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Exercise‐induced oxidative–nitrosative stress is associated with impaired dynamic cerebral autoregulation and blood–brain barrier leakage
Author(s) -
Bailey Damian M.,
Evans Kevin A.,
McEneny Jane,
Young Ian S.,
Hullin David A.,
James Philip E.,
Ogoh Shigehiko,
Ainslie Philip N.,
Lucchesi Céline,
Rockenbauer Antal,
Culcasi Marcel,
Pietri Sylvia
Publication year - 2011
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2011.060178
Subject(s) - oxidative stress , cerebral blood flow , cerebral autoregulation , medicine , chemistry , nitric oxide , autoregulation , nitrotyrosine , enolase , blood–brain barrier , endocrinology , anesthesia , blood pressure , nitric oxide synthase , central nervous system , immunohistochemistry
The present study examined whether dynamic cerebral autoregulation and blood–brain barrier function would become compromised as a result of exercise‐induced oxidative–nitrosative stress. Eight healthy men were examined at rest and after an incremental bout of semi‐recumbent cycling exercise to exhaustion. Changes in a dynamic cerebral autoregulation index were determined during recovery from continuous recordings of blood flow velocity in the middle cerebral artery (MCAv) and mean arterial pressure during transiently induced hypotension. Electron paramagnetic resonance spectroscopy and ozone‐based chemiluminescence were employed for direct detection of spin‐trapped free radicals and nitric oxide metabolites in venous blood. Neuron‐specific enolase, S100β and 3‐nitrotyrosine were determined by ELISA. While exercise did not alter MCAv, it caused a mild reduction in the autoregulation index (from 6.9 ± 0.6 to 5.5 ± 0.9 a.u., P < 0.05) that correlated directly against the exercise‐induced increase in the ascorbate radical, 5‐(diethoxyphosphoryl)‐5‐methyl‐1‐pyrroline N ‐oxide and N ‐ tert ‐butyl‐α‐phenylnitrone adducts, 3‐nitrotyrosine and S100β ( r =–0.66 to –0.76, P < 0.05). In contrast, no changes in neuron‐specific enolase were observed. In conclusion, our findings suggest that intense exercise has the potential to increase blood–brain barrier permeability without causing structural brain damage subsequent to a free radical‐mediated impairment in dynamic cerebral autoregulation.