202205160144高海拔適應之後的紅血球濃度, 回到低海拔多長時間會降低

2022-05-16 01:49 剛好看到FB有人討論. 順便查詢一下. 先用google翻譯, 之後再修改. 
直接看最後一段結論.
拉巴斯/海拔高度 3,625 公尺
從海平面到達拉巴斯. 約 40天紅血球會到達最高濃度. 從拉巴斯回到海平面, 約 20 天會下降.

這篇是 2007年的研究
Altitude adaptation through hematocrit changes
RESULT 結果
上升時血細胞比容值的初始增加反映了由於紅細胞生成素增加的高度刺激,紅細胞的最大可能產生和釋放。曲線逐漸變平直到達到穩定的峰值平台將對應於逐漸增加的反饋機制(圖 1)。當血細胞比容為 43%(起始 Ht 為 36% + 7%,即總體 14% 增加的一半)時,達到了 50% 的適應。該點 (A50) 在大約 1 週時達到。由於曲線的指數形狀和下面描述的促紅細胞生成素,在初始階段有更大程度的適應。相反,在下降到海平面時,紅細胞比容的下降是逐漸的並且幾乎是線性的(圖 2)。實心菱是一名男性高海拔本地人(第一作者)在高海拔停留2個月後。實心方塊是男性海平面原住民(第二作者),空三角形是女性海平面原住民,兩者都是在高海拔地區停留 2 週後。這表明由於紅細胞壽命以及新細胞溶解的新理論,即選擇性破壞最年輕的循環紅細胞(見討論),導致正常的紅細胞破壞。最初的 18-23 天衰減是線性相關的,因為沒有新的紅細胞替代。可能涉及其他因素 - 但沒有明確定義。然而,一旦心肺系統能夠維持最節能的水平,斜率將達到一個平台。圖 3 顯示了到達拉巴斯後的三個血細胞比容階段:1) 急性適應(從到達時間到 3 天),可能發生急性高山病, 2) 亞急性適應,其中亞急性高山病,例如 高海拔適應因子 = 海拔時間(以天為單位)/海拔高度(以千米為單位)(公里)。40 天后,血細胞比容完全適應 3500 m(圖 1)。因此,拉巴斯海拔高度為 40 天/3.5 公里 = 11.4 天/公里。假設這個線性因子通常是可以接受的,我們可以計算從海平面上升時完全適應其他固定高度所需的天數。作為使用這個高海拔適應因子的第一個例子,我們可以計算適應 2500 米所需的時間長度:2.5 x 11.4 = 28.5 天。同樣,為了適應 5000 m:需要 5.0 x 11.4 = 57 天。為適應8812米(珠穆朗瑪峰頂峰):8.8×11.4=100天,不包括溫差、風、物流、食物等其他因素。然而,在這些極端高度的情況下,需要不同階段的高度適應似乎是合乎邏輯的,就像目前所做的那樣,因為沒有飛機可以降落在珠穆朗瑪峰的山頂上。這些數據表明,大多數人在攀登珠穆朗瑪峰時並沒有花足夠的時間來適應。因此,由於海拔高度的並發症。適應公式應僅適用於 2000 m 以上的高度,因為在此高度之前,變化是微不足道的。為了計劃從高於海平面的高度開始的運動,如登山,這需要進一步研究。放血已在高海拔地區用於治療紅細胞增多症。然而,我們強烈反對它,因為在大多數情況下,紅細胞增多症的根本原因尚不清楚 (3)。CMS 中的低通氣和高血細胞比容被認為是最有效的節能機制 (4)。所以放血會給身體帶來不必要的額外負擔。但放血將是在前往海平面的高海拔居民中進行的合理選擇。此外,高海拔居民在停留在海平面後,經常被誤診為患有貧血症。從現在開始,這應該被認為是一個正常的適應過程。在這項研究中,分析了三名到達海平面或固定高度的人的血細胞比容,他們在那裡保持久坐和舒適的生活條件。這與不斷上升和變化高度的登山者形成鮮明對比。登山者還面臨運動、脫水、寒冷、失眠和壓力。海平面城市的高海拔遊客的正常飲食與登山者攝入的食物形成鮮明對比。脫水和/或出血會改變血細胞比容,但這些是對真實血細胞比容的錯誤觀察,假設液體沒有異常變化。先前的研究 (5) 表明,隨著海拔升高,血紅蛋白 (Hb) 濃度會增加。最初的增加基本上歸因於水從血管系統中移出,血漿體積 (PV) 減少高達 20% 和血容量 (BV) 的相關減少,這由濃度增加證實血漿蛋白 (6)。因暴露於缺氧而釋放的心房利鈉肽被認為是潛在的機制 (7)。然而,紅細胞體積 (RCV) 具有隨變化的個體差異,在 +20% 至 13% 之間增加和減少。在高海拔地區一年後,有報導稱 RCV 可增加高達 50 % (5)。女性的鐵補充劑已被證明可以改善高海拔地區的血細胞比容增加 (8)。這表明攝入紅肉是登上高海拔地區的基礎。適應是一個複雜的主題,因為多個變量在不同反應的個體中發揮著作用。此外,任何疾病都可以改變適應性。從 3510 m 的玻利維亞拉巴斯到 35 m 的哥本哈根,這意味著三個坐標的一系列變化:緯度、經度和高度,如上所述。提交人從拉巴斯向東到達海平面時遭遇了嚴重的時差反應。調整睡眠時間大約需要二十天,沒有藥物。這不僅是由於時差;它還影響氧氣增加和二氧化碳壓力從拉巴斯的 30 毫米汞柱增加到 40 毫米汞柱的正常海平面值。這種相對的二氧化碳積累最初會在白天引起疲勞和嗜睡。這一直持續並且相關性很好,直到達到完全的血細胞比容適應 A100。同樣,在長途旅行中,由於坐在飛機上,腳也會腫脹。到達海平面後,吸入空氣中增加的氧張力會導致換氣不足和呼吸性酸中毒。在急性適應階段,動脈血中較高的 CO2 張力會導致血管舒張和體液瀦留。在從拉巴斯前往海平面比賽的足球運動員中已經觀察到了這種情況。很可能存在某種程度的腦水腫,但這尚未得到 MR 掃描的證實。正如腎臟在長期海拔適應中發揮著重要作用一樣,它也在海平面適應中發揮作用,調節一種新的體液瀦留狀態。個體差異是由於種族、體能訓練、通氣和心臟特徵、遺傳,從根本上是心肺疾病。這與所有三個適應階段有關。在最初的急性適應期之後,易感個體可能會出現急性高山病。在極少數情況下,這是由於極其嚴重的血液系統疾病造成的,例如鐮狀細胞性貧血。如果受試者在亞急性期進行劇烈運動,很容易發展為高原亞急性心髒病。Anand 等人 (9) 在士兵上升到 5800 和 6700 m 之間的高度並進行劇烈的體育鍛煉時對此進行了描述。根據我們上面提出的方程,士兵至少需要 66 天(11.4 x 5.8)才能適應那個高度。士兵們最好通過低水平的運動逐漸訓練,因為他們只在高空停留了 70 天。這將顯著減少心功能不全。士兵們沒有足夠的時間適應新的缺氧環境。當血細胞比容值不再增加時,獲得最終的慢性適應階段。該階段之前已被證明是最節能的生物高海拔條件(4)。這裡,最初的心肺和腎臟過度活躍反應逐漸達到最低的耗氧量,但代價是紅細胞數量的增加。慢性適應階段最初是在 CMS 患者中描述的,但也與正常的高海拔居民有關。從高海拔到海平面,血細胞比容反應是線性的,在 18-23 天左右達到完全適應。該反應是線性的,因為它是由新紅細胞生成的突然停止和逐漸減少引起的,可能是由於新細胞增多以及正常的體液變化。紅細胞比容反應是線性的,在 18-23 天左右達到完全適應。該反應是線性的,因為它是由新紅細胞生成的突然停止和逐漸減少引起的,可能是由於新細胞增多以及正常的體液變化。紅細胞比容反應是線性的,在 18-23 天左右達到完全適應。該反應是線性的,因為它是由新紅細胞生成的突然停止和逐漸減少引起的,可能是由於新細胞增多以及正常的體液變化。
即使外部高度高於 10000 m,飛機機艙壓力通常對應於大約 2500 高度。在超過 8 小時的長途飛行中,這有助於在玻利維亞拉巴斯的埃爾阿爾托機場進行初始逐漸適應過程,達到 4100 米。在一小時或更短時間內到同一機場的短途航班可能會導致更大的急性高山病風險。在一項受控的低壓缺氧研究中,受試者在 3 小時/天、每週 5 天、總共 4 週期間暴露於 4000 米,血清促紅細胞生成素 (EPO) 水平翻了一番 (10)。然而,RCV 和 Hb 沒有增加。我們的研究假設類似的 EPO 上升。新細胞溶解 (11) 最初由 Alfrey 等人 (12, 13) 在太空逗留期間的宇航員中描述,已被證明在下降到海平面後對紅細胞增多症患者以及運送到海平面的紅細胞增多症高海拔居民中發揮作用。由於壁結構的變化,年輕和中年紅細胞更容易發生吞噬作用。這就提出了一個問題,上升是否比下降對健康更不利。向上是通過增加紅細胞數量來構建身體的策略。下降到海平面時,人體會通過溶血破壞紅細胞,增加尿膽素原(定期尿檢證明)以及糞便鐵和膽汁色素(深藍綠色糞便證明)的產生。乍一看,血統對健康的危害最大。因此,提出在到達海平面時放血(放血)是有益的是合乎邏輯的。這除了構成獻血者的資源外,還意味著有機體的節能機制。作者反對 CMS 患者在高海拔地區出血,因為我們認為紅細胞增多症是一系列疾病的結果 (3)。因此,通過放血降低攜氧能力對高海拔地區的身體來說是一種不必要的壓力。不是這樣,往下走,氧氣供應相對過剩。
我們的研究表明,當血細胞比容達到一個新的血細胞比容平台確認完全適應時,實現了新的完全適應。作者認為,響應環境慢性缺氧而增加紅細胞比容是允許氧氣運輸的最有效機制,因此不能像其他一些作者提出的那樣將其歸類為過度或不必要的 (5),以及最佳紅細胞比容的限制已設置。從海平面到拉巴斯的海拔高度需要大約 40 天才能完全適應。相反,回到海平面需要大約 20 天才能適應。

RESULTS The initial increase of the hematocrit value upon ascent reflects the maximum possible production and release of red blood cells due to a high stimulation through increased erythropoietin. A gradual flattening of the curve until the stable peak plateau is reached would correspond to a gradually increasing feedback mechanism (Fig. 1). A 50% of the adaptation is reached when the hematocrit is at 43% (starting Ht of 36% + 7% that is half of the overall 14% increase). This point (A50) is achieved at around 1 week. There is a greater degree of adaptation in the initial stages due to the exponential shape of the curve and erythropoietin described below. On the contrary, upon descent to sea level, the decrease in hematocrit is gradual and almost linear (Fig. 2).



The solid rhombus is a male high altitude native (first author) after 2 months’ stay at high altitude. The solid square is a male sea level native (second author) and the empty triangle is a female sea level native both after a 2 weeks’ stay at high altitude. This is suggestive of normal red blood cell destruction due to red blood cell life span along with the new theory of neocytolysis, i.e., selective destruction of the youngest circulating red cells (see discussion). The initial 18-23 days decay is linearly correlated, because there is no new replacement of red cells. Other factors could possibly be involved - yet not clearly defined. The slope, however, will reach a plateau once the cardio-pulmonary systems are able to sustain the most energy efficient level. Fig. 3 shows the three hematocrit stages after arrival to La Paz: 1) Acute adaptation (from the time of arrival up to 3 days), where acute mountain sickness can occur, 2) Subacute adaptation, where subacute mountain sickness such as where High altitude adaptation factor = Time at altitude in days/Altitude in kilometers (km). Complete hematocrit adaptation to 3500 m was achieved after 40 days (Fig. 1). Hence, 40 days/3.5 km = 11.4 days/km for the altitude of La Paz. Assuming that this linear factor is generally acceptable, we can calculate the number of days necessary to achieve a complete adaptation to other fixed altitudes, when ascending from sea level. As a first example of the use of this high altitude adaptation factor, we can calculate the length of time required to adapt to 2500 m: 2.5 x 11.4 = 28.5 days. Likewise, in order to adapt to 5000 m: 5.0 x 11.4 = 57 days are needed. In order to adapt to 8812 m (the summit of Mt Everest): 8.8 x 11.4 = 100 days, excluding other factors such as temperature differences, wind, logistics, and food. However, in the case of these extreme altitudes it seems logical to require different stages of altitude adaptation, as currently done, since no airplane can land on the summit of Mt. Everest. These data indicates that most people do not take enough time to adapt when ascending Mount Everest. Hence, the complications due to altitude. The adaptation formula should only be applied to altitudes above 2000 m, since up to this altitude, changes are insignificant. In order to plan for movements starting from higher than sea level altitudes, as in mountain climbing, this would require further studies. Phlebotomy has been used at high altitude to treat polyerythrocythemia. However, we strongly oppose it, as the underlying cause of polyerythrocythemia is not well understood in most cases (3). Hypoventilation along with a high hematocrit in CMS has been considered the most efficient energy saving mechanism (4). So that phlebotomy would produce an unnecessary extra load on the body. But phlebotomy would be a logic choice to perform in high altitude residents going to sea level. Furthermore, the high altitude residents, after staying at sea level, are often wrongly diagnosed as suffering from anemia. This should, from now on be considered a normal adaptation process. In this study, hematocrit was analyzed in three persons that arrived to sea level or to a fixed altitude, where they remained sedentary and in comfortable living conditions. This contrasts with mountaineers who are constantly ascending and changing altitudes. The mountaineers are also exposed to exercise, dehydration, cold, sleep loss, and are under stress. A normal diet for a high altitude visitor to a sea level city contrasts with the food ingested by mountaineers. Dehydration and/or bleeding alters the hematocrit, but these are false observations of the true hematocrit that assumes no abnormal fluid changes. Previous studies (5) haveshown that hemoglobin (Hb) concentration increases upon altitude ascent. The initial increase is attributed fundamentally to a shift of water out of the vascular system, with a decrease in the plasma volume (PV) up to 20 % and a correlated decrease of blood volume (BV), confirmed by an increase in the concentration of plasma proteins (6). Atrial natriuretic peptide, released by exposure to hypoxia is believed to be the underlying mechanism (7). However, red cell volume (RCV) has individual variations with changes, both increasing and decreasing between +20% down to 13%. After a year at high altitude, there are reports that RCV can increase up to 50 % (5). Iron supplementation in women has been shown to improve the hematocrit increase at high altitude (8). This shows that red meat ingestion is fundamental on ascent to high altitude. Adaptation is a complex subject due to multiple variables playing their role in differently reacting individuals. Also, any disease can alter adaptation. Going from La Paz, Bolivia at 3510 m to Copenhagen at 35 m, implies a series of changes in the three coordinates: latitude, longitude and altitude, as stated above. The author suffered a serious jet lag going to sea level from La Paz towards the East. It took around twenty days for regularization of sleep hours, without medication. This is not only due to the time difference; it also compromises the oxygen increase and the carbon dioxide tension increase from 30 mmHg in La Paz to the normal sea level value of 40 mmHg. This relative CO2 accumulation initially induces fatigue and sleepiness during the day. This lasted and correlated quite well until the full hematocrit adaptation A100 was achieved. There is, likewise, swelling of the feet during long trips, due to being seated in a plane. Upon arrival to sea level, the increased oxygen tension in the inspired air induces hypoventilation and respiratory acidosis. A higher CO2 tension in the arterial blood gives rise to vasodilatation and fluid retention during the acute adaptation stage. This has been observed in soccer players going from La Paz to compete at sea level. It is highly probable that some degree of cerebral edema may be present, but this has not been corroborated by MR scans. Just as the kidney plays a fundamental role in long-term altitude adaptation, it also functions in the sea level adaptation, regulating a new fluid retention status. Individual variations are due to race, physical training, ventilatory and cardiac characteristics, genetics, and fundamentally to cardio-pulmonary disease. This is relevant for all three adaptation stages. After the initial acute phase of adaptation, acute mountain sickness may occur in susceptible individuals. Rarely, it is due to hematological disorders that are extremely serious, such as sickle cell anemia. If the subject is exposed to intense exercise in the subacute stage, he can easily develop high altitude subacute cardiac disease. This was described by Anand et al (9) in soldiers ascending to altitudes between 5800 and 6700 m and performing intense physical exercise. According to our equation presented above, it would take at least 66 days (11.4 x 5.8) for the soldiers to adapt to that altitude. It would have been better for the soldiers to train gradually with low level exercise, since they remained only at altitude for 70 days. This would have reduced significantlythe cardiac insufficiency. The soldiers had insufficient time to adapt to the new hypoxic environment. The final chronic adaptation stage is acquired when the hematocrit value no longer increases. This stage has previously been shown to be the most energy efficient biological high altitude condition (4). Here, the initial cardio-respiratory and renal hyperactive response gradually achieves the lowest oxygen consumption at the expense of an increase in the number of red blood cells. The chronic adaptation stage was originally described in CMS patients, but it is also pertinent to normal high altitude residents. Going from high altitude to sea level, the hematocrit response is linear and complete adaptation is achieved at around 18-23 days. The response is linear, because it is caused by a sudden stop in new red blood cell production and a gradual decrease, possibly by neocytosis along with normal fluid changes.
Airplane cabin pressures typically correspond to around 2500 of altitude even though the exterior altitude is above 10000 m. On long flights for over 8 hours, this helps in the initial gradual adaptive process to 4100 m at the El Alto airport in La Paz, Bolivia. Short flights, in one hour or less to the same airport can lead to a greater risk of acute mountain sickness. In a controlled hypobaric hypoxia study, where subjects were exposed to 4000 m during 3 hours/day, 5 days per week in a total period of 4 weeks, the serum erythropoietin (EPO) levels doubled (10). However, there was no increase in RCV and Hb. Our study assumes a similar EPO rise. Neocytolysis (11) originally described by Alfrey et al (12, 13) in astronauts during space sojourn, has been shown to play a role on polycythemic patients after the descent to sea level and also in polycythemic high altitude dwellers transported to sea level. Young and middle-aged RBCs were more prone to phagocytosis due to changes in their wall structure. This poses a question of whether it would be more compromising to health to go up than to go down. Going up is a building strategy of the body by increasing the number of red blood cells. Going down to sea level, the human body destructs red blood cells through hemolysis with an increased production of urobilinogen (evidenced by a regular urine test) and also fecal iron and bile pigments (evidenced by dark blue-green stools). At first glance, the descent would compromise health most. Consequently, it is logical to propose that bleeding (phlebotomy) upon arrival to sea level is of benefit. This would, aside from constituting a resource for blood donors, mean an energy saving mechanism for the organism. The authors have opposed bleeding at high altitude in CMS patients, because we consider polyerythrocythemia a result of a spectrum of medical conditions (3). Hence, diminishing the oxygen carrying capacity by phlebotomy is an unnecessary stress to the body at high altitude. Not so, going down, where there is a relative excess of oxygen supply.
Our study shows that new full adaptation is achieved when the hematocrit reaches a new hematocrit plateau confirming complete adaptation. The authors believe that the increase of hematocrit in response to environmental chronic hypoxia is the most efficient mechanism to allow for oxygen transport and cannot be thus classified, as some other authors propose, as excessive or unnecessary (5), and where a limit of optimal hematocrit is set. Going from sea level to the altitude of La Paz requires about 40 days to achieve a complete adaptation. Conversely, going back down to sea level requires about 20 days for the adaptation to occur.

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