About this Research Topic
Professional organizations throughout the world recommend adults with hypertension participate in >20 min/day of aerobic exercise on most days of the week because, on average, exercise lowers BP by 5-8 mmHg. Reductions of this magnitude substantially decrease the overall cardiovascular risk. Moreover, the resting blood pressure (BP) of some people with hypertension may lower into normal ranges, reducing the need for antihypertensive medication.
There is evidence that a single bout of exercise may reduce BP for a few hours compared with control values. These reductions in BP are immediate, persist for up to 24 hr after the exercise session, and are termed postexercise hypotension (PEH). The PEH phenomenon is clinically important because: (1) it occurs immediately; (2) a person does not have to be physically fit to experience its BP benefits; (3) PEH is strongly correlated with the magnitude of the BP reductions that result from more long-term exercise training, suggesting that the BP benefits that result from exercise training are largely due to PEH; and simply, (4) because of PEH, BP is lower on exercise than non-exercise days has been suggested to be related to long term BP lowering due to chronic exercise. Indeed, the reason that professional organizations recommend exercise as antihypertensive lifestyle therapy on most, and preferably all, days of the week is due to PEH. We and others have long suspected that educating adults with hypertension about PEH may increase their motivation to exercise and, consequently, their adherence to exercise as antihypertensive lifestyle therapy.
In view of that, acute reductions in BP would be a desirable effect of exercise training designed to improve health, particularly BP management. In this context, a better understanding of mechanisms underlying the PEH phenomenon would be important to optimize the hypotensive effects of acute bouts of exercise. However, the role of the different potential systems contributing to PEH remain undefined. Overall, the literature suggests that central and peripheral factors concur for a reduction of BP after acute exercise, particularly lowered sympathetic nerve activity, decreased cardiac output, and increased local vasodilation. However, this is not consensual. Regardless of the exercise mode, there are trials reporting a reduction in sympathetic activity concomitant to PEH, while others observed sympathetic increasing with or without lowered parasympathetic outflow. Prior studies also produced discrepant data on the role of cardiac output and systemic vascular resistance as mechanisms of PEH in different populations (e.g., young vs. older adults, or normal vs. high BP). Such disparities probably result from the fact that determinants of PEH may vary due to confounding factors as the BP at rest, age/clinical status, or exercise characteristics (intensity, duration, or modality).
The present Research Topic focuses on providing evidence of clinical applications and mechanisms underlying the PEH phenomenon. Therefore, we invite researchers to investigate through experimental trials and meta-analyses the role of PEH as a central variable contributing to chronic effects of exercise on chronic changes in BP, as well as to identify potential mechanisms of BP lowering after acute exercise.
The studies should deepen our understanding of:
• The effects of different exercise modalities upon PEH in different populations;
• The influence of exercise intensity and volume on the magnitude and duration of PEH;
• The role of the autonomic nervous system in PEH after different exercise modalities;
• Central and peripheral mechanisms of BP reduction following acute exercise;
• Potential vascular mechanisms of post-exercise hypotension;
• Mechanisms of PEH in individuals with normal and high BP at rest;
• Clinical applications of the PEH phenomenon (responders vs. no responders, association with chronic responses etc);
• Factors optimizing the PEH response in populations with different characteristics (elderly, obese, hypertensive etc).
Disclosure statement: Topic Editor Linda Pescatello is a scientific consultant for Aytu BioScience. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
There is evidence that a single bout of exercise may reduce BP for a few hours compared with control values. These reductions in BP are immediate, persist for up to 24 hr after the exercise session, and are termed postexercise hypotension (PEH). The PEH phenomenon is clinically important because: (1) it occurs immediately; (2) a person does not have to be physically fit to experience its BP benefits; (3) PEH is strongly correlated with the magnitude of the BP reductions that result from more long-term exercise training, suggesting that the BP benefits that result from exercise training are largely due to PEH; and simply, (4) because of PEH, BP is lower on exercise than non-exercise days has been suggested to be related to long term BP lowering due to chronic exercise. Indeed, the reason that professional organizations recommend exercise as antihypertensive lifestyle therapy on most, and preferably all, days of the week is due to PEH. We and others have long suspected that educating adults with hypertension about PEH may increase their motivation to exercise and, consequently, their adherence to exercise as antihypertensive lifestyle therapy.
In view of that, acute reductions in BP would be a desirable effect of exercise training designed to improve health, particularly BP management. In this context, a better understanding of mechanisms underlying the PEH phenomenon would be important to optimize the hypotensive effects of acute bouts of exercise. However, the role of the different potential systems contributing to PEH remain undefined. Overall, the literature suggests that central and peripheral factors concur for a reduction of BP after acute exercise, particularly lowered sympathetic nerve activity, decreased cardiac output, and increased local vasodilation. However, this is not consensual. Regardless of the exercise mode, there are trials reporting a reduction in sympathetic activity concomitant to PEH, while others observed sympathetic increasing with or without lowered parasympathetic outflow. Prior studies also produced discrepant data on the role of cardiac output and systemic vascular resistance as mechanisms of PEH in different populations (e.g., young vs. older adults, or normal vs. high BP). Such disparities probably result from the fact that determinants of PEH may vary due to confounding factors as the BP at rest, age/clinical status, or exercise characteristics (intensity, duration, or modality).
The present Research Topic focuses on providing evidence of clinical applications and mechanisms underlying the PEH phenomenon. Therefore, we invite researchers to investigate through experimental trials and meta-analyses the role of PEH as a central variable contributing to chronic effects of exercise on chronic changes in BP, as well as to identify potential mechanisms of BP lowering after acute exercise.
The studies should deepen our understanding of:
• The effects of different exercise modalities upon PEH in different populations;
• The influence of exercise intensity and volume on the magnitude and duration of PEH;
• The role of the autonomic nervous system in PEH after different exercise modalities;
• Central and peripheral mechanisms of BP reduction following acute exercise;
• Potential vascular mechanisms of post-exercise hypotension;
• Mechanisms of PEH in individuals with normal and high BP at rest;
• Clinical applications of the PEH phenomenon (responders vs. no responders, association with chronic responses etc);
• Factors optimizing the PEH response in populations with different characteristics (elderly, obese, hypertensive etc).
Disclosure statement: Topic Editor Linda Pescatello is a scientific consultant for Aytu BioScience. All other Topic Editors declare no competing interests with regards to the Research Topic subject.
Keywords: blood pressure, hemodynamics, cardiovascular, exercise physiology, health
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