Term Paper on "Acclimatization Ascending to Higher Altitudes Requires"

Term Paper 6 pages (1766 words) Sources: 4 Style: MLA

[EXCERPT] . . . .

Acclimatization

Ascending to higher altitudes requires the body to make several compensatory changes. This process is known as acclimatization, and it involves various physiological systems adapting to lower levels of partial pressure of oxygen (PO2). There are acute responses to altitude changes that can be observed immediately, as well as more complex responses that can be observed among people experiencing prolonged, or chronic, exposure. Hypoxia, or reduction in oxygen, associated with exposure to altitude necessitates changes in several physiological systems, and these systems respond interactively with each other rather than in isolation (Wyatt, 2002). Some of the observed responses to altitude are an increase in pulmonary ventilation, polycythemia, a rightward shift in the oxygen dissociation curve, changes in the number of capillaries in peripheral tissues, as well as changes in intracellular oxidative enzymes.

Increased Pulmonary Ventilation

Increased resting and submaximal ventilation is observed in immediate response to altitude related hypoxia (Wyatt, 2002). This increased ventilation is achieved through increased volume and rate of breaths, and individual variation in hypoxic ventilatory response has been demonstrated (Wyatt, 2002). Research has shown that individuals with strong hypoxic ventilatory drives exhibit better performance at high altitudes than individuals with less efficient drives (Wyatt, 2002). The stimulated ventilation that results from exposure to high altitudes is due to aortic and carotid sensitivity to reduced PO2 in arterial blood. This increase in ventilation increases PO2 in the alveoli and reduces end-tidal partial pressure of carbon dioxide (PETCO2), which lends to reduced carbon dioxide and H+ in the blood. In response to these reductions during the initial few days of exposure to altitude, the kidneys gradually excrete bicarbonate (HCO3), which is associated with decreased plasma volume. Increased pulmonary ventilation also results in a reduction in total water in the body due to loss of water vapor that occurs during respiration, which results in rapid dehydration during acute altitude exposure (Wyatt, 2002).

Researchers Donoghue et al. (2005) investigated changes in ventilation that occurred during acclimatization to hypoxia, and whether these ventilatory adaptations could be induced by alterations in end-tidal PO2 (PETO2). This was executed through comparison of two 5-day exposures. One of the exposures was mild hypoxia with PETO2 sustained at 10 Torr below normal value, while the other exposure was mild hyperoxia with PETO2 sustained at 10 Torr above normal value. In addition, PETCO2 was uncontrolled in both conditions. The results of this study indicated that participants exposed to mild hypoxia demonstrated an increase in acute ventilatory sensitivity to hypoxia, and those exposed to mild hyperoxia showed a significant decrease in this sensitivity. Furthermore, the findings of this study suggested that ventilatory sensitivity to hypoxia varies in a linear fashion with PETO2, and that this sensitivity continuously varies in response to normal PETO2 fluctuations that occur physiologically.

Polycythemia second physiological response that occurs during acclimatization to ascending altitude is polycythemia. This refers to the presence of abnormally high numbers of red blood cells in the circulatory system. The increased alveolar PO2 that occurs as a result of increased pulmonary ventilation necessitates many hematological adjustments (Wyatt, 2002). Within the first day of exposure to altitude, the concentration of hemoglobin (Hb) and hematocrit (Hct) increase. Also, PO2 sensitive cells located in the kidneys stimulate the release of erythropoietin (EPO), which acts to stimulate the production of red blood cells and results in polycythemia. The increases in Hb, Hct, and red blood cells in response to acclimatization to altitude act to facilitate greater PAO2 and oxygen per lieter of cardiac output (Wyatt, 2002).

Populations of individuals that live in high altitudes often demonstrate polycythemia, such as high-altitude dwellers in the Andes of South America. Norcliffe et al.(2005) sought to examine whether cerebral blood flow increased among these high-altitude dwellers who were known to be chronically hypoxic and polycythemic. Cerebrovascular responses to hypoxia and hypocapnia were determined in high-altitude dwellers at high altitude and also after descent to sea level. The findings among this group were then compared to sea-level residents who were not chronically hypoxic or polycythemic. The changes in cerebral blood flow that were examined in this study were estimated from changes in the velocity of cerebral blood flow determined by transcranial Doppler ultrasonography of the middle cerebral artery (Norcliffe et al., 2005).

There were two main findings of this study of polycythemic individuals conducted by Norcliffe et al. (2005). First, there were no observed differences in responses of cerebral circulation to hypoxia or hypocapnia between the two groups in the study (polycythemic high-altitude dwellers and non-polycythemic sea-level residents). The second main finding was that at sea level, both groups responded similarly to hypoxia, in that there cerebral blood flow increased. Moreover, polycythemia individuals display the same cerebrovascular responses to non-polycythemic individuals at sea level. This indicates that Hct, which increases at altitude and is related to polycythemia, does not significantly affect cerebrovascular reactions to hypoxia, and that the maladaptations in cerebrovascular responses observed at high altitude are rapidly reversed through acclimatization to lower altitudes (Norcliffe et al., 2005).

Rightward Shift in the Oxygen Dissociation Curve

The stimulated production of red blood cells in response to acclimatization to high altitudes results not only in polycythemia, but also in stimulated elevation of 2,3-diphosphoglycerate (2,3-DPG) in response to a rise in intracellular pH (Wyatt, 2002). This elevation in 2,3-DPG facilitates increased oxygen dissociation, and therefore results in a rightward shift of the oxyhemoglobin dissociation curve. At high altitudes, these changes contribute to the promotion of oxygen unloading at the muscle and furthermore increased utilization of oxygen (Wyatt, 2002). This oxyhemoglobin shift is facilitated by increased chemoreceptor ventilation control that results from decreased bicarbonate due to excretion from the kidneys. Examining this shift in the oxygen dissociation curve as it relates to all other processes involved in acclimatization to high altitudes further demonstrates how all these physiological responses are interactive, and they do not occur in isolation without influence on or from other processes.

Changes in Capillarization?

It is often believed that increased capillary density in skeletal muscle in response to hypoxic conditions due to high altitude would be physiologically adaptive, but Lundby et al. (2004) demonstrated that this may not be so. These researchers hypothesized that prolonged exposure to high altitude results in increased capillary density in muscles due to the enhanced expression of a target gene for hypoxia inducible factor 1

HIF-1) and subsequent increased expression of vascular endothelial growth factor (VEGF). However, the results of the study contradicted their hypothesis.

This study of capillarization in response to hypoxic conditions at high altitude by Lundby et al. (2004) yielded three main findings. First, in sea level residents, no conditions of exposure to hypoxia of high altitude resulted in any significant change in HIF-1 or VEGF. The second main finding was that sea level residents did not display any significant changes in mean muscle fiber or capillary density at high altitude. The third and final main finding of this study was that capillary density among high-altitude dwellers was not significantly different than sea-level residents, but tended, on the contrary, to be lower. Overall, no indication of new formations of capillaries in human skeletal muscle was observed, even after prolonged exposure to high altitude (Lundby et al., 2004), and these findings are contrary to some other research, such as the study conducted by Green et al. (1989), who observed increased capillarization in muscle in response to high altitude. Furthermore, the preservation of oxygen delivery to skeletal muscles during hypoxic conditions at high altitudes is accomplished sufficiently by the acclimatization-dependent increase in concentration of hemoglobin, and increased numbers of capillaries in peripheral tissues is not required (Lundby et al., 2004).

Changes in Oxidative Enzymes Within Cells

Exposure to hypoxic conditions at high altitudes causes changes in intracellular oxidative enzymes. Hoppeler & Vogt (2001) explored adaptations that muscular tissues make in response to exposure to hypoxia, and they determined that sustained exposure to severely hypoxic conditions can result in detrimental muscular effects. Initial detrimental effects can be observed in low-landers after only 2 months of acute exposure to hypoxic conditions experienced at high altitude. Populations living permanently at high altitudes, such as Tibetans and Quechuas who have existed at extremely high altitudes for thousands of years, demonstrate genetic adaptations that prevent any detrimental muscular effects from occurring. These adaptations involve a decrease in muscle oxidative capacity (Hoppeler & Vogt, 2001).

Hoppeler et al. (2003) also investigated intracellular changes in oxidative enzymes. These researchers established that that long-term or permanent exposure to hypoxic conditions at high altitude resulted in decreased mitochondrial content of muscle fibers. In these conditions, there is an increased reliance in carbohydrates as fuel for oxidative muscle metabolism, and there is a reduction in stores of intramyocellular lipid substrate stores. Furthermore, accumulations of lipofuscin, known to be a product of mitochondrial degradation, are found among individuals returning from time spent at extremely high altitudes. Performance appeared to be improved among these individuals by improved coupling between ATP supply and demand pathways and improved metabolite homeostasis (Hoppeler et al., 2003).

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