Effects of Altitude Exposure

carotid body, which causes activation of the sympathetic nervous system, are stimulated by short-term altitude exposure (less than three or four days) (Wahrenberger, 2003). These changes occur within a few minutes of altitude exposure and are related to a transient epinephrine secretion combined with a more sustained secretion of norepinephrine. These cause immediate changes which include an increase in ventilation, increased heart rate, increased cardiac output, and an elevation of blood pressure. There is also an increase in coronary blood flow. The increased ventilating which occurs with high altitude causes hypocapnia and respiratory alkalosis, which can inhibit the ability to hyperventilate and improve oxygenation. The rapid and significant increase in pressure in the pulmonary artery with initial exposure to attitude is most likely caused by hypoxia, which is induced by vasoconstriction. It is a universal finding, and may be important in the development of pulmonary edema.

The cardiovascular effects of high altitude are particularly noticeable during exercise (Wahrenberger, 2003). A study of 12 healthy office workers found that they showed only a minor elevation of resting heart rate at 8856 feet and 12,136 feet, but when asked to perform a Master's double-step exercise their heart rate increased significantly at these altitudes. Similar findings were observed for blood pressure and rate-pressure pr

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003). Sympathetic nervous system activity actually falls below pre-ascent levels, and is associated with a lower cardiac output wider arterio-venous oxygen differences, and lower blood pressure. More physiologic adaptations take place with prolonged high altitude exposure, including: resetting of the "hypoxic ventilatory response" to allow increased ventilation at a given hypoxic stimulus; leftward shift of the oxygen hemoglobin dissociation curve; increased tissue capillary density; and reduction in alveolar arterial gradient. Acclimatization occurs primarily through mechanisms other than the cardiovascular system, and the cardiovascular system responds to them, rather than the cardiovascular system initiating these changes. There is some evidence that long-term residence at high altitude may lower the risk of coronary artery disease. Burtscher et al (2001) studied 20 voluntary healthy elderly subjects who were randomly assigned to a low altitude (600 m) or a high altitude (2,000 m) group. Both groups increased their daily hiking from 2.5 to 5 hours daily during the 1-week study. Pre- and post-hiking cardiopulmonary variables at rest were measured daily. Exercise tests were performed on days 1, 4, and 7 of the study.
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Some common words found in the essay are:
Shimada Saito, Mount Everest, , Philadelphy Nachbauer, Environmental Health, wahrenberger 2003, oxygen saturation, altitude exposure, arterial oxygen, arterial oxygen saturation, blood pressure, heart rate, sea level, cardiac output, blood flow, Applied Physiology, low altitude, European Journal, sympathetic nervous system, Nishihara Shimada, et al 2001, blood pressure arterial, pressure arterial oxygen,
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Approximate Pages = 6 (250 words per page)

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