Clinical Implications for Exercise at Altitude Among Individuals With Cardiovascular Disease: A Scientific Statement From the American Heart Association

Abstract

An increasing number of individuals travel to mountainous environments for work and pleasure. However, oxygen availability declines at altitude, and hypoxic environments place unique stressors on the cardiovascular system. These stressors may be exacerbated by exercise at altitude, because exercise increases oxygen demand in an environment that is already relatively oxygen deplete compared with sea-level conditions. Furthermore, the prevalence of cardiovascular disease, as well as diseases such as hypertension, heart failure, and lung disease, is high among individuals living in the United States. As such, patients who are at risk of or who have established cardiovascular disease may be at an increased risk of adverse events when sojourning to these mountainous locations. However, these risks may be minimized by appropriate pretravel assessments and planning through shared decision-making between patients and their managing clinicians. This American Heart Association scientific statement provides a concise, yet comprehensive overview of the physiologic responses to exercise in hypoxic locations, as well as important considerations for minimizing the risk of adverse cardiovascular events during mountainous excursions.

Keywords: AHA Scientific Statements; altitude; cardiovascular diseases; exercise; heart failure; hypertension; sudden cardiac death; syncope.

Figure 1. Environmental changes at altitude.

Classification of altitude ranges with associated reductions in the fraction of inspired oxygen (Fio ₂) relative to sea level and percent reduction in functional capacity according to maximal oxygen uptake (Vo ₂max) as altitude increases. Popular tourist destinations are included for reference.

Figure 2. Physiologic response to hypoxia.

Response to hypoxia at altitude involves systemic arterial vasodilatation, hypoxic pulmonary vasoconstriction, and activation of peripheral chemoreceptors, with downstream effects including sympathetic activation, which increases blood pressure and cardiac output, as well as hyperventilation and pulmonary hypertension. Adapted from Bärtsch et al. © 2007 American Heart Association, Inc.

Figure 3. Cardiovascular hemodynamic changes that occur in response to acute (minutes to hours) and chronic (days to weeks) exposure to hypoxia compared with sea level.

Acutely, heart rate, cardiac output, muscle flow, and stroke volume increase. However, with sustained exposure, all of these variables decrease to levels at or below sea level. Blood pressure and systemic vascular resistance decrease during acute exposure, but may increase progressively with time to levels at or above sea level values. From Baggish et al. Reprinted by permission from Springer. © 2014.

Figure 4. Pretravel assessment for patients who are at risk of adverse cardiovascular events in mountainous environments.

BP indicates blood pressure; CSA, central sleep apnea; PAP, pulmonary arterial pressure; SCD, sudden cardiac death; and Spo ₂, systemic oxygen saturation.