Dehydration affects cerebral blood flow but not its metabolic rate for oxygen during maximal exercise in trained humans.
Bottom Line: In all conditions, reductions in ICA and MCA Vmean were associated with declining cerebral vascular conductance, increasing jugular venous noradrenaline, and falling arterial carbon dioxide tension (P aCO 2) (R(2) ≥ 0.41, P ≤ 0.01) whereas CCA flow and conductance were related to elevated blood temperature.In conclusion, dehydration accelerated the decline in CBF by decreasing P aCO 2 and enhancing vasoconstrictor activity.However, the circulatory strain on the human brain during maximal exercise does not compromise CMRO2 because of compensatory increases in O2 extraction.
Affiliation: Centre for Sports Medicine and Human Performance, Brunel University, London, UK.Show MeSH
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Mentions: At rest, ICA O2 delivery, a–v O2 and v–a CO2 difference, and CMRO2 and brain rate of CO2 production () indices were not significantly different across the three experimental conditions of the dehydration trial. From rest to sub-maximal exercise (40% WRmax) in control, ICA O2 delivery increased, v–a CO2 difference decreased, while the a–v O2 difference was unchanged (Fig. 3B, E and F). When exercise intensity became strenuous (≥60%), ICA O2 delivery declined to baseline values, as with ICA blood flow, and v–a CO2 and a–v O2 difference increased progressively to exhaustion (∼32% increase vs. rest, P < 0.05). Additionally, there was a progressive increase in brain index up to WRmax (Fig. 3G). During DEH, ICA O2 delivery remained constant up to 60% WRmax, before declining to below resting values. Moreover, v–a CO2 difference, a–v O2 difference and brain index were elevated at WRmax (P < 0.05). ICA O2 delivery was somewhat restored in REH whereas v–a CO2 and a–v O2 difference, and brain index were similar to control. Overall, these responses resulted in a maintained CMRO2 index at rest and throughout exercise to exhaustion (Fig. 3H). Brain a–v lactate concentration ([La]) difference was maintained at sub-maximal exercise intensities in control conditions before increasing at WRmax, resulting in net uptake of [La] by the brain (Fig. 4A and C). Conversely, in DEH and REH, a–v [La] was unchanged. Brain a–v glucose concentration ([Glu]) difference was stable in all conditions (except WRmax in control conditions), resulting in a stable uptake of glucose across exercise intensities (Fig. 4B and D).
Affiliation: Centre for Sports Medicine and Human Performance, Brunel University, London, UK.