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Cardiovascular Physiology Concepts

Richard E. Klabunde, PhD


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Skeletal Muscle Blood Flow

The regulation of skeletal muscle blood flow is important for two reasons. First, skeletal muscle serves important locomotory functions in the body because of its contractile properties. This is important for voluntary movement (e.g., walking, swimming), postural control, and involuntary movement (e.g., respiration). Contracting muscle consumes large amounts of oxygen to replenish ATP that is hydrolyzed during contraction; therefore, contracting muscle needs to be able to increase its blood flow and oxygen delivery in order to support its metabolic and contractile activities. Second, about 20% of the cardiac output at rest goes to skeletal muscle, which means that about 20% of resting systemic vascular resistance is determined by the vascular resistance of skeletal muscle. For this reason, changes in skeletal muscle resistance and blood flow can greatly influence arterial pressure.

As in all tissues, the microcirculation, particularly small arteries and arterioles, is the most important site for the regulation of vascular resistance and blood flow within the muscle. Like cardiac muscle, each muscle fiber (cell) is surrounded by several capillaries. This reduces diffusion distances for the efficient exchange of gasses (O2 and CO2) and other molecules between the blood and the skeletal muscle cells.

Characteristics of Skeletal Muscle Blood Flow

  1. Skeletal muscle accounts for about 20% of cardiac output and systemic vascular resistance. During extreme physical exertion, more than 80% of cardiac output can be directed to contracting muscles; therefore, skeletal muscle resistance becomes the primary determinant of systemic vascular resistance during exercise.
  2. At rest, skeletal muscle blood flows may be 1-4 ml/min per 100g; maximal blood flows may reach 50-100 ml/min per 100g depending upon the muscle type. Therefore, blood flow can increase 20 to 50-fold with maximal vasodilation or active hyperemia.
  3. Coordinated, rhythmical contractions (e.g., running) enhance blood flow by means of the skeletal muscle pump mechanism.
  4. Sympathetic innervation produces vasoconstriction through alpha1 and alpha2 adrenoceptors located on the vascular smooth muscle. There is a significant amount of sympathetic tone at rest so that abrupt removal of sympathetic influences (e.g., by using an alpha-adrenoceptor blocker) can increase resting flow 2 to 3-fold.
  5. Vascular beta2-adrenoceptors produce vasodilation when stimulated by agonists such as epinephrine.
  6. There is evidence for sympathetic cholinergic innervation of skeletal muscle arteries in some species such as dogs and cats; however, there is no convincing evidence that this occurs in human skeletal muscle. In species having sympathetic cholinergic innervation, activation during exercise can cause vasodilation through the release of acetylcholine binding to muscarinic receptors.
  7. There is a close coupling between oxygen consumption and blood flow.
  8. Blood flow is strongly determined by local regulatory (tissue and endothelial) factors such as tissue hypoxia, adenosine, K+, CO2, H+, and nitric oxide. During exercise, these local regulatory mechanisms override the sympathetic vasoconstrictor influences (termed functional sympatholysis).
  9. Skeletal muscle blood flow shows a moderate degree of autoregulation.
  10. Like the coronary circulation, muscle blood flow can be significantly compromised by extravascular compression that occurs during strong muscular contractions, especially during sustained tetanic contractions.

The figure below shows how blood flow changes during phasic contractions. An example of this would be measuring brachial artery inflow during rhythmical contraction of the forearm.

blood flow in contracting skeletal muscle
When the contractions first begin, blood flow briefly decreases because of compressive forces exerted by the contracting muscles on the vasculature within the muscle. Each time the muscles contract arterial inflow decreases due to extravascular compression, and then arterial inflow increases as the muscles relax. This is repeated each time the muscles contract and relax. If flow were measured in the outflow vein, the venous outflow would increase during contraction and decrease during relaxation - the opposite of what occurs on the arterial side of the circulation. After just a couple of seconds, mean and peak flows begin to increase (active hyperemia). After 15-20 seconds the increased flow will reach a steady state that is determined by the force and frequency of contraction, and the metabolic demands of the tissue. When contractions cease, blood flow may transiently increase because of the loss of compressive forces, and then over the next minute or so the flow will return to control.

Revised 01/27/12

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.