exp Pharmacol Physiol, 24(2), 117-125. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9075582&dopt=Abstract

Thomas, G.D., & Segal, S. S. (2004).  “Neural control of muscle blood flow during exercise.” J Appl Physiol, 97(2), 731-738.  http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=15247201&query_hl=2&itool=pubmed_docsum