As muscles begin exercising, the arterioles serving the muscle dilate to provide more blood flow. By itself, this vasodilation would lower the total peripheral resistance and thus mean arterial pressure. However, arterial pressure does not decrease because other parts of the cardiovascular system are adjusted to support the increased blood flow to the muscles. Let's first look at the muscle arterioles and then at the various changes in the cardiovascular system that support the increased flow of blood to the exercising muscles.
As a muscle begins exercising, the arterioles serving that muscle dilate due to local chemical effects. These occur within a muscle as a result of the muscle fibers using more energy. This mechanism greatly simplifies the response to exercise because it automatically ensures that muscles using more energy get more blood flow. The nervous system need not be concerned with dividing up the blood flow to all the numerous muscles in body.
Various local chemical factors can trigger vasodilation of arterioles. The specific factors we discuss are increased carbon dioxide, increased hydrogen ion, increased K+ and increased osmolarity. (The latter occurs as metabolic reactions break larger molecules down into more smaller molecules.)
Due to such factors, blood flow can increase up to 20 times as a muscle exercises.
What triggers the autonomic actions that prevent the fall in arterial pressure? First, the carotid baroreceptor reflex is constantly adjusting the autonomic control of the cardiovascular system in response to any changes in the arterial pressure. However, physiologists do not, in fact, detect changes in arterial pressure as exercise begins. Thus, while the carotid baroreceptor reflex is important, it cannot by itself explain the response to exercise, since typically the pressure does not change as exercise begins.
The regulatory system, in other words, is very effective at anticipating changes. The higher areas of the brain that start the muscles contracting at the same time signal the autonomic nervous system to begin corresponding changes in the cardiovascular system. This feedfoward signal is usually called the central command. Both the cardiac output and the arterioles are adjusted.
The cardiac output is increased, of course, via sympathetic nerves that increase the heart rate and increase the stroke volume. Also, the stroke volume potentially can increase via the Frank-Starling mechanism. This is because contracting skeletal muscles tend to squeeze blood in their veins back to the central veins via muscle pumping. The elevated pressure in the central veins then in some circumstances can increase the end diastolic volume and thus the stroke volume.
At the same time as skeletal muscle arterioles dilate, arterioles to certain other areas help compensate by constricting. The primary organs for this sympathetic vasoconstriction are the gut, skin and inactive skeletal muscles.
The gut usually can get by with less blood flow because most of the blood flowing to the digestive system is for absorbing food molecules rather than for keeping the organs alive. However, in long-term, endurance exercise, digestion and absorption at some point starts taking place again.
Likewise, blood flow to the skin is not primarily for keeping the skin alive and thus can be reduced, at least for a short while. But reductions in blood flow to the skin are likely to be transient because it is imperative that enough blood flow through the skin to give off the extra heat generated in exercise.
In the end, in a healthy person the mean arterial pressure stays constant. because the increased flow of blood through exercising muscles is compensated for remarkably well by an increased cardiac output and adjustments to arterioles.