Specific effect of hypobaria on cerebrovascular hypercapnic responses in hypoxia.

It remains unknown whether hypobaria plays a role on cerebrovascular reactivity to CO2 (CVR). The present study evaluated the putative effect of hypobaria on CVR and its influence on cerebral oxygen delivery (cDO2 ) in five randomized conditions (i.e., normobaric normoxia, NN, altitude level of 440 m; hypobaric hypoxia, HH at altitude levels of 3,000 m and 5,500 m; normobaric hypoxia, NH, altitude simulation of 5,500 m; and hypobaric normoxia, HN). CVR was assessed in nine healthy participants (either students in aviation or pilots) during a hypercapnic test (i.e., 5% CO2 ). We obtained CVR by plotting middle cerebral artery velocity versus end-tidal CO2 pressure (PET CO2 ) using a sigmoid model. Hypobaria induced an increased slope in HH (0.66 ± 0.33) compared to NH (0.35 ± 0.19) with a trend in HN (0.46 ± 0.12) compared to NN (0.23 ± 0.12, p = .069). PET CO2 was decreased (22.3 ± 2.4 vs. 34.5 ± 2.8 mmHg and 19.9 ± 1.3 vs. 30.8 ± 2.2 mmHg, for HN vs. NN and HH vs. NH, respectively, p < .05) in hypobaric conditions when compared to normobaric conditions with comparable inspired oxygen pressure (141 ± 1 vs. 133 ± 3 mmHg and 74 ± 1 vs. 70 ± 2 mmHg, for NN vs. HN and NH vs. HH, respectively) During hypercapnia, cDO2 was decreased in 5,500 m HH (p = .046), but maintained in NH when compared to NN. To conclude, CVR seems more sensitive (i.e., slope increase) in hypobaric than in normobaric conditions. Moreover, hypobaria potentially affected vasodilation reserve (i.e., MCAv autoregulation) and brain oxygen delivery during hypercapnia. These results are relevant for populations (i.e., aviation pilots; high-altitude residents as miners; mountaineers) occasionally exposed to hypobaric normoxia.

Active Preconditioning With Blood Flow Restriction or/and Systemic Hypoxic Exposure Does Not Improve Repeated Sprint Cycling Performance.

PURPOSE: The aim of this study was to evaluate the effects of active preconditioning techniques using blood flow restriction or/and systemic hypoxic exposure on repeated sprint cycling performance and oxygenation responses. METHODS: Participants were 17 men; 8 were cycle trained (T: 21 ± 6 h/week) and 9 were untrained but physically active (UT). Each participant completed 4 cycles of 5 min stages of cycling at 1.5 W⋅kg-1 in four conditions [Control; IPC (ischemic preconditioning) with partial blood flow restriction (60% of relative total occlusion pressure); HPC (hypoxic preconditioning) in normobaric systemic hypoxia (FIO2 13.6%); and HIPC (hypoxic and ischemic preconditioning combined)]. Following a 40 min rest period, a repeated sprint exercise (RSE: 8 × 10 s sprints; 20 s of recovery) was performed. Near-infrared spectroscopy parameters [for each sprint, change in deoxyhemoglobin (Δ[HHb]), total hemoglobin (Δ[tHb]), and tissue saturation index (ΔTSI%)] were measured. RESULTS: Trained participants achieved higher power outputs (+10-16%) than UT in all conditions, yet RSE performance did not differ between active preconditioning techniques in the two groups. All conditions induced similar sprint decrement scores during RSE in both T and UT (16 ± 2 vs. 23 ± 9% in CON; 17 ± 3 vs. 19 ± 6% in IPC; 18 ± 5 vs. 20 ± 10% in HPC; and 17 ± 3 vs. 21 ± 5% in HIPC, for T and UT, respectively). During the sprints, Δ[HHb] was larger after IPC than both HPC and CON in T (p < 0.001). The Δ[tHb] was greater after HPC than all other conditions in T, whereas IPC, HPC, and HIPC induced higher Δ[tHb] than CON in UT. CONCLUSION: None of the active preconditioning methods had an ergogenic effect on repeated sprint cycling performance, despite some specific hemodynamic responses (e.g., greater oxygen extraction and changes in blood volume), which were emphasized in the trained cyclists.

Cardiovascular and Cerebral Responses During a Vasovagal Reaction Without Syncope.

This clinical case report presents synchronous physiological data from an individual in whom a spontaneous vasovagal reaction occurred without syncope. The physiological data are presented for three main phases: Baseline (0-200 s), vasovagal reaction (200-600 s), and recovery period (600-1200 s). The first physiological changes occurred at around 200 s, with a decrease in blood pressure, peak in heart rate and vastus lateralis tissue oxygenation, and a drop in alpha power. The vasovagal reaction was associated with a progressive decrease in blood pressure, heart rate and cerebral oxygenation, whilst the mean middle cerebral artery blood flow velocity and blood oxygen saturation remained unchanged. Heart rate variability parameters indicated significant parasympathetic activation with a decrease in sympathetic tone and increased baroreflex sensitivity. The total blood volume and tissue oxygenation index (TOI) dropped in the brain but slightly increased in the vastus lateralis, suggesting cerebral hypoperfusion with blood volume pooling in the lower body part. Cerebral hypoperfusion during the vasovagal reaction was associated with electroencephalography (EEG) flattening (i.e., decreased power in beta and theta activity) followed by an EEG high-amplitude "slow" phase (i.e., increased power in theta activity). The subject developed signs and symptoms of pre-syncope with EEG flattening and slowing during prolonged periods of symptomatic hypotension, but did not lose consciousness.