Journal of applied physiology
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Randomized Controlled Trial
Worsening of central sleep apnea at high altitude--a role for cerebrovascular function.
Although periodic breathing during sleep at high altitude occurs almost universally, the likely mechanisms and independent effects of altitude and acclimatization have not been clearly reported. Data from 2005 demonstrated a significant relationship between decline in cerebral blood flow (CBF) at sleep onset and subsequent severity of central sleep apnea that night. We suspected that CBF would decline during partial acclimatization. ⋯ Over 10 days, the increases resolved and AHI worsened. During sleep at high altitude large oscillations in mean CBF velocity (CBFv) occurred, which were 35% higher initially (peak CBFv = 96 cm/s vs. peak CBFv = 71 cm/s) than at days 12-15. Our novel findings suggest that elevations in CBF and its reactivity to CO(2) upon initial ascent to high altitude may provide a protective effect on the development of periodic breathing during sleep (likely via moderating changes in central Pco2).
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Randomized Controlled Trial
Interindividual relationships between blood pressure and cerebral blood flow variability with intact and blunted cerebrovascular control.
The relationships between blood pressure variability (BPV) and cerebral blood flow variability (CFV) across individuals in the presence of intact and blunted cerebrovascular control are poorly understood. This study sought to characterize the interindividual associations between spontaneous BPV and CFV under conditions of normal and blunted [calcium channel blockade (CCB)] cerebrovascular control in healthy humans. We analyzed blood pressure and flow velocity data from 12 subjects treated with CCB (60 mg oral nimodipine) and 11 subjects treated with a placebo pill. ⋯ Compared with placebo, CCB reduced very-low-frequency MAP (P < 0.05) and MCAv(mean) power (P < 0.01) and the low-frequency cross-spectral phase angle (P < 0.05). The magnitude of change in MAP and MCAv(mean) power with CCB (i.e., change scores) was positively related in the very-low-frequency range. Collectively, these findings indicate that CFV may be an explanatory factor in the association between elevated BPV and adverse cerebrovascular outcomes and support the possibility of using CCB to improve hemodynamic stability under resting conditions.
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Methods to classify activity types are often evaluated with an experimental protocol involving prescribed physical activities under confined (laboratory) conditions, which may not reflect real-life conditions. The present study aims to evaluate how study design may impact on classifier performance in real life. Twenty-eight healthy participants (21-53 yr) were asked to wear nine triaxial accelerometers while performing 58 activity types selected to simulate activities in real life. ⋯ Walking time was systematically overestimated, except for lower back sensor data (range: 7-757%). In conclusion, classifier performance under confined conditions may not accurately reflect classifier performance in real life. Future studies that aim to evaluate activity classification methods are warranted to pay special attention to the representativeness of experimental conditions for real-life conditions.
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Chronic obstructive pulmonary disease (COPD) patients often show asynchronous movement of the lower rib cage during spontaneous quiet breathing and exercise. We speculated that varying body position from seated to supine would influence rib cage asynchrony by changing the configuration of the respiratory muscles. Twenty-three severe COPD patients (forced expiratory volume in 1 s = 32.5 ± 7.0% predicted) and 12 healthy age-matched controls were studied. ⋯ Rib cage paradox was noticed in approximately one-half of the COPD patients while seated, but was not related to impaired diaphragm motion. In the supine posture, the rib cage paradox disappeared, suggesting that, in this posture, diaphragm mechanics improves. In conclusion, changing body position induces important differences in the chest wall behavior in COPD patients.
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Hyperbaric oxygen (HBO(2)) stimulates presumptive central CO2-chemoreceptor neurons, increases minute ventilation (V(min)), decreases heart rate (HR) and, if breathed sufficiently long, produces central nervous system oxygen toxicity (CNS-OT; i.e., seizures). The risk of seizures when breathing HBO(2) is variable between individuals and its onset is difficult to predict. We have tested the hypothesis that a predictable pattern of cardiorespiration precedes an impending seizure when breathing HBO2. ⋯ Breathing HBO2 induced an early transient increase in V(min) (Phase 2) and HR during the chamber pressurization, followed by a second significant increase of V(min) ≤8 min prior to seizure (Phase 3). HR, which subsequently decreased during sustained hyperoxia, showed no additional changes prior to seizure. We conclude that hyperoxic hyperpnea (Phase 3 of the compound hyperoxic ventilatory response) is a predictor of an impending seizure while breathing poikilocapnic HBO(2) at rest in unanesthetized rats.