Dylan Sieck

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.

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.