Blood pressure is measured as two values: systolic pressure and the lower diastolic pressure. Systolic pressure represents the pressure inside arteries when the heart contracts and pushes blood out. Diastolic pressure reflects the pressure in the arteries when the heart is relaxed and refilling with blood. During dynamic exercise, such as running or cycling, systolic pressure increases significantly, often rising by 60 mmHg or more. Despite this dramatic increase in the heart’s output, diastolic pressure remains relatively unchanged or may even slightly decrease in healthy individuals, indicating an adaptive cardiovascular system.
Diastolic Pressure and Total Peripheral Resistance
Diastolic pressure is governed by the resistance the blood encounters as it flows through the body’s network of blood vessels, known as Total Peripheral Resistance (TPR). TPR is the cumulative resistance offered by the arterioles, capillaries, and veins in the systemic circulation. Arterioles are the primary regulators of TPR because their muscular walls can constrict or dilate, controlling the amount of blood flow into specific tissue beds.
The relationship between blood pressure, cardiac output (the volume of blood pumped by the heart per minute), and TPR shows that a change in one variable affects the others. During exercise, cardiac output increases substantially, which would drive up both systolic and diastolic pressures if resistance remained constant. Diastolic pressure stability indicates that the increase in cardiac output is counteracted by a significant and simultaneous drop in the body’s overall resistance. This resistance decreases because the small arteries in the working muscles dramatically widen, creating a much larger channel for the blood to flow through.
The Primary Mechanism: Localized Vasodilation
The reason diastolic pressure does not increase is the profound localized vasodilation that occurs in the skeletal muscles performing the work. As muscle cells increase their activity, they rapidly consume oxygen and produce metabolic byproducts. These local chemical changes signal the smooth muscle cells surrounding the arterioles that supply the active muscle tissue.
The resulting vasodilation, or widening of the blood vessels, is a direct response to the accumulation of substances like adenosine, nitric oxide (NO), potassium ions, and lactic acid. Nitric oxide is a potent vasodilator released by endothelial cells in response to increased blood flow shear stress. This locally mediated widening of the resistance vessels causes a massive drop in blood flow resistance in those areas.
This dramatic fall in resistance within the exercising muscle beds effectively lowers the entire body’s TPR. This prevents the increased blood volume from elevating the pressure during the heart’s relaxation phase. This local mechanism ensures that blood flow to the active muscles increases up to 25 times the resting rate, precisely matching oxygen supply to metabolic demand.
Systemic Regulation and Pressure Maintenance
While local vasodilation drops resistance in the working muscles, the body employs a centralized countermeasure to prevent overall blood pressure from plummeting. The sympathetic nervous system (SNS) becomes highly active during exercise. The SNS causes widespread vasoconstriction, or narrowing, of blood vessels in non-exercising areas, such as the digestive tract, kidneys, and inactive muscle tissue.
This sympathetic-driven vasoconstriction redirects blood flow away from non-essential organs and toward the demanding skeletal muscles. This action helps maintain the overall systemic vascular tone, preventing blood pressure from compromising flow to the brain and heart.
The net effect is a balance where the massive local vasodilation in active muscles is partially offset by generalized vasoconstriction in inactive tissues. This coordinated control mechanism is why diastolic pressure remains stable, as the total resistance change is minimized despite the local changes.
How Exercise Type Affects Diastolic Pressure
The stability or slight decrease in diastolic pressure is characteristic of dynamic, or aerobic, exercise, like running or swimming. This activity involves rhythmic muscle contractions that allow for continuous blood flow and effective metabolic vasodilation. The rhythmic pumping action of the muscles also assists in venous return, supporting efficient circulation.
In contrast, static, or isometric, exercise, such as holding a plank or a heavy weight, results in a significant increase in diastolic pressure. During a strong static contraction, the sustained tension in the muscle physically compresses the blood vessels. This mechanical compression severely limits blood flow, preventing metabolic vasodilation from fully taking effect. Since the vessels cannot widen, the TPR does not drop sufficiently to counteract the increased cardiac output, causing the diastolic pressure to rise.