Short-term High Altitude Exposure Research Articles

Effects of short-term exposure to high altitude on cardiac function

Abstract Background What effect does short-term high altitude exposure have on heart function? Can people exercise in the highlands? what changes occur in heart function during exercise in highland areas? This study will explore these topics. Objectives To investigate the difference of heart function between people at sea level and at high altitude, and to study the changes of short time exercise on heart function at high altitude. Methods 36 healthy subjects were recruited to go to high altitude area after underwent exercise echocardiography on a supine bicycle at sea level. They ascended to 3600m within 24 hours by bus.Another exercise echocardiography was performed on the day of arrival.Heart rate (HR), blood pressure (BP) and blood oxygen saturation (SaO2) were monitored in real time during both examinations. Parameters such as left ventricular ejection fraction, E/ E 'and mean pulmonary artery pressure (mPAP) after rest and exercise were calculated.ΔmPAP /CO was calculated by (mean mPAP at peak -mean mPAP at rest )/(mean CO at peak-mean CO at rest). Results At peak exercise,SaO2,TRV,RVD2,SPAP,mPAP,PVR, ePLAR,RVAS,ΔMpap/CO were much higher at high altitude levels. (P < 0.001); E,A,FAC,ΔS were significantly lower than that of the sea leval; at rest, HR,TRV,sPAP,mPAP ,PVR were much higher at high altitude levels than at sea leval(P < 0.001)，SaO2,RVOT ACT, were significantly lower than that of the sea leval(P < 0.001). Conclusions When healthy people are in high altitude environment, the heart function changes obviously. Supine bicycle exercise stress echocardiography can well monitor the heart function changes and provide quantitative data, providing new technical methods for future related research.

Comprehensive Evaluation of Acute Physiological and Psychological Responses to a Short-Term High-Altitude Exposure at 2500 Meters

Comprehensive Evaluation of Acute Physiological and Psychological Responses to a Short-Term High-Altitude Exposure at 2500 Meters

Impact of flight and equivalent short-term high-altitude exposure on ocular structures and function.

Exposure to high-altitude conditions during flight or similar activities affects many aspects of visual function, which is critical not only for flight safety but for any altitude-related activity. We aimed to summarize the available literature pertaining to ocular changes during flight or equivalent short-term high-altitude exposure (e.g., hypobaric chamber, effortless ascent lasting ≤ 24 h) and to highlight future research priorities. Using the PubMed/MEDLINE and Web of Science/ISI Web of Knowledge databases with structured search syntax, we conducted a systematic review of the literature spanning a 40-year period (January 1, 1983, to October 10, 2023). Articles pertaining to ocular changes during flight or flight-equivalent exposure to altitude were retrieved. The reference lists of retrieved studies were also searched, and citations of these references were included in the results. Of 875 relevant PubMed and ISI publications, 122 qualified for inclusion and 20 more were retrieved from the reference lists of initially selected records, for a total of 142 articles. Reported anterior segment changes included deterioration in tear film stability and increased dry eye incidence, increased corneal thickness, discomfort and bubble formation in contact lens users, refraction changes in individuals with prior refractive surgery, decreased intraocular pressure, and alterations in pupillary reaction, contrast sensitivity, and visual fields. Photoreceptor-visual pathway changes included alterations in both photoreceptors and neuro-transduction, as evidenced in dark adaptation, macular recovery time, reduction in visual field sensitivity, and optic neuritis (likely an element of decompression sickness). Retinochoroidal changes included increases in retinal vessel caliber, retinal blood flow, and choroidal thickness; central serous chorioretinopathy; and retinal vascular events (non-arteritic ischemic optic neuropathy, high-altitude retinopathy, and retinal vein occlusion). The effect of short-term high-altitude exposure on the eye is, in itself, a difficult area to study. Although serious impairment of visual acuity appears to be rare, ocular changes, including tear film stability, contact lens wear, central corneal thickness, intraocular pressure, contrast sensitivity, stability of refractive surgeries, retinal vessels, visual fields, and macula recovery time, should be considered in civilian aviators. Our report provides guidance to climbers and lowlanders traveling to altitude if they have pre-existing ocular conditions or if they experience visual symptoms while at altitude. However, key outcomes have been contradictory and comprehensive studies are scarce, especially those pertaining to the choroid and retina. Such studies could not only deepen our understanding of high-altitude ocular pathophysiology, but could also offer valuable information and treatment possibilities for a constellation of other vision-threatening diseases.

Effect of High-Altitude Exposure on the Heart

High altitude brings a great physiological change in human beings, both during short-term exposure and in lifelong residents, especially in the cardiovascular system. Hypoxia notably induces pulmonary vasoconstriction, thus resulting in a moderate increase in pulmonary arterial pressure. Acclimatized inhabitants exhibit lower pulmonary pressure and better exercise capacity than lowlanders during short-term high-altitude exposure. Rapid ascent to high altitude without adequate acclimatization can cause high-altitude pulmonary edema in susceptible individuals, with a rapid increase in pulmonary pressure. Cardiac output increases initially following acute high-altitude exposure and returns to normal as at sea level after a few days of acclimatization. Ventricular volumes at high altitude change consistently with decreases in plasma volume. Left ventricular systolic function is enhanced after acute high-altitude exposure and during chronic acclimatization. However, there are controversies on whether right ventricular systolic function is preserved or decreases after high-altitude exposure, probably due to variable hypoxic pulmonary vasoconstriction. High altitude induces altered ventricular diastolic patterns. Recently, a new perspective has emerged, whereby ventricular intrinsic relaxation is not impaired, as assessed by untwisting through speckle-tracking imaging. Persistent hypoxic pulmonary hypertension probably induced right ventricular dilation and hypertrophy, and even right heart failure, described as high-altitude heart diseases. Descent to lower altitude should be the best treatment for them, and potential pharmacological agents majorly focus on the inhabitation of pulmonary vasoconstriction, such as phosphodiesterase-5 inhibitors and endothelin receptor antagonists. Evidence on the risks of high-altitude exposure for patients with previous cardiovascular diseases is limited, and thus they should be prudent when ascending to high altitude. Further randomized large-scale studies are needed to explore cardiac performance at high altitudes and provide more evidence for the prevention and clinical management of medical complications at high altitude.

Atrial performance in healthy subjects following high altitude exposure at 4100\xa0m: 2D speckle-tracking strain analysis

High altitude (HA) exposure has been considered as a cardiac stress and might impair ventricular diastolic function. Atrial contraction is involved in ventricular passive filling, however the atrial performance to HA exposure is poorly understood. This study aimed to evaluate the effect of short-term HA exposure on bi-atrial function. Physiological and 2D-echocardiographic data were collected in 82 healthy men at sea level (SL, 400 m) and 4100 m after an ascent within 7 days. Atrial function was measured using volumetric and speckle-tracking analyses during reservoir, conduit and contractile phases of cardiac cycle. Following HA exposure, significant decreases of reservoir and conduit function indexes were observed in bi-atria, whereas decreases of contractile function indexes were observed in right atrium (RA), estimated via RA active emptying fraction (SL 41.7 ± 13.9% vs. HA 35.4 ± 12.2%, p = 0.001), strain during the contractile phase [SL 13.5 (11.4, 17.8) % vs. HA 12.3 (9.3, 15.9) %, p = 0.003], and peak strain rate during the contractile phase [SL − 1.76 (− 2.24, − 1.48) s−1 vs. HA − 1.57 (− 2.01, − 1.23) s−1, p = 0.002], but not in left atrium (LA). In conclusion, short-term HA exposure of healthy individuals impairs bi-atrial performance, mostly observed in RA. Especially, atrial contractile function decreases in RA rather than LA, which seems not to compensate for decreased ventricular filling after HA exposure. Our findings may provide a novel evidence for right-sided heart dysfunction to HA exposure.

Pulmonary function tests at low altitude predict pulmonary pressure response to short-term high altitude exposure

Background: Travelling to high altitude (HA) presents a risk of the high levels of pulmonary artery pressure (PAP) at altitude, which is associated with impaired exercise capacity and fatal HA pulmonary oedema. However, prediction of high levels of PAP at altitude is still unclear.Methods: Echocardiography and pulmonary function tests were performed on 121 healthy men at low altitude (LA) and 4100 m (5 ± 2 h after a 7 day ascent).Results: HA exposure increased the levels of FEV1/FVC ratio, FEF25%, 50%, 75%, MMEF, mPAP, total pulmonary vascular resistance (PVR) and systolic pulmonary arterial pressure (SPAP). More smokers and lower forced expiratory flow at 25% of forced vital capacity (FEF25%) at LA were observed in subjects with mPAP≥30 mmHg than those with mPAP<30 mmHg at HA. Multivariate logistic regression identified that FEF25% at LA [odds ratio (OR) 0.50, 95%CI 0.33−0.76, p = 0.001] and smoking (OR 3.09, 95%CI 1.31–7.27, p = 0.010) were the independent predictors for identifying subjects with mPAP≥30 mmHg at HA. Moreover, FEF25% at LA was linearly correlated with mPAP at HA (r = -0.31, p < 0.001), which mainly existed in smokers. Compared to subjects with FEF25% ≥7.55 L/sec at LA, those with FEF25% <7.55 L/sec at LA showed higher levels of mPAP, and total PVR, and a multivariable OR of 11.16 (95%CI, 3.48–35.81) for developing mPAP ≥ 30 mmHg at HA. However, there was no significant difference in the incidences of AMS and its related clinical symptoms in subjects with different levels of FEF25%.Conclusions: Thus, these findings suggest that subjects with low FEF25% values at LA are susceptible to high levels of PAP at altitude but not the incidence of AMS following short-term HA exposure, especially in smokers.

Short-Term High-Altitude Exposure (3600 m) Alters the Type Distribution of Sperm Deformity.

Background: The effect of short-term exposure to high altitudes below 4000 m on the distribution of sperm abnormality is a matter of concern with regard to the ability for fertilization, and rarely reported. Materials and Methods: The survey subjects, who had not visited the high plateau previously, were divided into three groups: two high-plateau groups and the low-altitude control group. In the high-plateau groups, healthy young men had been living in Lhasa City, Tibet (3600 m), for 1 or 3 months. Similar subjects in Chongqing City (400 m) were used as the control group. Semen was collected, and semen volume, pH, and sperm concentration were analyzed. After observing sperm morphology by light microscopy, we measured the percentage of sperm abnormality and statistically analyzed its type distribution. Results: Sperm concentration was decreased significantly after 3 months of high-altitude exposure (p < 0.01). The total sperm malformation rate did not change, but the head malformation rate was increased (p < 0.05). In addition, there were changes in the distribution of sperm malformation. The occurrence and frequency of sperm with excessive head size, neck crimp, and tailless were increased significantly (p < 0.01, p < 0.01, and p < 0.05, respectively) at 3 months. Conclusion: Our study demonstrates that short-term high-altitude exposure of >1 month at 3600 m increases the distribution of sperm deformities.

Retinal vessel oxygen saturation and vessel diameter in healthy individuals during high-altitude exposure.

To assess changes of retinal vessel oxygen saturation and vessel diameter in healthy individuals during high-altitude exposure. Retinal oxygen saturation and vessel diameter were obtained at sea level (SL, 40m) and high altitude (HA, 3681m) on 17 healthy individuals from Beijing (six males, 28.06±8.06years) using Oxymap T1 and then compared with 21 residents from Yushu (10 males, 28.63±6.00years). Systemic and ocular parameters were also measured before and after high-altitude exposure. Data were presented as mean±SD and analysed using paired and independent Student t-test with significance accepted at p<0.05. Short-term high-altitude exposure of Beijing Group significantly affected all the systemic and ocular parameters, as well as retinal oxygen saturation and vessel diameter ranging from overall quadrant to different quadrants, other than retinal venous oxygen saturation and retinal arterial diameter. However, these changes were not evident in those permanently living at HA. Pearson's correlation analysis revealed correlations between retinal oxygen saturation and systemic and ocular parameters (all p<0.05). The multivariate linear regression analysis indicated that retinal arterial oxygen saturation was significantly associated with arterial peripheral arterial oxygen saturation (SpO2 ) and subfoveal choroidal thickness. Short-term exposure to HA induces retinal microcirculation disturbance and auto-regulatory response in healthy individuals, which is probably attributed to arterial SpO2 and endothelial dysfunction under hypoxic conditions.

Patent foramen ovale: a novel cardiovascular risk factor in patients with sleep disordered breathing and high altitude dwellers?

Diseases associated with chronic hypoxaemia are a leading cause of morbidity and mortality in Western countries. Epidemiological data indicate that cardiovascular diseases contribute substantially to this problem, but the underlying mechanisms are incompletely understood. Sleep disordered breathing and high altitude exposure are frequent conditions associated with hypoxaemia. Recent evidence suggests that in these conditions the concomitant presence of a patent foramen ovale plays an important pathogenic role. For example, in patients with obstructive sleep apnoea the presence of a patent foramen ovale is associated with more severe sleep disordered breathing, nocturnal oxygen desaturation, generalised endothelial dysfunction and arterial hypertension. After patent foramen ovale closure, both sleep disordered breathing and cardiovascular phenotype improve, suggesting the existence of a possible causal link. During short-term high altitude exposure, the presence of a patent foramen ovale, by aggravating altitude-induced hypoxaemia, facilitates exaggerated pulmonary hypertension. Interestingly, there is increasing evidence showing that in high-altitude dwellers a patent foramen ovale also alters the cardiovascular phenotype. In this article we will summarise recent evidence demonstrating how a patent foramen ovale alters the cardiovascular phenotype and increases cardiovascular risk in patients with sleep disordered breathing and high-altitude dwellers.

Cardiopulmonary adaptation to short-term high altitude exposure in adult Fontan patients

ObjectiveHigh altitude-related hypoxia induces pulmonary vasoconstriction. In Fontan patients without a contractile subpulmonary ventricle, an increase in pulmonary artery pressure is expected to decrease circulatory output and reduce exercise capacity....

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<i>Circulation</i> Editors’ Picks

Mechanisms and Drug Therapy of Pulmonary Hypertension at High Altitude

Pulmonary vasoconstriction represents a physiological adaptive mechanism to high altitude. If exaggerated, however, it is associated with important morbidity and mortality. Recent mechanistic studies using short-term acute high altitude exposure have provided insight into the importance of defective vascular endothelial and respiratory epithelial nitric oxide (NO) synthesis, increased endothelin-1 bioavailability, and overactivation of the sympathetic nervous system in causing exaggerated hypoxic pulmonary hypertension in humans. Based on these studies, drugs that increase NO bioavailability, attenuate endothelin-1 induced pulmonary vasoconstriction, or prevent exaggerated sympathetic activation have been shown to be useful for the treatment/prevention of exaggerated pulmonary hypertension during acute short-term high altitude exposure. The mechanisms underpinning chronic pulmonary hypertension in high altitude dwellers are less well understood, but recent evidence suggests that they differ in some aspects from those involved in short-term adaptation to high altitude. These differences have consequences for the choice of the treatment for chronic pulmonary hypertension at high altitude. Finally, recent data indicate that fetal programming of pulmonary vascular dysfunction in offspring of preeclampsia and children generated by assisted reproductive technologies represents a novel and frequent cause of pulmonary hypertension at high altitude. In animal models of fetal programming of hypoxic pulmonary hypertension, epigenetic mechanisms play a role, and targeting of these mechanisms with drugs lowers pulmonary artery pressure. If epigenetic mechanisms also are operational in the fetal programming of pulmonary vascular dysfunction in humans, such drugs may become novel tools for the treatment of hypoxic pulmonary hypertension.

Compromised White Matter Microstructural Integrity after Mountain Climbing: Evidence from Diffusion Tensor Imaging

The aim of the present study was to investigate cerebral microstructural alterations after single short-term mountain climbing. Voxel-based morphometry (VBM) analysis of gray matter (GM) and white matter (WM) volumes and Tract-Based Spatial Statistics (TBSS) analysis of WM fractional anisotropy (FA) based on MRI images were carried out on 14 mountaineers before and after mountain climbing (6206 m). In addition, verbal and spatial 'two-back' tasks and serial reaction time task were also tested. No significant changes were detected in total and regional volumes of GM, WM, and cerebral spinal fluid after mountain climbing. Significant decreased FA values were found in the bilateral corticospinal tract, corpus callosum (anterior and posterior body, splenium), reticular formation of dorsal midbrain, left superior longitudinal fasciculus, right posterior cingulum bundles, and left middle cerebellar peduncle. In all the above regions, the radial diffusivity values tended to increase, except in the left superior longitudinal fasciculus the change was statistically significant. There were no significant changes in the two cognitive tests after mountain climbing. These findings indicate that short-term high-altitude exposure leads to disturbances mainly in cerebral WM, showing compromised fiber microstructural integrity, which may clarify the mechanisms underlining some cognitive and motor deficits tested previously.

Paracrine erythropoietin (EPO) signaling and anti‐apoptosis in the lungs of guinea pigs exposed to high altitude (HA)

HA residence stimulates erythropoiesis as well as lung growth and remodeling in young animals, suggesting parallel upregulation of endocrine and paracrine/autocrine EPO signaling. To examine this possibility, we exposed weanling male guinea pigs to 3,800 m HA for 3 d, 7 d or 1 mo compared to matched controls at sea level (SL) (n = 5–8 each), and measured mRNA and/or protein expression of hypoxia‐inducible factors (HIF‐1alpha and ‐2alpha), EPO and its receptor (EPOR), Jak2, VEGF and its receptors (−R1, −R2), endothelin‐1 (ET‐1), proliferation marker (PCNA), and an apoptotic suppressor (Bcl‐2) and a promoter (BAD). Compared to SL, HA‐exposed lungs showed 100% and 50% higher HIF‐1alpha mRNA at 3 and 7 d and 55% lower HIF‐2alpha mRNA at 3 d, although HIF‐2alpha protein was 120% higher. Lung EPO mRNA and cytoplasmic EPOR protein increased 150% and 25% at 3 d without significant changes in membrane EPOR or Jak2. Plasma and urine EPO protein increased 56% and 160% at 3 d. Lung VEGF‐R2 protein increased 72% at 3 d while VEGF increased 27% at 7 d. ET‐1 mRNA increased 3‐fold at 3 and 7 d. BAD was 50% lower and Bcl‐2 100% higher at 3 d. PCNA was unaltered. All changes resolved by 1 mo. Thus, short‐term HA exposure stimulates both endocrine and paracrine/autocrine EPO signaling. Enhanced EPO signaling in the lung occurs primarily at the ligand but not the receptor level and is associated with anti‐apoptosis. Support: NIH R01 HL045716.

Maximal performance at altitude and on return from altitude in conditioned runners.

Maximal performance at altitude and on return from altitude in conditioned runners.