The High-Altitude Environment

Chapter 6 Altitude CHAPTER 6 ALTITUDE Prepared for the Course Team my Patricia Ash 6.1 Introduction: the high-altitude en8ironment As in previous chapters, this chapter looks at both phenotypic and genotypic adaptations to what may be regarded as an ‘extreme’ environment. People who live at sea-level and ascend to high altitude are exposed to hypoxia; there then follows a suite of physiological and biochemical changes that maintain an oxygen supply to the respiring tissues. These physiological changes are known as acclimatization, and are possible because of phenotypic flexibility. The chapter also considers long-term physiological and biochemical adaptations to life at high altitude. Increasing numbers of people are emigrating from sea-level to high altitude, e.g. from China to Tibet. Long-term physiological adaptations for life at high altitude may also be derived from phenotypic plasticity which, as you will recall from Chapter 2 (Section 2.10.2), is the process by which factors in the environment, e.g. aridity, low T or low P of a neonate or immature animal, can a O 2 shape the anatomy and influence the physiology and biochemistry of the adult. We should remember too that phenotypic plasticity and flexibility (and therefore the ability to adapt physiologically) are themselves under genetic control. Low atmospheric pressures at high altitude mean low P O 2 , and therefore hypoxia in respiring tissues. Sudden exposure to high altitude, say 4000 m, by means of a helicopter flight to the upper slopes of a mountain, may result in a set of symptoms known as mountain sickness, which is caused by the effects of acute hypoxia on the blood circulatory system and the brain. Acute exposure to even higher altitudes, and hence lower P O 2 , may result in loss of consciousness, followed by death (Figure 6.1). Figure 6.1 The total air pressure and the partial pressure of oxygen in the atmosphere at various altitudes with a summary of the effects usually observed in non-acclimatized people. 0_8 S324Book 2 .n8ironmental Physiology Nevertheless, more than 22 million people live permanently at high altitude, with domestic animals grazing the alpine pastures, where crops such as barley can also be grown. It is estimated that humans have lived on the Qinghai- Tibetan plateau for about 4000–5500 years, and on the high Andes (altitudes 3000–4000 m) for up to 12000 years. The Bolivian village of Morococha is at an altitude of 4500 m and the capital, La Paz, is at 3800 m. Cusco in Peru is at 3400m, and villages around Lake Titicaca at 3800 m. The ethnic Andean population living at high altitude numbers around 8 million, about 75% of whom are Quechuan people and the remainder Aymara. In Section 6.4 we explore and evaluate research studies that investigated whether Quechuan people have heritable traits that can be linked to adaptations for life at high altitude. Animal species have lived at high altitudes for much longer than humans. In Figure 6.2 Vicuna fact, fossils of pika have been found on the Tibetan plateau and dated at about ( Vicugna vicugna ). 37 million years old. Camelids such as llama and vicuna ( Vicugna vicugna ; Figure 6.2) live at high altitudes in the Andes and have no apparent problems with hypoxia. The yak ( Bos gruniens ; Figure 6.3) is an important livestock species in mountainous areas in Asia. Small mammalian species such as pika ( Ochotona sp.; Figure 6.4) and root voles ( Microetus sp.) live in the same high-altitude alpine meadows as yak. Reptiles including iguanids ( Liolaemus sp.) from the Andes and amphibians such as the Andean frog ( Telmatobius peruvianus) are also permanent residents at high altitudes. Birds fly over mountain ranges on their migratory flights. The bar-headed goose ( Anser indicus; Figure 6.5) migrates over the Himalayas, flying over Mount Everest at 9000 m altitude whilst honking loudly, and so clearly not suffering from shortness of breath! Figure 6.3 Yak ( Bos gruniens ). Tourists, trekkers and climbers who live at sea-level or at low altitudes, visit high mountains in ever-increasing numbers. Many people living at sea-level can walk up mountains, even those as high as Everest, as long as they do so gradually. Rapid transport of a lowlander to high altitude, e.g. in a car or a helicopter, may result in a suite of symptoms known as acute mountain sickness (AMS). The well-known symptoms include headache, fatigue, shortness of breath, dizziness, sleep disturbance and vomiting. The physiology of mountain sickness is covered in Sections 6.2.4 and 6.2.5. Domestic animals are also vulnerable when transported to high altitude. In the summer, farmers transport large numbers of cattle to rich pastures at high altitudes. The cow ( Bos taurus) is a lowland species and, like humans, suffers from symptoms linked to hypoxia. In Section 6.4 we return to the initial Figure 6.4 Pika ( Ochotona sp.). response to hypoxia, this time at the molecular level. Hypoxia-inducible factor (HIF-1α ), a transcription factor, plays a crucial role in mediating the cellular response to hypoxia (Section 6.4.1). We end in Section 6.5 with a research study comparing the activities of three catabolic enzymes in the muscle tissue of three pika species and look at enzyme properties that could be linked to low tissue P . O 2 We begin our study of high-altitude physiology with a brief survey of the physiological and biochemical responses to high altitude. Figure 6.5 Bar-headed goose ( Anser indicus). 016 Chapter 6 Altitude 6.0 Initial physiological and miochemical responses to high altitude 6.0.1 The control of respiration Before we study how animals and humans cope in atmospheres with low oxygen pressure, we need to understand oxygen transfer. The ‘oxygen cascade’ (Figure 6.6) describes the partial pressure of oxygen as it passes from air to the deep body tissues. Figure 6.6 Oxygen cascade in human tissues. Mean P gradients O 2 from inspired air to tissues in human subjects native to sea-level and in subjects native to 4540m. Although the P O 2 in the atmosphere at high altitude is much less than that at sea- level, and the P O 2 gradient down the oxygen cascade is much less steep than that for sea-level residents, the venous P O 2 is not greatly different. Therefore, the P O 2 gradient for oxygen transfer to the mitochondria is maintained. The dashed portions of the lines represent estimates of the P changes and are not precise O 2 measurements. The labels identify the four steps in the cascade where oxygen transfer is governed by diffusive conductance (Fick’s law), or by mechanical movement of fluid (ventilation or perfusion). In large animals, it is possible to separate the oxygen cascade into steps that describe gradients of: G diffusive conductance , where oxygen transfer is by physical diffusion. So, it is directly proportional to the exchange area and P O 2 gradient, and inversely proportional to the diffusion distance (e.g. lungs/gills to blood and blood to tissues). G convective conductance , where oxygen transfer is by mechanical movements of the surrounding fluid, e.g. lung/gill ventilation with air/water and perfusion of lung/gill and tissue capillaries by blood that is carrying oxygen bound to haemoglobin. In vertebrates, an oxygen cascade with four steps from the environment to the tissues may be identified. G Step 1 – delivery of water or air containing oxygen to the respiratory gas exchange surfaces of the animal. This process of external convection is termed ventilation. 017 S324Book 2 .n8ironmental Physiology G Step 2 – passage of oxygen from the air/water presented to the respiratory gas exchange surfaces (gills/lungs), across the epithelium, by diffusion into the body fluids. G Step 3 – transport of oxygen (combined with haemoglobin) to the metabolizing tissues by internal convection, or perfusion, through the cardiovascular system. G Step 4 – passage of oxygen from the circulating body fluids to the metabolizing mitochondria, by diffusion through the tissues. Hence the stages in the cascade (Figure 6.6) are alternately convection, diffusion, convection and then diffusion again. For a human ascending from sea-level to high altitude in a helicopter flight, from sea-level to say 4000 m, the immediate challenge is low atmospheric P O 2 and the initial failure of the lungs to increase ventilation to compensate. Why is there such a delay? In order to understand why lungs cannot increase ventilation immediately, we need to investigate the chemical control of breathing. At sea-level, as long as the alveoli in the lungs are ventilated and the cardiovascular system is working normally, respiring tissues receive blood containing sufficient oxygen and normal levels of carbon dioxide. Changes in both P CO2 and P O 2 can have damaging effects however. A fall in P O 2 in the blood (known as hypoxia ) compromises the oxygen supply to tissues when people are exposed to high altitude without the opportunity for gradual acclimatization. Even small changes in P are significant. Chapter 2 (Section 2.4.2) explained CO2 that when carbon dioxide dissolves in blood, it reacts slowly with water forming + carbonic acid (H 2 CO3 ), which dissociates reversibly to form hydrogen ions (H ) − and hydrogen carbonate ions (HCO3 ). + − CO2 + H 2 O 0 H 2 CO3 0 H + HCO3 (6.1) Like all chemical equilibria, the reactions proceed to an extent determined by the relative concentrations of the reactants and the products. Note that plasma − contains hydrogen carbonate ions (HCO3 ) derived from a reaction in red blood cells, which pushes the reaction to the left.

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