Introduction

To mountaineers, acclimatization is the process by which they become more comfortable at altitude and find they can perform better than when they first arrived (Houston 1955; Roach 2019). The concept is nicely encapsulated by a statement from Charles Houston (1955), who, following decades of experience climbing at very high altitudes, wrote: “There is an altitude frontier beyond which humans cannot become accustomed to oxygen lack, but the approach to that frontier … is made possible by acclimatization—the process of becoming accustomed to an environment foreign to the organism.” For individuals traveling to high altitude, acclimatization prevents or alleviates symptoms and signs of acute altitude illness and restoration of some of the exercise performance lost on arrival at altitude (Latshang et al. 2013; Subudhi et al. 2014), whereas for physiologists, altitude acclimatization is, strictly, the sum of all the beneficial changes in response to altitude hypoxia that occur with time spent at a given altitude, and that eventually disappear on descent to low altitude. It refers only to the changes in response to hypoxia seen as beneficial as opposed to changes that result in illnesses such as acute mountain sickness (AMS), high altitude cerebral edema (HACE), or high altitude pulmonary edema (HAPE) and are considered pathological.

This chapter considers the issue of acclimatization in greater detail. After clarifying the concept of acclimatization, the chapter provides an overview of the major physiological responses to hypoxia, which serves as a preview to the more detailed information in the chapters that follow. We then consider factors affecting the success of acclimatization and how long the beneficial responses last following descent to lower elevation. Because there are elevations above which individuals can no longer acclimatize, the chapter concludes with a discussion of the issue of high altitude deterioration seen at very high altitudes.

Acclimatization versus Adaptation

Acclimatization is often defined by the increase in ventilation and the consequent reduction in PCO₂ and increase in PO₂. However, these alone are not satisfactory measures since many other processes are involved. The processes of acclimatization all tend to reduce the fall in PO₂ as oxygen is transported through the body from the outside air to the tissues. However, even in the best acclimatized individual the tissue PO₂ is not restored to the sea level value and performance remains impaired. This is illustrated in Figure 7.1, which shows the inspired and alveolar PO₂ (P_AO₂) of a subject exposed to acute hypoxia and after acclimatization. Also shown are the normal P_AO₂ at sea level and the arterial PO₂ (P_aO₂) at which continuous oxygen therapy is advised for patients with chronic obstructive pulmonary disease (COPD); even acclimatized subjects are below this level at altitudes above 4000 m.

The major benefits of acclimatization are to protect against acute altitude illness (Subudhi et al. 2014), to improve cognitive performance to near sea-level values (Roach et al. 2014), and to boost submaximal exercise performance (Fulco et al. 2005; Horstman et al. 1980; Latshang et al. 2013; Subudhi et al. 2014) without changing peak oxygen consumption (Beidleman et al. 1997; Calbet et al. 2003a; Calbet et al. 2003b; Calbet et al. 2004; Fulco et al. 2002; Fulco et al. 2005; Lundby et al. 2004; Lundby et al. 2007; Sutton et al. 1988; Wolfel et al. 1991). To understand the effects of acclimatization on exercise, tests of submaximal endurance are more useful than peak oxygen consumption or all-out time trial performance over a short distance, as high altitude travelers rarely perform at these levels of exertion. For example, mountaineers try to preserve energy to sustain efforts across multiple days and might actually put themselves at risk of serious harm, or death, if they truly reached the point of exhaustion. Their ability to cover more ground faster while preserving a functional reserve is a hallmark of acclimatization supported by anecdotal accounts (Houston 2005; Messner 1989). Despite this, the physiology behind the improvement in sustained, self-regulated submaximal performance at altitude remains unexplored.

The transient phenomenon of acclimatization must be distinguished from the concept of adaptation, which refers to characteristics present in long-term high altitude residents that have arisen as a result of natural selection working on the gene pool. These characteristics serve to distinguish people born and bred at high altitude from even well-­acclimatized lowlanders. There is debate about whether these characteristics are due to environmental factors operating during early growth or due to genetic causes. Recent genetic evidence points to adaptation happening in people resident at high altitude for generations in South America, Tibet, and Ethiopia (Chapter 4). The remainder of this chapter will focus on the issue of acclimatization while issues related to adaptation are discussed in Chapters 4 and 6.

The Consequences of Exposure to Acute Hypoxia

To further explore the process of human adjustment to hypoxia, one must turn to an understanding of the oxygen transport system in an oxygen-limited environment. The response of the body to hypoxia depends crucially on the rate of onset as well as the degree of hypoxia. For instance, the effect on a pilot of sudden loss of oxygen supply in an unpressurized aircraft at the height of the summit of Mount Everest is quite different from the effect of similar altitude on a climber who has spent some weeks at altitude. The pilot would probably lose consciousness in a few minutes (Figure 7.2), whereas the climber, though very breathless, will not only remain conscious but also be able to perform meaningful physical work. The difference in outcomes between the pilot and the climber is due to the process of acclimatization.

The effect of acute, often severe, hypoxia has been studied intensively since Paul Bert first pointed out the danger of ascent to high altitude to early balloonists (Chapter 1). Figure 7.2 shows the effect of sudden exposure to various increasing altitudes. At modest altitude, breathlessness may be felt on exertion and some rise in heart rate noticed, but the main effect is on the central nervous system. At 4000–5000 m some tingling of the fingers and mouth may be noticed, but although the subject would now definitely be hypoxemic, there is very little subjective sensation to indicate this fact. Above about 5000 m, some subjects may become unconscious, and above 7000 m, most will be so (Pickard and Gradwell 2008). There is considerable individual variation in response to acute hypoxia. From Figure 7.2, we can see that, on acute exposure to the altitude equivalent to the summit of Everest, the unacclimatized subject remains conscious for only about two minutes.

The Oxygen Transport System

Figure 7.3 shows the oxygen transport system at sea level and at high altitude. This diagram can be used as a “table of contents” of changes resulting from acclimatization and serves as a preview of more detailed discussions of the physiologic responses to hypoxia in the chapters that follow. PO₂ falls at each stage as oxygen is transported from ambient air to inspired air (P_IO₂) to the alveolar space (P_AO₂), arterial blood (P_aO₂), and mixed venous blood ( Pv–O₂), which approximates to the mean tissue PO₂. This forms a staircase or cascade of PO₂. The process of acclimatization can be thought of as mitigating the drop in PO₂ seen at each step in this cascade. Each step is considered below.

Factors Impacting Successful Acclimatization

No objective test can tell a mountaineer or other high altitude traveler if they are fully or only partially acclimatized. In practice, this is not a serious limitation because the positive benefits of transitioning from unacclimatized to acclimatized are readily apparent (Roach 2019). For the acclimatized individual at a given altitude, tasks of daily living become easier to accomplish, tolerance of low to moderate intensity exertion markedly improves, and the symptoms of AMS, if present initially, fade.

The investigation of the underlying molecular and physiological mechanisms driving acclimatization has been largely stagnant until recently. For example, research into the pathophysiology of AMS often uses models of cross-over control conditions at sea level or comparisons of those with and without AMS at high altitude, or, even worse, a cross-over design where individual variation is ignored. Only recently have studies begun to compare the unacclimatized AMS subject to themselves when they become acclimatized (Subudhi et al. 2014). As pointed out more than 60 years ago by Charles Houston, the acclimatized climber is largely protected from the challenges of acute hypoxia (Houston 1955). Determining how this happens and if it can be artificially induced holds promise to advance our understanding of the mechanisms driving acclimatization and AMS. The following is a summary of the science regarding aspects supporting successful acclimatization. Because hard data are notably absent in this area, much of the discussion necessarily relies on anecdotal evidence and common sense.

Rate of acclimatization

The changes involved in acclimatization occur in various systems and with varying time courses. These are illustrated in Figure 7.4, which shows the futility of the frequently asked question, “How long does it take to become acclimatized?”

Of these changes, the most important are the responses in the cardiorespiratory system and the blood, which occur over the course of days or a few weeks. Figure 7.5 shows the changes in a number of physiological systems over the first 10 days of altitude 4300 m (Muza et al. 2010). Lundby et al. (2004) studied early changes in acclimatization in six lowlanders. Subjects were studied at sea level (normoxia and acute hypoxia) and after two and eight weeks of acclimatization at 4100 m in Bolivia. Local high altitude residents were also studied at altitude. Some results from this study are shown in Figure 7.6 for rest (Figure 7.6a) and maximum exercise (Figure 7.6b). It can be seen that the hematocrit rises during the first two weeks to close to the high altitude residents’ value and is no higher at eight weeks. The P_aO₂ continues to rise for eight weeks and is still below that of the high altitude residents. Changes in P_aCO₂ appear to be complete at two weeks while the (A-a)ΔO₂ rises with acute hypoxia, is greater at two weeks, and falls slightly at eight weeks. The situation at maximum work rate is similar except that the P_aCO₂ continues to fall due to increased exercise ventilation. Subudhi et al. (2014) studied 21 college students at sea level and after 16 days at 5200 m in Bolivia; results showed a similar time course for acclimatization. The elevations in arterial oxygenation and [Hb] from day 1 to 16 at 5200 m were similar to those measured in individuals acclimatized for at least 10 days at altitudes ranging from 3800 m to 5260 m (Bebout et al. 1989; Lundby et al. 2004; Wagner et al. 1987; Wagner et al. 2002). Thus, it seems that 10–16 days at 4000–5000 m results in significant acclimatization, and that this duration of exposure can be effective to test acclimatization and its subsequent retention.

Surprisingly, when subjects descended for one to three weeks to 1500 m, they experienced neocytolysis (Ryan et al. 2014), a destruction of red blood cells that led to a 13% drop in hemoglobin concentration and thus in arterial oxygen content (C_aO₂

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