Journal of applied physiology
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Randomized Controlled Trial
Effects of respiratory time ratio on heart rate variability and spontaneous baroreflex sensitivity.
Paced breathing is a frequently performed technique for cardiovascular autonomic studies. The relative timing of inspiration and expiration during paced breathing, however, is not consistent. We, therefore, examined whether indexes of heart rate variability and spontaneous baroreflex sensitivity would be affected by the respiratory time ratio that is set. ⋯ At the same time, Porta's and Guzik's indexes obtained during 0.1-Hz breathing were greater than during 0.25-Hz breathing in both positions. The authors suggest that setting the I/E during paced breathing is not necessary when measuring spectral indexes of heart rate variability and spontaneous baroreflex sensitivity under the conditions used in this study. The necessity of paced breathing for the measurement of heart rate asymmetry, however, requires further investigation.
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Randomized Controlled Trial
Intravenous adenosine activates diffuse nociceptive inhibitory controls in humans.
Experimentally induced pain can be attenuated by concomitant heterotopic nociceptive stimuli (counterirritation). Animal data indicate that this stems from supraspinal "diffuse noxious inhibitory controls" (DNICs) triggered by C and Aδ fibers. In humans, only noxious stimuli induce counterirritation. ⋯ The temporal dynamics of adenosine-induced dyspnea and RIII inhibition differed (immediate onset followed by a slow decrease for dyspnea, slower onset for RIII inhibition). Intravenous adenosine in normal humans induces counterirritation, fueling the notion that C-fiber stimulation trigger DNICs in humans. The temporal dissociation between adenosine-induced dyspnea and RIII inhibition suggests that C fibers other than pulmonary ones might be involved.
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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 Comparative Study
Mechanisms of nasal high flow on ventilation during wakefulness and sleep.
Nasal high flow (NHF) has been shown to increase expiratory pressure and reduce respiratory rate but the mechanisms involved remain unclear. Ten healthy participants [age, 22 ± 2 yr; body mass index (BMI), 24 ± 2 kg/m(2)] were recruited to determine ventilatory responses to NHF of air at 37°C and fully saturated with water. We conducted a randomized, controlled, cross-over study consisting of four separate ∼60-min visits, each 1 wk apart, to determine the effect of NHF on ventilation during wakefulness (NHF at 0, 15, 30, and 45 liters/min) and sleep (NHF at 0, 15, and 30 liters/min). ⋯ In the nasal cavity model, NHF increased expiratory but decreased inspiratory resistance depending on both the cannula size and the expiratory flow rate. The mechanisms of action for NHF differ from those of CPAP and are sleep/wake-state dependent. NHF may be utilized to increase tidal breathing during wakefulness and to relieve respiratory loads during sleep.
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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.