Regional cerebral perfusion and sympathetic activation during exercise in hypoxia and hypercapnia: preliminary insight into 'Cushing's mechanism'

We examined the interactive influence of hypoxia and exercise, and hypercapnia and exercise, on regional cerebral perfusion and sympathetic activation. Twenty healthy young adults (seven women) completed study trials including (1) rest in normoxia (SpO(2) : similar to 96%, P-ETCO2 : similar to 36 mmHg), normocapnic hypoxia (SpO(2) : similar to 84%, P-ETCO2 : similar to 36 mmHg), and normoxic hypercapnia (SpO(2) : similar to 98%, P-ETCO2 : similar to 46 mmHg) and (2) unilateral rhythmic handgrip exercise (45% of maximal voluntary contraction at 1 Hz for 3 min) under the same gas conditions. Based on the exercising arm, blood flow in the contralateral internal carotid (ICA(BF)) and ipsilateral vertebral (VA(BF)) arteries, anterior and posterior cerebral O-2 delivery (CDO2), and muscle sympathetic nerve activity (MSNA) were measured in each trial. During exercise in hypoxia, ICA(BF), VA(BF), anterior and posterior CDO2 were significantly lower, whereas totalMSNA was significantly greater, than the sumof the responses evoked by either hypoxia or exercise alone. During exercise in hypercapnia, ICA(BF) and anterior CDO2 were significantly greater, whereas MSNA was lower, than the sum of the responses evoked by either hypercapnia or exercise alone. The VABF and posterior CDO2 responses to hypercapnic exercise were not different from the summated responses. These findings suggest that the brain is hypoperfused and sympathetic outflow potentiated during hypoxic exercise, and that the brain is hyperperfused and sympathetic discharge constrained during hypercapnic exercise. The contrasting consequences for cerebral perfusion and sympathetic activation indicate a potential involvement of Cushing's mechanism in the autonomic control during exercise in healthy humans.