Time-varying signal analysis to detect high-altitude periodic breathing in climbers ascending to extreme altitude

This work investigates the performance of cardiorespiratory analysis detecting periodic breathing (PB) in chest wall recordings in mountaineers climbing to extreme altitude. The breathing patterns of 34 mountaineers were monitored unobtrusively by inductance plethysmography, ECG and pulse oximetry using a portable recorder during climbs at altitudes between 4497 and 7546 m on Mt. Muztagh Ata. The minute ventilation (VE) and heart rate (HR) signals were studied, to identify visually scored PB, applying time-varying spectral, coherence and entropy analysis. In 411 climbing periods, 30–120 min in duration, high values of mean power (MPVE) and slope (MSlopeVE) of the modulation frequency band of VE, accurately identified PB, with an area under the ROC curve of 88 and 89 %, respectively. Prolonged stay at altitude was associated with an increase in PB. During PB episodes, higher peak power of ventilatory (MPVE) and cardiac (MPLF HR) oscillations and cardiorespiratory coherence (MPLFCoher), but reduced ventilation entropy (SampEnVE), was observed. Therefore, the characterization of cardiorespiratory dynamics by the analysis of VE and HR signals accurately identifies PB and effects of altitude acclimatization, providing promising tools for investigating physiologic effects of environmental exposures and diseases.Peer ReviewedPostprint (author’s final draft

Alterations of cardiovascular complexity during acute exposure to high altitude: A multiscale entropy approach

Stays at high altitude induce alterations in cardiovascular control and are a model of specific pathological cardiovascular derangements at sea level. However, high-altitude alterations of the complex cardiovascular dynamics remain an almost unexplored issue. Therefore, our aim is to describe the altered cardiovascular complexity at high altitude with a multiscale entropy (MSE) approach. We recorded the beat-by-beat series of systolic and diastolic blood pressure and heart rate in 20 participants for 15 min twice, at sea level and after arrival at 4554 m a.s.l. We estimated Sample Entropy and MSE at scales of up to 64 beats, deriving average MSE values over the scales corresponding to the high-frequency (MSEHF) and low-frequency (MSELF) bands of heart-rate variability. We found a significant loss of complexity at heart-rate and blood-pressure scales complementary to each other, with the decrease with high altitude being concentrated at Sample Entropy and at MSEHF for heart rate and at MSELF for blood pressure. These changes can be ascribed to the acutely increased chemoreflex sensitivity in hypoxia that causes sympathetic activation and hyperventilation. Considering high altitude as a model of pathological states like heart failure, our results suggest new ways for monitoring treatments and rehabilitation protocols

Aerospace medicine and biology: A continuing bibliography with indexes (supplement 327)

This bibliography lists 127 reports, articles and other documents introduced into the NASA Scientific and Technical Information System during August, 1989. Subject coverage includes: aerospace medicine and psychology, life support systems and controlled environments, safety equipment, exobiology and extraterrestrial life, and flight crew behavior and performance

Aerospace medicine and biology: A continuing bibliography with indexes (supplement 299)

This bibliography lists 96 reports, articles, and other documents introduced into the NASA scientific and technical information system in June, 1987

Does acute hypoxia and high altitude exposure adversely affect cardiovascular performance?

Introduction: The cardiovascular adaptations to high altitude (HA) exposure and its relationship to acute mountain sickness (AMS) are incompletely understood. Aims: This thesis addresses four main hypotheses 1. HA adversely affects biventricular cardiac function leading to an increase in estimated filling pressures which is influenced by the mode of hypoxia. 2. HA exposure leads to myocardial injury that is linked to the development of AMS. 3. HA exposure is associated with a reduction in arterial compliance and an increase in central blood pressure (BP). 4. HA exposure reduces heart rate (HR) variability (HRV) that is linked to AMS an increased risk of cardiac arrhythmias. Methods: This consisted of eight independent studies conducted at terrestrial and ‘simulated’ HA (hypobaric hypoxia [HH] and normobaric hypoxia [NH] Cardiac function and arterial compliance were examined using portable transthoracic echocardiography and pulse contour analysis respectively. Myocardial injury was measured in venous blood by cardiac troponin T (cTnT) quantification. Cardiac inter-beat interval data for HRV analysis was acquired using single lead ECGs and novel finger and patch sensor technologies. Cardiac rhythm was investigated using a novel implantable cardiac monitor. Results: HA exposure was associated with a non-pathological increase in cTnT, and mild diastolic changes without adversely affecting systolic function or ventricular filling pressures. Resting cardiovascular responses were similar with HH, NH and HA, though notable differences emerged with exercise. Resting central BP, HR and BP-augmentation increased at terrestrial HA. HRV fell (eg reduced time-domain measures, increased LF/HF ratios and less chaos) at HA and was consistently different between men and women. Significant HA (>3500m) was associated with the development of tachyarrhythmia (atrial fibrillation and supraventricular tachycardia) and asymptomatic nocturnal bradycardias and pauses (>3.0 seconds). There were no independent predictors of AMS and its severity. Conclusion: HA-related hypoxia induces early sympathetic activation leading to an increase in resting HR and central BP and may be proarrhythmic. Parasympathetic activation with acclimatisation can trigger nocturnal pauses at higher altitudes. HA exposure does not adversely affect cardiac function

Aerospace Medicine and Biology: A continuing bibliography with indexes, supplement 145

This bibliography lists 301 reports, articles, and other documents introduced into the NASA scientific and technical information system in August 1975

Aerospace Medicine and Biology: A continuing bibliography with indexes, supplement 127, April 1974

This special bibliography lists 279 reports, articles, and other documents introduced into the NASA scientific and technical information system in March 1974

Aerospace medicine and biology: A continuing bibliography with indexes (supplement 292)

This bibliography lists 192 reports, articles and other documents introduced into the NASA scientific and technical information system in December, 1986

The Influence of Cerebral Blood Flow and Carbon Dioxide on Neuromuscular Responses During Environmental Stress

Although reductions in cerebral blood flow (CBF) may be implicated in the development of central fatigue during environmental stress, the contribution from hypocapnia-induced reductions in CBF versus reductions in CBF per se has yet to be isolated. The current research program examined the influence of CBF, with and without consequent hypocapnia, on neuromuscular responses during hypoxia and passive heat stress. To this end, neuromuscular responses, as indicated by motor evoked potentials (MEP), maximal M-wave (Mmax) and cortical voluntary activation (cVA) of the flexor carpi radialis muscle during isometric wrist flexion, was assessed in three separate projects: 1) hypocapnia, independent of concomitant reductions in CBF; 2) altered CBF during severe hypoxia and; 3) thermal hyperpnea-mediated reductions in CBF, independent of hypocapnia. All projects employed a custom-built dynamic end-tidal forcing system to control end-tidal PCO2 (PETCO2), independent of the prevailing environmental conditions, and cyclooxygenase inhibition using indomethacin (Indomethacin, 1.2 mg·Kg-1) to selectively reduce CBF (estimated using transcranial Doppler ultrasound) without changes in PETCO2. A primary finding of the present research program is that the excitability of the corticospinal tract is inherently sensitive to changes in PaCO2, as demonstrated by a 12% increase in MEP amplitude in response to moderate hypocapnia. Conversely, CBF mediated reductions in cerebral O2 delivery appear to decrease corticospinal excitability, as indicated by a 51-64% and 4% decrease in MEP amplitude in response to hypoxia and passive heat stress, respectively. The collective evidence from this research program suggests that impaired voluntary activation is associated with reductions in CBF; however, it must be noted that changes in cVA were not linearly correlated with changes in CBF. Therefore, other factors independent of CBF, such as increased perception of effort, distress or discomfort, may have contributed to the reductions in cVA. Despite the functional association between reductions in CBF and hypocapnia, both variables have distinct and independent influence on the neuromuscular system. Therefore, future studies should control or acknowledge the separate mechanistic influence of these two factors