Steven Romero

Postexercise hypotension and sustained postexercise vasodilatation: what happens after we exercise?

•u2002 What is the topic for this review? During the exercise recovery period, the combination of centrally mediated decreases in sympathetic nerve activity with a reduced signal transduction from sympathetic nerve activation into vasoconstriction, as well as local vasodilator mechanisms, contributes to the fall in arterial blood pressure seen after exercise. •u2002 What advances does it highlight? Important findings from recent studies include the recognition that skeletal muscle afferents may play a primary role in postexercise resetting of the baroreflex via discrete receptor changes within the nucleus tractus solitarii and that sustained postexercise vasodilatation of the previously active skeletal muscle is primarily the result of histamine H1 and H2 receptor activation.

Blood pressure regulation X: what happens when the muscle pump is lost? Post-exercise hypotension and syncope

Syncope which occurs suddenly in the setting of recovery from exercise, known as post-exercise syncope, represents a failure of integrative physiology during recovery from exercise. We estimate that between 50 and 80xa0% of healthy individuals will develop pre-syncopal signs and symptoms if subjected to a 15-min head-up tilt following exercise. Post-exercise syncope is most often neurally mediated syncope during recovery from exercise, with a combination of factors associated with post-exercise hypotension and loss of the muscle pump contributing to the onset of the event. One can consider the initiating reduction in blood pressure as the tip of the proverbial iceberg. What is needed is a clear model of what lies under the surface; a model that puts the observational variations in context and provides a rational framework for developing strategic physical or pharmacological countermeasures to ultimately protect cerebral perfusion and avert loss of consciousness. This review summarizes the current mechanistic understanding of post-exercise syncope and attempts to categorize the variation of the physiological processes that arise in multiple exercise settings. Newer investigations into the basic integrative physiology of recovery from exercise provide insight into the mechanisms and potential interventions that could be developed as countermeasures against post-exercise syncope. While physical counter maneuvers designed to engage the muscle pump and augment venous return are often found to be beneficial in preventing a significant drop in blood pressure after exercise, countermeasures that target the respiratory pump and pharmacological countermeasures based on the involvement of histamine receptors show promise.

Effect of antioxidants on histamine receptor activation and sustained postexercise vasodilatation in humans

What is the central question of this study? Is exercise‐induced oxidative stress the upstream exercise‐related signalling mechanism that leads to sustained postexercise vasodilatation via activation of H1 and H2 histamine receptors? What is the main finding and its importance? Systemic administration of the antioxidant ascorbate inhibits sustained postexercise vasodilatation to the same extent as seen previously with H1 and H2 histamine receptor blockade following small muscle‐mass exercise. However, ascorbate has a unique ability to catalyse the degradation of histamine. We also found that systemic infusion of the antioxidant N‐acetylcysteine had no effect on sustained postexercise vasodilatation, suggesting that exercise‐induced oxidative stress does not contribute to sustained postexercise vasodilatation.

Postexercise syncope: Wingate syncope test and effective countermeasure

•u2002 What is the central question of this study? Does a modified version of the Wingate anaerobic power test produce presyncopal signs and symptoms in healthy individuals? Does an inspiratory threshold device work as a countermeasure against postexercise syncope? •u2002 What is the main finding and its importance? A modified Wingate test is a good model to induce postexercise syncope, and syncopal symptoms can be ameliorated by an inspiratory threshold device.

Neurovascular control following small muscle-mass exercise in humans

Sustained postexercise vasodilation, which may be mediated at both a neural and vascular level, is seen in previously active skeletal muscle vascular beds following both large and small muscle‐mass exercise. Blunted sympathetic vascular transduction and a downward resetting of the arterial baroreflex contribute to this vasodilation after cycling (large muscle‐mass exercise), but it is unknown if these responses also contribute to sustained vasodilation following small muscle‐mass exercise. This study aimed to determine if baroreflex sensitivity is altered, the baroreflex is reset, or if sympathetic vascular transduction is blunted following small muscle‐mass exercise. Eleven healthy, college‐aged subjects (five males, six females) completed one‐leg dynamic knee‐extension exercise for 1 h at 60% of peak power output. While cardiovagal baroreflex sensitivity was increased ~23% postexercise relative to preexercise (P < 0.05), vascular and integrated baroreflex sensitivity were not altered following exercise (P = 0.31 and P = 0.48). The baroreflex did not exhibit resetting (P > 0.69), and there was no evidence of changes in vascular transduction following exercise (P = 0.73). In conclusion, and in contrast to large muscle‐mass exercise, it appears that small muscle‐mass exercise produces a sustained postexercise vasodilation that is largely independent of central changes in the baroreflex.

Post-exercise syncope: Wingate syncope test and visual-cognitive function.

Adequate cerebral perfusion is necessary to maintain consciousness in upright humans. Following maximal anaerobic exercise, cerebral perfusion can become compromised and result in syncope. It is unknown whether post‐exercise reductions in cerebral perfusion can lead to visual‐cognitive deficits prior to the onset of syncope, which would be of concern for emergency workers and warfighters, where critical decision making and intense physical activity are combined. Therefore, the purpose of this experiment was to determine if reductions in cerebral blood velocity, induced by maximal anaerobic exercise and head‐up tilt, result in visual‐cognitive deficits prior to the onset of syncope. Nineteen sedentary to recreationally active volunteers completed a symptom‐limited 60° head‐up tilt for 16 min before and up to 16 min after a 60 sec Wingate test. Blood velocity of the middle cerebral artery was measured using transcranial Doppler ultrasound and a visual decision‐reaction time test was assessed, with independent analysis of peripheral and central visual field responses. Cerebral blood velocity was 12.7 ± 4.0% lower (mean ± SE; P < 0.05) after exercise compared to pre‐exercise. This was associated with a 63 ± 29% increase (P < 0.05) in error rate for responses to cues provided to the peripheral visual field, without affecting central visual field error rates (P = 0.46) or decision‐reaction times for either visual field. These data suggest that the reduction in cerebral blood velocity following maximal anaerobic exercise contributes to visual‐cognitive deficits in the peripheral visual field without an apparent affect to the central visual field.