Ainslie PN, Barach A, Murrell C, Hamlin M, Hellemans J, Ogoh S. Alterations in cerebral autoregulation and cerebral blood flow velocity during acute hypoxia: rest and exercise. Am J Physiol Heart Circ Physiol 292: H976 -H983, 2007. First published September 29, 2006; doi:10.1152/ajpheart.00639.2006.-We examined the relationship between changes in cardiorespiratory and cerebrovascular function in 14 healthy volunteers with and without hypoxia [arterial O2 saturation (SaO 2 ) ϳ80%] at rest and during 60 -70% maximal oxygen uptake steady-state cycling exercise. During all procedures, ventilation, end-tidal gases, heart rate (HR), arterial blood pressure (BP; Finometer) cardiac output (Modelflow), muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAV; transcranial Doppler ultrasound) were measured continuously. The effect of hypoxia on dynamic cerebral autoregulation was assessed with transfer function gain and phase shift in mean BP and MCAV. At rest, hypoxia resulted in increases in ventilation, progressive hypocapnia, and general sympathoexcitation (i.e., elevated HR and cardiac output); these responses were more marked during hypoxic exercise (P Ͻ 0.05 vs. rest) and were also reflected in elevation of the slopes of the linear regressions of ventilation, HR, and cardiac output with SaO 2 (P Ͻ 0.05 vs. rest). MCAV was maintained during hypoxic exercise, despite marked hypocapnia (44.1 Ϯ 2.9 to 36.3 Ϯ 4.2 Torr; P Ͻ 0.05). Conversely, hypoxia both at rest and during exercise decreased cerebral oxygenation compared with muscle. The low-frequency phase between MCAV and mean BP was lowered during hypoxic exercise, indicating impairment in cerebral autoregulation. These data indicate that increases in cerebral neurogenic activity and/or sympathoexcitation during hypoxic exercise can potentially outbalance the hypocapniainduced lowering of MCAV. Despite maintaining MCAV, such hypoxic exercise can potentially compromise cerebral autoregulation and oxygenation.hypocapnia; hypoxemia AN IMPORTANT PROTECTIVE FEATURE of the cerebral circulation is the ability to maintain cerebral blood flow (CBF) over a wide range of cerebral perfusion pressures (36). At rest, lowering of arterial PCO 2 (Pa CO 2 ) (hypocapnia) as a result of hyperventilation and elevations in sympathetic activation act to enhance cerebral autoregulation (i.e., by widening the cerebral autoregulation curve and causing a rightward shift, respectively), thus preventing cerebral hyperperfusion (36). During exercise, however, it has been shown that dynamic cerebral autoregulation was impaired by exhaustive exercise despite a hyperventilation-induced reduction in Pa CO 2 and likely exercise-induced elevations in sympathetic activation (35).Acute hypoxia in resting and exercising humans results in an enhanced muscle sympathetic discharge, cardiac output, skeletal muscle blood flow, and increased heart rate with little or no alteration in mean arterial blood pressure (MAP) (15, 38). In the brain, the vasod...

We tested the hypothesis that intermittent hypoxia (IH) and/or continuous hypoxia (CH) would enhance the ventilatory response to acute hypoxia (HVR), thereby altering blood pressure (BP) and cerebral perfusion. Seven healthy volunteers were randomly selected to complete 10-12 days of IH (5-min hypoxia to 5-min normoxia repeated for 90 min) before ascending to mild CH (1,560 m) for 12 days. Seven other volunteers did not receive any IH before ascending to CH for the same 12 days. Before the IH and CH, following 12 days of CH and 12-13 days post-CH exposure, all subjects underwent a 20-min acute exposure to poikilocapnic hypoxia (inspired fraction of O(2), 0.12) in which ventilation, end-tidal gases, arterial O(2) saturation, BP, and middle cerebral artery blood flow velocity (MCAV) were measured continuously. Following the IH and CH exposures, the peak HVR was elevated and was related to the increase in BP (r = 0.66 to r = 0.88, respectively; P < 0.05) and to a reciprocal decrease in MCAV (r = 0.73 to r = 0.80 vs. preexposures; P < 0.05) during the hypoxic test. Following both IH and CH exposures, HVR, BP, and MCAV sensitivity to hypoxia were elevated compared with preexposure, with no between-group differences following the IH and/or CH conditions, or persistent effects following 12 days of sea level exposure. Our findings indicate that IH and/or mild CH can equally enhance the HVR, which, by either direct or indirect mechanisms, facilitates alterations in BP and MCAV.

Some adults with an intellectual disability, who have a history of falling, may have delayed responses to postural perturbations and this impairment could be targeted in physiotherapy interventions aimed at improving balance capabilities and preventing falls.

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