Cerebral Oxygenation and Blood Flow Velocity at Maximal Exercise: The Effect of Clamping Carbon Dioxide

Abstract

During incremental exercise tests to exhaustion, reductions in PETCO2 above the respiratory compensation point (RCP) are associated with parallel decreases in cerebral blood flow velocity (CBFv) and cerebral oxygenation. Exercise performance may be limited by this low flow, low oxygenation state. To date, no group has clamped PETCO2 near maximal exercise to characterize interactions between PETCO2, CBFv, cerebral oxygenation, and performance. PURPOSE: We hypothesized that by preventing the decrease in PETCO2 at maximal exercise, we could prevent the fall in CBFv and cerebral oxygenation and thus possibly extend exercise if cerebral oxygen delivery were a limiting factor. METHODS: In this single-blind crossover experiment, ten professional or category I cyclists performed two sequential maximal exercise tests (25W+25W/min; Pbar=630mmHg) in a randomly assigned and counterbalanced order. With a normocapnic test as a control, we clamped PETCO2 in the intervention trial by using a rebreathing circuit combined with real-time CO2 monitoring to prevent the decrease in PETCO2 after the RCP. Changes in middle cerebral artery CBFv (transcranial Doppler), tissue oxygenation (frontal lobe and vastus lateralis, near infrared spectroscopy; peripheral pulse oximetry), end-tidal CO2 (PETCO2), ventilation, and non-invasive blood pressure were analyzed across percent of peak power and at the RCP (significance at P < 0.05). RESULTS: During the intervention trial, we prevented the fall in PETCO2 at maximal exercise (40.9+/-5.2 mmHg vs. 32.8+/-5.7 mmHg during unclamped, p < 0.05). CBFv was higher at peak power with CO2 clamping (47.5 +/- 8.3 cm/s vs. 38.2 +/- 7.3 cm/s, P< 0.05), but brain and muscle oxygenation were unchanged, and peak power was lower (384.3+/-22.1Watts vs. 407.9+/-28.7 Watts, P < 0.05). CONCLUSION: At maximal exercise, CO2 is a key determinant of CBFv, but cerebral oxygenation and maximal aerobic power do not change in parallel to CBFv under normoxic conditions. Acknowledgements This study supported by NIH RO1 HL-070362, the Altitude Research Center, the Cystic Fibrosis Foundation Grant OLIN08B0 and the Pediatric Pulmonary Fellowship of the University of Colorado.