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高海拔减压前 24 小时进行偏置运动增加减压应激。

Eccentric exercise 24 h prior to hypobaric decompression increases decompression strain.

机构信息

Division of Environmental Physiology, Swedish Aerospace Physiology Center, KTH Royal Institute of Technology, Stockholm, Sweden.

Department of Neuroscience, Experimental Traumatology, KI Karolinska Institutet, Stockholm, Sweden.

出版信息

Eur J Appl Physiol. 2023 Sep;123(9):2001-2011. doi: 10.1007/s00421-023-05214-3. Epub 2023 May 4.

DOI:10.1007/s00421-023-05214-3
PMID:37140728
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10460726/
Abstract

PURPOSE

Animal studies have shown that recent musculoskeletal injuries increase the risk of decompression sickness (DCS). However, to date no similar experimental study has been performed in humans. The aim was to investigate if exercise-induced muscle damage (EIMD)-as provoked by eccentric work and characterized by reduced strength and delayed-onset muscle soreness (DOMS)-leads to increased formation of venous gas emboli (VGE) during subsequent hypobaric exposure.

METHODS

Each subject (n = 13) was on two occasions exposed to a simulated altitude of 24,000 ft for 90 min, whilst breathing oxygen. Twenty-four hours prior to one of the altitude exposures, each subject performed 15 min of eccentric arm-crank exercise. Markers of EIMD were reduction in isometric m. biceps brachii strength and DOMS as assessed on the Borg CR10 pain scale. The presence of VGE was measured in the right cardiac ventricle using ultrasound, with measurements performed at rest and after three leg kicks and three arm flexions. The degree of VGE was evaluated using the six-graded Eftedal-Brubakk scale and the Kisman integrated severity score (KISS).

RESULTS

Eccentric exercise induced DOMS (median 6.5), reduced the biceps brachii strength (from 230 ± 62 N to 151 ± 8.8 N) and increased the mean KISS at 24,000 ft, both at rest (from 1.2 ± 2.3 to 6.9 ± 9.2, p = 0.01) and after arm flexions (from 3.8 ± 6.2 to 15.5 ± 17.3, p = 0.029).

CONCLUSION

EIMD, induced by eccentric work, provokes release of VGE in response to acute decompression.

摘要

目的

动物研究表明,近期的肌肉骨骼损伤会增加减压病(DCS)的风险。然而,迄今为止,尚未在人类中进行类似的实验研究。本研究旨在探讨运动诱导的肌肉损伤(EIMD)——通过离心运动引起,表现为力量下降和迟发性肌肉酸痛(DOMS)——是否会导致随后的低压暴露期间静脉气体栓塞(VGE)形成增加。

方法

每位受试者(n=13)在两次情况下均接受 24000 英尺模拟高度 90 分钟的吸氧暴露。在其中一次海拔暴露前 24 小时,每位受试者均进行 15 分钟的离心手臂曲柄运动。EIMD 的标志物为等长肱二头肌力量下降和用 Borg CR10 疼痛量表评估的 DOMS。使用超声在右心室测量 VGE 的存在,测量在休息时和三次腿部踢腿和三次手臂弯曲后进行。使用 Eftedal-Brubakk 六级量表和 Kisman 综合严重程度评分(KISS)评估 VGE 程度。

结果

离心运动引起 DOMS(中位数 6.5),降低肱二头肌力量(从 230±62 N 降至 151±8.8 N),并增加 24000 英尺时的平均 KISS,无论在休息时(从 1.2±2.3 增至 6.9±9.2,p=0.01)还是在手臂弯曲后(从 3.8±6.2 增至 15.5±17.3,p=0.029)。

结论

离心运动引起的 EIMD 会引起 VGE 释放,从而导致急性减压时出现 VGE。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb6/10460726/6216373113f3/421_2023_5214_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb6/10460726/c963a723b1cd/421_2023_5214_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb6/10460726/68b937bedfe8/421_2023_5214_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb6/10460726/6216373113f3/421_2023_5214_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb6/10460726/c963a723b1cd/421_2023_5214_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb6/10460726/68b937bedfe8/421_2023_5214_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddb6/10460726/6216373113f3/421_2023_5214_Fig3_HTML.jpg

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