Increased metabolic activity of skeletal muscle

- Vasodilator metabolites (lactate, K+, and adenosine) accumulate because of increased metabolism of the exercising muscle.

- These metabolites cause arteriolar dilation in the active skeletal muscle, thus increasing skeletal muscle blood flow (active hyperemia).

-As a result of the increased blood flow, 02 delivery to the muscle is increased. The number of perfused capillaries is increased so that the diffusion distance for 02 is decreased.

- This vasodilation accounts for the overall decrease in TPR that occurs with exercise. Note that activation of the sympathetic nervous system alone (by the central command) would cause an increase in TPR.

C. Hemorrhage (Table 3-6 and Figure 3-18)

- The compensatory responses to acute blood loss are as follows: 1. A decrease in blood volume produces a decrease in mean systemic pressure. As a result, there is a decrease in both cardiac output and arterial pressure.

Table 3-5. Summary of Effects of Exercise

Heart rate


Stroke volume


Cardiac output


Arterial pressure

T (slight)

Pulse pressure

Î (due to increased stroke volume)


-l-i (due to vasodilation of skeletal muscle beds)

AV 02 difference

ÎÎ (due to increased 02 consumption)

AV = arterial-venous; TPR = total peripheral resistance.

AV = arterial-venous; TPR = total peripheral resistance.

Table 3-6. Summary of Responses to Hemorrhage

Heart rate TPR

Contractility Unstressed volume Renin

Angiotensin II Aldosterone

Circulating epinephrine and norepinephrine ADH

1 (T stressed volume)

ADH = antidiuretic hormone; TPR = total peripheral resistance.

Baroreceptor reflex t Sympathetic outflow t Angiotensin II

t Heart rate Constriction of Constriction t TPR t Aldosterone t Fluid absorption t Contractility arterioles of veins I I

t TPR I Unstressed T T

volume t Na+ reabsorption t Blood volume

t Blood volume t Arterial pressure toward normal

Figure3-18. Cardiovascular responses to hemorrhage. Pc=capillary hydrostatic pressure; TPR=total peripheral resistance.

2. The carotid sinus baroreceptors detect the decrease in arterial pressure. As a result of the baroreceptor reflex, there is increased sympathetic outflow to the heart and blood vessels and decreased parasympathetic outflow to the heart, producing:

a. t heart rate b. T contractility c. T TPR (due to arteriolar constriction)

d. i unstressed volume and T stressed volume (due to venous constriction)

- Vasoconstriction occurs in skeletal, splanchnic, and cutaneous vascular beds. However, it does not occur in coronary or cerebral vascular beds, ensuring that adequate blood flow will be maintained to the heart and brain.

- These responses attempt to restore normal arterial blood pressure.

3. Chemoreceptors in the carotid and aortic bodies are very sensitive to hypoxia. They supplement the baroreceptor mechanism by increasing sympathetic outflow to the heart and blood vessels.

4. Cerebral ischemia (if present) causes an increase in Pco2, which activates chemoreceptors in the vasomotor center to increase sympathetic outflow.

5. Arteriolar vasoconstriction causes a decrease in Pc. As a result, capillary absorption is favored, which helps to restore circulating blood volume.

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