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The mechanism(s) for the increased occurrence of a grayout or blackout, syncope, immediately after heavy resistance exercise are unclear. It is well-known that orthostatic stress increases the occurrence of postexercise syncope. In addition, previous findings have suggested that hypo-perfusion, especially in the posterior cerebral circulation rather than anterior cerebral circulation, may be associated with the occurrence of syncope. Herein, we hypothesized that the postexercise decrease in posterior, but not anterior, cerebral blood flow (CBF) would be greater during orthostatic stress. Nine healthy subjects performed 3-min isometric handgrip (HG) at 30% maximum voluntary contraction without (CONTROL) and during lower body negative pressure (LBNP; -40 Torr) while vertebral artery (VA) blood flow, as an index of posterior CBF, and middle cerebral artery blood velocity (MCAv), as an index of anterior CBF, were measured. Immediately after HG (0 to 15 sec of recovery phase), mean arterial pressure decreased but there was no difference in this reduction between CONTROL and LBNP conditions (-15.4 ± 4.0% and -17.0 ± 6.2%, P = 0.42). Similarly, MCAv decreased following exercise and was unaffected by the application of LBNP (P = 0.22). In contrast, decreases in VA blood flow immediately following HG during LBNP were significantly greater compared to CONTROL condition (-24.2 ± 9.5% and -13.4 ± 6.6%, P = 0.005). These findings suggest that the decrease in posterior CBF immediately following exercise was augmented by LBNP, whereas anterior CBF appeared unaffected. Thus, the posterior cerebral circulation may be more sensitive to orthostatic stress during the postexercise period.
This article was published in the following journal.
Name: Physiological reports
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