Tahisha M. Buck

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

•  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. •  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.

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. Using a string phantom, we found the average beam width of four different probes varied across probes from 2.93 ± 0.05 to 4.41 ± 0.06 mm (mean ± SD) and with depth of insonation. Using this information, we tested the validity of a calculated correction factor to minimize the thin-beam error in mean velocity observed in a flow phantom with known diameter. Use of a correction factor reduced the overestimation from 39 ± 11 to 7 ± 9% (P < 0.05). Lastly, in vivo we explored how knowledge of beam width improves understanding of physiological flow conditions. In vivo, use of a correction factor reduced the overestimation of mean velocity from 23 ± 11 to -4 ± 9% (P < 0.05). Thus this large source of error is real, has been largely ignored by the early adaptors of Doppler ultrasound for vascular physiology studies in humans, and is correctable by the described techniques.

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

•  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? •  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.

Mast cell degranulation and de novo histamine formation contribute to sustained post-exercise 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 H1 and H2 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. Subjects performed 1 h of unilateral dynamic knee-extension exercise or sham (seated rest). We measured the interstitial histamine concentration and local blood flow (ethanol washout) via skeletal muscle microdialysis of the vastus lateralis. In some probes, we infused either α-fluoromethylhistidine hydrochloride (α-FMH), a potent inhibitor of histidine decarboxylase, or histamine H1/H2-receptor blockers. We also measured interstitial tryptase concentrations, a biomarker of mast cell degranulation. Compared with preexercise, histamine was increased after exercise by a change (Δ) of 4.2 ± 1.8 ng/ml (P < 0.05), but not when α-FMH was administered (Δ-0.3 ± 1.3 ng/ml, P = 0.9). Likewise, local blood flow after exercise was reduced to preexercise levels by both α-FMH and H1/H2 blockade. In addition, tryptase was elevated during exercise by Δ6.8 ± 1.1 ng/ml (P < 0.05). Taken together, these data suggest that interstitial histamine in skeletal muscle increases with exercise and results from both de novo formation and mast cell degranulation. This suggests that exercise produces an anaphylactoid signal, which affects recovery, and may influence skeletal muscle blood flow during exercise.NEW & NOTEWORTHY Blood flow to previously active skeletal muscle remains elevated following an acute bout of aerobic exercise and is dependent on activation of histamine H1 and H2 receptors. The intramuscular source of histamine that drives this response to exercise has not been identified. Using intramuscular microdialysis in exercising humans, we show both mast cell degranulation and formation of histamine by histidine decarboxylase contributes to the histamine-mediated vasodilation that occurs following a bout of aerobic exercise.