ABSTRACT
Skeletal muscle receives around 20% of CO at rest and, during exercise, can receive up to 17 times more blood per minute (80% of CO). Thus, some degree of vasodilatation in skeletal muscle must also occur in response to exercise. Although metabolic factors and circulating epinephrine (see Topic D6) play an important role in mediating the increase in skeletal muscle blood flow that is observed during exercise, there is debate about whether neurogenic vasodilatation takes place. Whatever the mechanisms involved, it is clear that if skeletal muscle is receiving 80% of CO and the vascular bed is dilated, then the contribution that skeletal muscle makes to total peripheral resistance (TPR) must be high, and that TPR should fall during exercise. As explained in Topic Dl, if TPR falls, then mean arterial blood pressure (MABP) should fall, since MABP = CO x TPR. However, the changes in TPR during exercise are compensated for by
GTP cGMP Relaxation
NO
increases in CO, and the resultant effect on MABP is minimal. During moderate exercise, MABP is usually increased by only around 20 mmHg, and during heavy exercise, by only 10 mmHg, as activity-induced vasodilatation begins to predominate. Systolic blood pressure (SBP) tends to rise during exercise, and diastolic blood pressure (DBP) tends to fall slightly, resulting in a much smaller change in MABP than one might expect.
