I just read through a research paper written by Bärtsch P., Saltin, B. General introduction to altitude adaptation and mountain sickness. Scand. J. Med. Sci. Sports 2008 (Suppl. 1):1-10.
I have put a few excerpts from the paper into this blog to inform my fellow climbers. The text below is a mixture of paraphrasing and quotes from the paper. This is a really good paper and I highly recommend tracking it down and giving it a complete read.
Abstract
The key elements in acclimatization aim at securing the oxygen supply to tissues and organs of the body with an optimal oxygen tension of the arterial blood. In acute exposure, ventilation and heart rate are elevated with a minimum reduction in stroke volume. In addition, plasma volume is reduced over 24–48 h to improve the oxygen carrying capacity of the blood, and is further improved during a prolonged sojourn at altitude through an enhanced erythropoiesis and larger Hb mass, allowing for a partial or full restoration of the blood volume and arterial oxygen content. Most of these adaptations are observed from quite low altitudes [1000m above sea level (m a.s.l.)] and become prominent from 2000 m a.s.l. At these higher altitudes additional adaptations occur, one being a reduction in the maximal heart rate response and consequently a lower peak cardiac output. Thus, in spite of a normalization of the arterial oxygen content after 4 or more weeks at altitude, the peak oxygen uptake reached after a long acclimatization period is essentially unaltered compared with acute exposure. What is gained is a more complete oxygenation of the blood in the lungs, i.e. SaO2 is increased. The alteration at the muscle level at altitude is minor and so is the effect on the metabolism, although it is debated whether a possible reduction in blood lactate accumulation occurs during exercise at altitude. Transient acute mountain sickness (headache, anorexia, and nausea) is present in 10–30% of subjects at altitudes between 2500 and 3000ma.s.l. Pulmonary edema is rarely seen below 3000ma.s.l. and brain edema is not seen below 4000ma.s.l. It is possible to travel to altitudes of 2500–3000ma.s.l., wait for 2 days, and then gradually start to train. At higher altitudes, one should consider a staged ascent (average ascent rate 300 m/day above 2000ma.s.l.), primarily in order to sleep and feel well, and minimize the risk of mountain sickness. A new classification of altitude levels based on the effects on performance and well-being is proposed and an overview given over the various modalities using hypoxia and altitude for improvement of performance.
Definitions:
Erythropoiesis is the process by which red blood cells (erythrocytes) are produced. It is stimulated by decreased O2 in circulation, which is detected by the kidneys, which then secrete the hormone erythropietin. This hormone stimulates proliferation and differentiation of red cell precursors, which activates increased erythropoiesis in the hemopoietic tissues, ultimately producing red blood cells.
Notes of Interest:
A significant increase in red blood cell mass may already occur after 3 wees at a minimum altitude of 2100 m a.s.l. (Schmitd & Prommer, 2008) and this gets more pronounced as altitude increases.
During the first 24-48 h, at even a low altitude (15000-2000 m a.s.l.), Hb concentration is elevated by 0.5-1.0g/100 mL blood, which may correspond to a loss of plasma water of 0.2-0.3 L. At 3000 and 4000 m a.s.l., the rise in Hb concentration may amount to another 0.5-0.8g/100 mL per 1000m, indicating a decrease in plasman volume of 0.600.9 L (Saltin, 1966; Svedenhag et al., 1997; Calbet et al., 2004).
Classic high-altitude training involves living and training at altitudes between 2000 and 2800 m a.s.l. for a period of 2-4 weeks. Living high and training low, introduced by Levine & Stray-Gundersen (1997), consists of living about 20h/day at an altitude of 2800 m a.s.l. and training at an altitude of 1200 m a.s.l., which already impairs maximum aerobic performance in well-trained subjects.
AMS (Acute Mountain Sickness)
There appears to be a threshold altitude of about 2100 m a.s.l. for significant development of AMS (acute mountain sickness) with exposure to hypobaric hypoxia at rest (Muhm et al., 2007). At altitudes between 2500 and 300 m, the prevalence of AMS is betwen 10% and 30%, depending on the population and the definition of AMS. At these altitudes, AMS is usually mild, transient, and does not progress to more severy symptoms of altitude illnesses, such as cerebral or pulmonary edema. [PHIL: note, they say nothing about cognitive function or neuronal damage]. At altitudes of 4000 - 4500 m a.s.l., the prevalence of AMS is 40%-60%, and in some susceptible individuals treatment with oxygen, dexamethasone, and descent ar necessary for improvement and prevention of progression to cerebral edema (Bärtsch & Roach, 2001). When going to altitudes above 3000m, staged ascent and /or prevention of AMS by acetazolamide (2 x 250 mg/day may be necessary to avoid physical discomfort within the first few days of altitude exposure. A low hypoxic ventilatory response (HVR) may be associated with increased susceptibility to AMS (Moor aet al., 1986; Richalet et al., 1988a), and HVR tends to be lower in endurance-trained athletes (Schoene, 1982). [PHIL: This means that if you're an endurance-trained athlete, it is a good idea to learn how to breath properly for a trip to the top of Kilimanjaro.)
The text below discussing HACE and HAPE comes directly from Bärtsch & Saltin, 2008.
HACE (High-Altitude Cerebral Edema)
HACE is usually preceded by progressive symptoms of AMS. It is characterized by progressive truncal ataxia, clouded consciousness, and variable focal neurologic symptoms. Without treatment, coma usually develops within 1–2 days, and death occurs rapidly because of brain herniation. Vasogenic edema has been demonstrated by MRI (Hackett et al., 1998). Treatment consists of administration of supplemental oxygen, dexamethasone, and descent. HACE rarely occurs below 4000ma.s.l. (Fig. 2), and the prevalence at 4000 5000ma.s.l. is 0.5–1.5%. HACE can be avoided by preventing AMS or by fast and adequate treatment of AMS.
HAPE (High-Altitude Pulmonary Edema)
HAPE is a non-cardiogenic edema that is due to a non-inflammatory capillary leak caused by an abnormally high hypoxic pulmonary vasoconstriction (Bärtsch et al., 2005). Early symptoms are dyspnoea, decreased performance, and cough. In advanced cases, dyspnoea at rest, orthopnoea, and pink frothy sputum occur (Bä rtsch, 1999). HAPE is rare below 3000ma.s.l. and is usually associated with abnormalities in the pulmonary circulation. Prevalence of HAPE after rapid ascent to 4550ma.s.l. within 24 h, including an overnight stay at 3600m a.s.l., is 6% in a general mountaineering population (Fig. 2) and 60–70% in HAPE-susceptible individuals (Bärtsch et al., 2002). Susceptible individuals are characterized by an abnormal increase in pulmonary artery pressure with exposure to hypoxia and also during normobaric exercise (Grünig et al., 2000). This abnormal response pattern of the pulmonary circulation can be found in about 10% of the population in Germany (Grünig et al., 2005). The rate of ascent, the altitude of exposure, and exertion are the major risk factors for development of HAPE, in addition to individual susceptibility based on an abnormal pulmonary hypoxic vasoconstriction. HAPE can be avoided in susceptible individuals with slow ascent (300–400 m/day above 2000ma.s.l.). If slow ascent is not possible, HAPE can also be prevented by drugs that lower pulmonary artery pressure, such as nifedipine (Baürtsch et al., 1991), sildenafil, or dexamethasone (Maggiorini et al., 2006). Treatment consists of administration of supplemental oxygen, application of pulmonary vasodilators (nifedipine or tadalafil), and descent. Mortality is estimated to be 50% if no treatment is possible (Lobenhoffer et al., 1982), while adequate treatment leads to a complete recovery without sequelae.
I have put a few excerpts from the paper into this blog to inform my fellow climbers. The text below is a mixture of paraphrasing and quotes from the paper. This is a really good paper and I highly recommend tracking it down and giving it a complete read.
Abstract
The key elements in acclimatization aim at securing the oxygen supply to tissues and organs of the body with an optimal oxygen tension of the arterial blood. In acute exposure, ventilation and heart rate are elevated with a minimum reduction in stroke volume. In addition, plasma volume is reduced over 24–48 h to improve the oxygen carrying capacity of the blood, and is further improved during a prolonged sojourn at altitude through an enhanced erythropoiesis and larger Hb mass, allowing for a partial or full restoration of the blood volume and arterial oxygen content. Most of these adaptations are observed from quite low altitudes [1000m above sea level (m a.s.l.)] and become prominent from 2000 m a.s.l. At these higher altitudes additional adaptations occur, one being a reduction in the maximal heart rate response and consequently a lower peak cardiac output. Thus, in spite of a normalization of the arterial oxygen content after 4 or more weeks at altitude, the peak oxygen uptake reached after a long acclimatization period is essentially unaltered compared with acute exposure. What is gained is a more complete oxygenation of the blood in the lungs, i.e. SaO2 is increased. The alteration at the muscle level at altitude is minor and so is the effect on the metabolism, although it is debated whether a possible reduction in blood lactate accumulation occurs during exercise at altitude. Transient acute mountain sickness (headache, anorexia, and nausea) is present in 10–30% of subjects at altitudes between 2500 and 3000ma.s.l. Pulmonary edema is rarely seen below 3000ma.s.l. and brain edema is not seen below 4000ma.s.l. It is possible to travel to altitudes of 2500–3000ma.s.l., wait for 2 days, and then gradually start to train. At higher altitudes, one should consider a staged ascent (average ascent rate 300 m/day above 2000ma.s.l.), primarily in order to sleep and feel well, and minimize the risk of mountain sickness. A new classification of altitude levels based on the effects on performance and well-being is proposed and an overview given over the various modalities using hypoxia and altitude for improvement of performance.
Definitions:
Erythropoiesis is the process by which red blood cells (erythrocytes) are produced. It is stimulated by decreased O2 in circulation, which is detected by the kidneys, which then secrete the hormone erythropietin. This hormone stimulates proliferation and differentiation of red cell precursors, which activates increased erythropoiesis in the hemopoietic tissues, ultimately producing red blood cells.
Notes of Interest:
A significant increase in red blood cell mass may already occur after 3 wees at a minimum altitude of 2100 m a.s.l. (Schmitd & Prommer, 2008) and this gets more pronounced as altitude increases.
During the first 24-48 h, at even a low altitude (15000-2000 m a.s.l.), Hb concentration is elevated by 0.5-1.0g/100 mL blood, which may correspond to a loss of plasma water of 0.2-0.3 L. At 3000 and 4000 m a.s.l., the rise in Hb concentration may amount to another 0.5-0.8g/100 mL per 1000m, indicating a decrease in plasman volume of 0.600.9 L (Saltin, 1966; Svedenhag et al., 1997; Calbet et al., 2004).
Classic high-altitude training involves living and training at altitudes between 2000 and 2800 m a.s.l. for a period of 2-4 weeks. Living high and training low, introduced by Levine & Stray-Gundersen (1997), consists of living about 20h/day at an altitude of 2800 m a.s.l. and training at an altitude of 1200 m a.s.l., which already impairs maximum aerobic performance in well-trained subjects.
AMS (Acute Mountain Sickness)
There appears to be a threshold altitude of about 2100 m a.s.l. for significant development of AMS (acute mountain sickness) with exposure to hypobaric hypoxia at rest (Muhm et al., 2007). At altitudes between 2500 and 300 m, the prevalence of AMS is betwen 10% and 30%, depending on the population and the definition of AMS. At these altitudes, AMS is usually mild, transient, and does not progress to more severy symptoms of altitude illnesses, such as cerebral or pulmonary edema. [PHIL: note, they say nothing about cognitive function or neuronal damage]. At altitudes of 4000 - 4500 m a.s.l., the prevalence of AMS is 40%-60%, and in some susceptible individuals treatment with oxygen, dexamethasone, and descent ar necessary for improvement and prevention of progression to cerebral edema (Bärtsch & Roach, 2001). When going to altitudes above 3000m, staged ascent and /or prevention of AMS by acetazolamide (2 x 250 mg/day may be necessary to avoid physical discomfort within the first few days of altitude exposure. A low hypoxic ventilatory response (HVR) may be associated with increased susceptibility to AMS (Moor aet al., 1986; Richalet et al., 1988a), and HVR tends to be lower in endurance-trained athletes (Schoene, 1982). [PHIL: This means that if you're an endurance-trained athlete, it is a good idea to learn how to breath properly for a trip to the top of Kilimanjaro.)
The text below discussing HACE and HAPE comes directly from Bärtsch & Saltin, 2008.
HACE (High-Altitude Cerebral Edema)
HACE is usually preceded by progressive symptoms of AMS. It is characterized by progressive truncal ataxia, clouded consciousness, and variable focal neurologic symptoms. Without treatment, coma usually develops within 1–2 days, and death occurs rapidly because of brain herniation. Vasogenic edema has been demonstrated by MRI (Hackett et al., 1998). Treatment consists of administration of supplemental oxygen, dexamethasone, and descent. HACE rarely occurs below 4000ma.s.l. (Fig. 2), and the prevalence at 4000 5000ma.s.l. is 0.5–1.5%. HACE can be avoided by preventing AMS or by fast and adequate treatment of AMS.
HAPE (High-Altitude Pulmonary Edema)
HAPE is a non-cardiogenic edema that is due to a non-inflammatory capillary leak caused by an abnormally high hypoxic pulmonary vasoconstriction (Bärtsch et al., 2005). Early symptoms are dyspnoea, decreased performance, and cough. In advanced cases, dyspnoea at rest, orthopnoea, and pink frothy sputum occur (Bä rtsch, 1999). HAPE is rare below 3000ma.s.l. and is usually associated with abnormalities in the pulmonary circulation. Prevalence of HAPE after rapid ascent to 4550ma.s.l. within 24 h, including an overnight stay at 3600m a.s.l., is 6% in a general mountaineering population (Fig. 2) and 60–70% in HAPE-susceptible individuals (Bärtsch et al., 2002). Susceptible individuals are characterized by an abnormal increase in pulmonary artery pressure with exposure to hypoxia and also during normobaric exercise (Grünig et al., 2000). This abnormal response pattern of the pulmonary circulation can be found in about 10% of the population in Germany (Grünig et al., 2005). The rate of ascent, the altitude of exposure, and exertion are the major risk factors for development of HAPE, in addition to individual susceptibility based on an abnormal pulmonary hypoxic vasoconstriction. HAPE can be avoided in susceptible individuals with slow ascent (300–400 m/day above 2000ma.s.l.). If slow ascent is not possible, HAPE can also be prevented by drugs that lower pulmonary artery pressure, such as nifedipine (Baürtsch et al., 1991), sildenafil, or dexamethasone (Maggiorini et al., 2006). Treatment consists of administration of supplemental oxygen, application of pulmonary vasodilators (nifedipine or tadalafil), and descent. Mortality is estimated to be 50% if no treatment is possible (Lobenhoffer et al., 1982), while adequate treatment leads to a complete recovery without sequelae.
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