Mast cell degranulation and de novo histamine formation contribute to sustained postexercise vasodilation in humans.

In humans, acute aerobic exercise elicits a sustained postexercise vasodilation within previously active skeletal muscle. This response is dependent on activation of histamine H and H receptors, but the source of intramuscular histamine remains unclear. We tested the hypothesis that interstitial histamine in skeletal muscle would be increased with exercise and would be dependent on de novo formation via the inducible enzyme histidine decarboxylase and/or mast cell degranulation.

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.

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.

Thin-beam ultrasound overestimation of blood flow: how wide is your beam?

It has been predicted that the development of thin-beam ultrasound could lead to an overestimation of mean blood velocity by up to 33% as beam width approaches 0% of vessel diameter. If both beam and vessel widths are known, in theory, this overestimation may be correctable. Therefore, we updated a method for determining the beam width of a Doppler ultrasound system, tested the utility of this technique and the information it provides to reliably correct for the error in velocity measurements, and explored how error-corrected velocity estimates impact the interpretation of in vivo data.

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 80% 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.

Postexercise syncope: Wingate syncope test and effective countermeasure.

Altered systemic haemodynamics following exercise can compromise cerebral perfusion and result in syncope. As the Wingate anaerobic test often induces presyncope, we hypothesized that a modified Wingate test could form the basis of a novel model for the study of postexercise syncope and a test bed for potential countermeasures. Along these lines, breathing through an impedance threshold device has been shown to increase tolerance to hypovolaemia, and could prove beneficial in the setting of postexercise syncope.

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

A single bout of aerobic exercise produces a postexercise hypotension associated with a sustained postexercise vasodilatation of the previously exercised muscle. Work over the last few years has determined key pathways for the obligatory components of postexercise hypotension and sustained postexercise vasodilatation and points the way to possible benefits that may result from these robust responses. 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.