Recent advances in exercise pressor reflex function in health and disease, 2020, Stone et al

Andy

Retired committee member
Autonomic alterations at the onset of exercise are critical to redistribute cardiac output towards the contracting muscles while preventing a fall in arterial pressure due to excessive vasodilation within the contracting muscles. Neural mechanisms responsible for these adjustments include central command, the exercise pressor reflex, and arterial and cardiopulmonary baroreflexes. The exercise pressor reflex evokes reflex increases in sympathetic activity to the heart and systemic vessels and decreases in parasympathetic activity to the heart, which increases blood pressure (BP), heart rate, and total peripheral resistance through vasoconstriction of systemic vessels.

In this review, we discuss recent advancements in our understanding of exercise pressor reflex function in health and disease. Specifically, we discuss emerging evidence suggesting that sympathetic vasoconstrictor drive to the contracting and non-contracting skeletal muscle is differentially controlled by central command and the metaboreflex in healthy conditions.

Further, we discuss evidence from animal and human studies showing that cardiovascular diseases, including hypertension, diabetes, and heart failure, lead to an altered exercise pressor reflex function. We also provide an update on the mechanisms thought to underlie this altered exercise pressor reflex function in each of these diseases. Although these mechanisms are complex, multifactorial, and dependent on the etiology of the disease, there is a clear consensus that several mechanisms are involved.

Ultimately, approaches targeting these mechanisms are clinically significant as they provide alternative therapeutic strategies to prevent adverse cardiovascular events while also reducing symptoms of exercise intolerance.
Paywall, https://www.autonomicneuroscience.com/article/S1566-0702(20)30132-6/fulltext
Sci hub, https://sci-hub.tw/10.1016/j.autneu.2020.102698
 
This is a useful introduction to the autonomic facets of exercise, but there is of course more going on with regards to the neurology, muscle physiology and biochemistry resulting from exercise.

A key point however is the autonomic responses are reactive and lag behind the increase in central drive to the muscles, resulting increase in muscle force (and thus pressor effect on blood vessels).

This latency can be part of the pattern of orthostatic intolerance, for example.

Also note that the autonomic regulation applies primarily to the arteries and veins, not the peripheral capillaries in the driven muscles. Otherwise the increase in sympathetically vasoconstriction would be counterproductive. Instead, the capillaries are locally regulated to maintain consistent blood flow into the veins and can vary the local pressure over a wide range to maintain this flow.
 
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