Objective To explore the dynamic changes of blood routine indicators and adaptation mechanisms during rapid ascent to high altitude. Methods A total of 80 healthy male soldiers were selected, whose blood routine was tested at 0, 2, 30, 90, and 120 days after rapid ascent to high altitude, and the changes of each indicator were observed. Results After rapid ascent to high altitude, the total WBC count showed no significant fluctuation. Neutrophil count and percentage significantly increased on the 2nd day and gradually returned to the 0 day level. Lymphocyte count and percentage significantly increased on the 90th day, showing statistically significant differences compared to the 0 day level (P<0.05). The RBC count significantly rose after rapid ascent and tended to stabilize after 30 days. HGB and mean corpuscular volume gradually increased on the 2nd, 30th, and 90th days, showing significant differences compared to the 0 day level (P<0.05), and fully stabilized after 90 days. PLT count initially showed a slight stress-induced increase, followed by a decline, and was significantly lower than the 0 day level at 120 days (P<0.05), but still within the normal range. Conclusions After rapid ascent to 4300 m high altitude, the hematopoietic and immune systems of the body exhibit sequential adaptive features. The red blood cell system stabilizes at 90 days after rapid ascent, while the PLT count shows a fluctuating pattern of initial increase and later decrease. These changes may be closely related with hypoxia-inducible factor regulation, iron metabolism balance and immune adjustment.
Key words
rapid ascent to high altitude /
white blood cells /
red blood cells /
platelets /
hypoxia adaptation
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
References
[1] 张成慧, 邬云红, 王溯源, 等. 糖代谢对高原环境的适应与疾病[J]. 四川大学学报(医学版), 2024,55(6):1460-1468.
[2] Thake C D, Mian T, Garnham A W, et al. Leukocyte counts and neutrophil activity during 4h of hypocapnic hypoxia equivalent to 4000 m[J]. Aviat Space Environ Med, 2004,75(9):811-817.
[3] Burtscher J, Samaja M. Healthy aging at moderate altitudes:hypoxia and hormesis[J]. Gerontology, 2024, 70(11):1152-1160.
[4] Schioppa T, Uranchimeg B, Saccani A, et al. Regulation of the chemokine receptor CXCR4 by hypoxia[J]. J Exp Med, 2003,198(9):1391-1402.
[5] Eash K J, Means J M, White D W, et al. CXCR4 is a key regulator of neutrophil release from the bone marrow under basal and stress granulopoiesis conditions[J]. Blood, 2009,113(19):4711-4719.
[6] Li H, Liu T, Wang Y, et al. Paraventricular nucleus CRH neurons regulate acute lung injury via sympathetic nerve-neutrophil axis[J]. Nat Commun, 2025,16(1):8870.
[7] Ince L M, Weber J, Scheiermann C. Control of leukocyte trafficking by stress-associated hormones[J]. Front Immunol, 2019,9:3143.
[8] Islam S M T, Won J, Khan M, et al. Hypoxia-inducible factor-1 drives divergent immunomodulatory functions in the pathogenesis of autoimmune diseases[J]. Immunology, 2021,164(1):31-42.
[9] Altınönder I, Kaya M, Yentür S P, et al. Thymic gene expression analysis reveals a potential link between HIF-1A and Th17/Treg imbalance in thymoma associated myasthenia gravis[J]. J Neuroinflammation, 2024, 21(1):126.
[10] Dang E V, Barbi J, Yang H Y, et al. Control of T(H)17/T(reg) balance by hypoxia-inducible factor 1[J]. Cell, 2011,146(5):772-784.
[11] Kietzmann T. Hypoxia-inducible erythropoietin expression:details matter[J]. Haematologica, 2020,105(12):2704-2706.
[12] Ryan B J, Wachsmuth N B, Schmidt W F, et al. AltitudeOmics:rapid hemoglobin mass alterations with early acclimatization to and de-acclimatization from 5260 m in healthy humans[J]. PLoS One, 2014, 9(10):e108788.
[13] Liu W, Zhang X, Liu J, et al. An erythroid-biased FOShi hematopoietic multipotent progenitor subpopulation contributes to adaptation to chronic hypoxia[J]. Cell Stem Cell, 2025,32(6):935-951.
[14] Yang Y, Gao C, Yang T, et al. Vascular characteristics and expression of hypoxia genes in Tibetan pigs’ hearts[J]. Vet Med Sci, 2022,8(1):177-186.
[15] Zhou S, Yan J, Song K, et al. High-altitude hypoxia induces excessive erythrocytosis in mice via upregulation of the intestinal HIF2a/iron-metabolism pathway[J]. Biomedicines, 2023,11(11):2992.
[16] Li M, Tang X, Liao Z, et al. Hypoxia and low temperature upregulate transferrin to induce hypercoagulability at high altitude[J]. Blood, 2022,140(19):2063-2075.
[17] Siebenmann C, Roche J, Schlittler M, et al. Regulation of haemoglobin concentration at high altitude[J]. J Physiol, 2024,602(21):5587-5600.
[18] Wang Z, Tenzing N, Xu Q, et al. Apoptosis is one cause of thrombocytopenia in patients with high-altitude polycythemia[J]. Platelets, 2023,34(1):2157381.
[19] Wang Z, Gomchok D, Ye Y, et al. Platelet reduction in rats exposed to chronic hypoxia is associated with interaction of glycoprotein ib alpha von willebrand factor[J]. Hamostaseologie, 2025, 28(1):5-82.
[20] Shang C, Wuren T, Ga Q, et al. The human platelet transcriptome and proteome is altered and pro-thrombotic functional responses are increased during prolonged hypoxia exposure at high altitude[J]. Platelets, 2020,31(1):33-42.
[21] Pham K, Vargas A, Frost S, et al. Changes in immune cell populations during acclimatization to high altitude[J]. Physiol Rep,2024, 12(22):e70024.
[22] Gassmann M, Muckenthaler M U. Adaptation of iron requirement to hypoxic conditions at high altitude[J].J Appl Physiol (1985), 119(12):1432-40.
PDF(909 KB)
