Exercise-induced cerebral oxygenation is preserved in the trained state

Background and Aims: It has been suggested that a decrease in brain oxygenation participates in the termination of exercise, especially in hypoxia (Subudhi et al. 2009; Vogiatis et al. 2011). Moreover, there is growing evidence suggesting that the cerebral vasculature of aerobically fit subjects (TRAINED) is more reactive than that of their sedentary counterparts (SEDENTARY) (Ainslie et al. 2008). Despite these facts, very little is known regarding the respective responses of these groups to maximal exercise. Therefore, the primary objective of the present study was to verify if TRAINED would have a greater increase in cerebral oxygenation than SEDENTARY during exercise. Methods: TRAINED (n=9) and SEDENTARY (n=9) responses to a standardised incremental test to volitional exhaustion were compared. Breath-by-breath gas exchanges, middle cerebral artery blood velocity (MCAv, Transcranial Doppler) and concentration in left prefrontal cortical oxyhaemoglobin (cO2Hb) (near-infrared spectroscopy) were monitored throughout the test performed on a semi-recumbent cycle ergometer. Relative changes in cO2Hb and MCAv were recorded throughout the test. Data were analysed using a 2-way repeated measures ANOVA (intensity x group) and Bonferroni corrected paired and independent samples t-tests. Results: MCAv increased steadily in both groups from rest up to a peak at 70% of oxygen uptake at exhaustion (VO2exhaust) before decreasing back towards resting level. Despite similar trends towards an increase during submaximal exercise, TRAINED MCAv was offset compared to SEDENTARY. This may be explained by the interaction effect that was identified. TRAINED cO2Hb also increased progressively throughout the submaximal intensities and continued to increase until exhaustion. On the contrary, SEDENTARY cO2Hb did not increase significantly at any point, leading to a significant difference between groups from 40% onwards. Finally, the changes in cO2Hb between rest and exhaustion were positively correlated with VO2exhaust (n=18, Pandlt;0.05). Conclusions: These findings suggest that in the first instance the brain copes with exercise by self-regulating increased blood flow. At intensities andgt;70% of VO2exhaust, while MCAv decreased due to the hyperventilatory-induced hypocapnia (Ogoh and Ainslie 2009), cO2Hb increased further in the TRAINED suggesting that the brain switches from more flow to more extraction. This can be seen as a protective mechanism since a hyper-perfusion could potentially induce a failure of the blood-brain barrier. From a clinical point of view, this adaptive response of the 'trained brain' seems to confirm the neuroprotective effect of chronic exercise.