Local Blood Flow and Exercise

Learning Objectives

By the end of this session, you should be able to:

Describe how local metabolic demand affects blood flow in a tissue
Explain acute and long-term control of local blood flow
List important vasoconstrictor and vasodilator factors
Explain how exercise affects blood flow to the skeletal muscle, blood pressure, and cardiac output.

Importance of Local Blood Flow Control

The blood flow to each tissue is always controlled at a level only slightly more than required to maintain full tissue oxygenation.
Tissues almost never suffer from oxygen nutritional deficiency, and yet the workload on the heart is kept at a minimum.
For example, in the resting state, the metabolic activity of the muscles is very low and so is the blood flow (4 ml/min/100 g muscle).
During heavy exercise, muscle metabolic activity increases more than 60-fold and the blood flow as much as 20-fold (80 ml/min/100 g muscle).

Mainly dependent on oxygen availability:

Acute Control: Local vasodilation/vasoconstriction within seconds to minutes.
Long-term Control: Increase/decrease in the physical sizes and numbers of blood vessels over days, weeks, and months.

Decreased availability of oxygen leads to adenosine release followed by vasodilation.
Best known in coronary arteries.
Researchers believe adenosine is an important controller of blood flow in skeletal muscle and other tissues as well.

Also known as nutrient lack theory.
Local precapillary and metarteriole sphincters open and close cyclically several times per minute.
The cyclic opening and closing requires oxygen (and nutrients).
When the oxygen concentration is high, the sphincters stay closed until the tissue consumes the excess oxygen.
When the oxygen concentration falls low enough, the sphincters open.

Present in almost all tissues.
Special areas have distinctly different mechanisms:
- Kidneys: Tubuloglomerular feedback.
- Brain: Concentrations of carbon dioxide and hydrogen ions play very prominent roles. Increase in either or both dilates the cerebral blood vessels.
When microvascular blood flow increases, upstream arteries are dilated through the endothelium-derived relaxing factor (EDRF, mostly nitric oxide).

When BP increases acutely, there is an immediate rise in local blood flow.
Within less than a minute, the blood flow in most tissues returns to almost the normal level, even though the arterial pressure is kept elevated. This is called "autoregulation of blood flow."

A BP increase leads to an increase in blood flow, followed by excess oxygen/nutrients, which leads to vasoconstriction and a return to normal blood flow.

BP increase leads to increased blood flow, vessel stretch, stretch-induced depolarization, vasoconstriction, and normal blood flow.
The precise mechanism behind stretch-induced depolarization is not completely understood but involves ion channels and extracellular proteins.
The myogenic mechanism may be important in preventing excessive stretch of blood vessels.

Acute mechanisms for blood flow control are effective but cannot fully adjust to the requirements.
Long-term regulation develops over hours, days, and weeks, giving far more complete regulation.
The principal mechanism of long-term regulation is to change "tissue vascularity," involving the actual physical reconstruction of the tissue vasculature.
Oxygen is important for both acute control and long-term control of blood flow.
Growth factors like VEGF, fibroblast growth factor, and angiogenin are involved in increasing the growth of new vessels.
Vascularity is determined by the maximal level of blood flow need rather than by average need.

This is a phenomenon of long-term local blood flow regulation.
When a blood vessel is blocked, a new vascular channel (collateral vessels) usually develops around the blockage and allows at least partial supply of blood.
Initial dilation of small vascular loops that already connect the vessel above the blockage to the vessel below (within 1-2 minutes).
Further dilation occurred within the ensuing hours, reaching ~ half of the needed flow over one day and often full capacity within a few days.
Continued growth of collateral vessels, almost always forming many small vessels rather than one large vessel.

Blood Flow in Skeletal Muscle

During strenuous exercise, skeletal muscle requires large amounts of blood flow.
Blood flow is not as high during contractions because the blood vessels are ‘squeezed’.

Local blood flow increase in skeletal muscle:
- Oxygen is used up rapidly, resulting in the release of vasodilators (e.g., CO2, H+, Adenosine, Lactose, and K+).
- Loss of arteriolar wall contraction due to oxygen lack.
Massive systemic sympathetic discharge leading to:
- Increased HR and contractility, causing a direct increase in cardiac output (CO).
- Systemic α1 vasoconstriction (and β2 vasodilation in skeletal muscle blood vessel) causing redirection of blood to skeletal muscle.
- Venoconstriction increasing mean systemic filling pressure/venous return, leading to an increase in CO.

Many different physiological effects occur to increase cardiac output (CO) approximately in proportion to the degree of exercise.
The ability to increase CO for delivery of oxygen and nutrients to the muscles during exercise is crucial for continued muscle work.

The cardiac function curve shifts up due to increased HR and contractility from sympathetic stimulation.
The venous return curve shifts right due to:
- Venoconstriction.
- Tensing of abdominal and other skeletal muscles.
A decrease in TPR (total peripheral resistance) increases the slope of both curves, contributing to the increase in CO.
At rest, cardiac function and venous return curves for normal circulation cross at point A, giving a CO of about 5 L/min.
During heavy exercise, both cardiac function and venous return curves change significantly, yielding a CO of over 20 L/min (point B).