Redistribution of Blood Flow During Exercise
Assessing Skeletal Muscle Blood Flow Redistribution with NIRS
Blood flow regulation is one of the most interesting aspects of human physiology. When we perform high-intensity exercise, we utilize oxygen faster than it can be supplied to the skeletal muscle. As a result, there is net deoxygenation of the skeletal muscle. In response to this hypoxia in the skeletal muscle, we experience ‘metabolic vasodilation,’ which increases blood flow. This process is relatively simple during single joint or small muscle mass exercise, like a bicep curl. However, it becomes increasingly complex when we progress to regional exercise using multiple muscle groups close to one another or full-body exercise. The reason for this is that we have a finite ability to metabolically vasodilate tissue before we outstrip’ our cardiac output and cannot maintain our blood pressure.
As a result, our body has built-in protective mechanisms to ensure that we never vasodilate so much that it threatens our arterial blood pressure, which would lead to a loss of consciousness. One mechanism by which this occurs is increased sympathetic nervous system activity [ie, sympathetic vasoconstriction]. This sympathetic regulation of peripheral resistance guards against the extreme vasodilator capacity of skeletal muscle invoked by exercise and protects us from extreme hypotension [low blood pressure].
For example, When intense upper body movement is added to intense lower body movement, blood flow to the legs at a given work rate will reduce by up to 10%. For example, if I was echo biking with my legs only for a few minutes and then started using my arms and legs, my lower body’s blood flow would be reduced. A similar effect also occurs in the upper body, as would be the case if I was doing an arms-only assault bike and then started using my legs as well.
These reductions in blood flow to the extremity muscles are a product of peripheral vasoconstriction caused by the arterial baroreflex, whose key functions include supporting and maintaining blood pressure.
This mechanism is also seen when an athlete is limited by delivery and cannot increase cardiac output to cope with an increased work demand. In these cases, cardiac output is not sufficient to maintain blood pressure, and the arterial baroreflex increases peripheral resistance by augmenting SNS activity and restricting blood flow to working skeletal muscles. This is an effective strategy because tiny changes in the radius of a blood vessel have huge impacts on resistance.
This is common in Crossfit athletes who are strong, have great local muscular endurance but weak cardiac output. These athletes often end up in a scenario where the demand for blood flow is higher than the cardiac system can supply. In these cases, blood flow to low priority areas is selectively reduced, which eventually impacts the working muscle. When this occurs, we can look for signs of vasoconstriction or occlusion to see if the cardiac system is implicated and other red flags. This can be seen on a step test where the working muscles progressively vasoconstrict as intensity increases.
