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High-altitude regions pose distinctive challenges for cardiovascular health because of decreased oxygen levels, reduced barometric pressure, and colder temperatures. Approximately 82 million people live above 2400 meters, while over 100 million people visit these heights annually. Individuals ascending rapidly or those with pre-existing cardiovascular conditions are particularly vulnerable to altitude-related illnesses, including Acute Mountain Sickness (AMS) and Chronic Mountain Sickness (CMS). The cardiovascular system struggles to adapt to hypoxic stress, which can lead to arrhythmias, systemic hypertension, and right ventricular failure. Pathophysiologically, high-altitude exposure triggers immediate increases in cardiac output and heart rate, often due to enhanced sympathetic activity. Over time, acclimatisation involves complex changes, such as reduced stroke volume and increased blood volume. The pulmonary vasculature also undergoes significant alterations, including hypoxic pulmonary vasoconstriction and vascular remodelling, contributing to conditions, like pulmonary hypertension and high-altitude pulmonary edema. Genetic adaptations in populations living at high altitudes, such as gene variations linked to hypoxia response, further influence these physiological processes. Regarding cardiovascular disease risk, stable coronary artery disease patients generally do not face significant adverse outcomes at altitudes up to 3500 meters. However, those with unstable angina or recent cardiac interventions should avoid high-altitude exposure to prevent exacerbation. Remarkably, high-altitude living correlates with reduced cardiovascular mortality rates, possibly due to improved air quality and hypoxia-induced adaptations. Additionally, there is a higher incidence of congenital heart disease among children born at high altitudes, highlighting the profound impact of hypoxia on heart development. Understanding these dynamics is crucial for managing risks and improving health outcomes in high-altitude environments.
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http://dx.doi.org/10.2174/011573403X308818241030051249 | DOI Listing |
J Appl Physiol (1985)
September 2025
Department of Human Physiology and Nutrition, William J. Hybl Sport Medicine and Performance Center, University of Colorado Colorado Springs, Colorado Springs, CO, USA.
Chronic exposure to high altitude leads to increases in hemoglobin mass (Hbmass), which may improve exercise performance and decrease acute mountain sickness (AMS) symptoms. We evaluated the influence of intravenous iron or erythropoietin (EPO) treatment on Hbmass, exercise performance, and AMS during a 14-day exposure to 3094 m. Thirty-nine participants (12F) completed the study conducted in Eugene, Oregon (sea level (SL), 130 m) and Leadville, Colorado (3094 m).
View Article and Find Full Text PDFBiology (Basel)
July 2025
Department of Physiology, School of Medicine, Ankara University, Ankara 06230, Türkiye.
Hypoxia can adversely affect multiple organ systems. This study investigated the impact of intermittent hypoxia on serotonin levels and depression-like behaviors across distinct neuroanatomical regions. Sixteen adult female Wistar albino rats were divided into two groups: control ( = 8) and hypoxia ( = 8).
View Article and Find Full Text PDFHigh Alt Med Biol
September 2025
Mountain Medicine Society of Nepal, Kathmandu, Nepal.
Shrestha, Suraj, Sanjeev Kharel, Suman Acharya, Gobi Basyal, and Sanjeeb S. Bhandari. A Retrospective Analysis of Altitude Illness at the Himalayan Rescue Association Aid Post Manang (2018-2023).
View Article and Find Full Text PDFHigh Alt Med Biol
September 2025
Hepatology, Department of Medicine II, University Hospital Wuerzburg, Wuerzburg, Germany.
A recent study of our group quantifying C-octanoate metabolism in HA (Capanna Margherita [MG]/4,559 m) showed that acute HA exposure might lead to an increase of the lipolytic and CO-producing pathways. To further test this hypothesis, we investigated intestinal biopsies from the same participants from simultaneously performed endoscopy studies for changes of mRNA-expression levels of the beta-oxidation enzymes and the decarboxylating tricarboxylic acid cycle (TCA) enzymes. Duodenal biopsies of 16 subjects exposed to HA were sampled via gastro-duodenoscopy at Zurich (baseline ZH, 490 m), on day 2 (MG2) and on day 4 at HA (MG4).
View Article and Find Full Text PDFLung India
September 2025
Department of Radiology, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.