Influence of aspirin on aging skeletal muscle: Insights from a cross-sectional cohort of septuagenarians.

Influence of aspirin on aging skeletal muscle: Insights from a cross-sectional cohort of septuagenarians.
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DOI:
10.14814/phy2.15669
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发表时间:
2023-04
影响因子:
2.5
通讯作者:
--
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其他
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阿司匹林是最常用的环氧合酶(COX)抑制剂和抗炎药之一,已被证明可以阻断COX产生的炎症调节和骨骼肌衰老。我们使用倾向分数匹配来比较健康ABC研究中不服用阿司匹林或任何其他COX抑制药物的个体(非消费者,n = 497,74 ± 3 Year,168 ± 9 cm,75.1 ± 13.8 Kg,33.1For± 7.4%体脂,37%女性,34%黑人)与那些每天服用阿司匹林(不服用任何其他COX抑制药物)和至少1 年(阿司匹林消费者,n = 515,74 ± 3 Year,168 ± 9 cm,76.2 ± 13.6 kg,33.8 ± 7.1%体脂,39%女性,30%黑人,平均阿司匹林消耗量:6 年。受试者根据年龄、身高、体重、体脂百分比、性别和种族进行匹配(p > 0.05)(倾向分数:0.33 ± 0.09 vs.0.33 ± 0.09,p > 0.05)。在计算机断层扫描确定的股四头肌(103.5 ± 0.9vs 104.9 ± 0.8 cm~2,p > 0.05)、腿肌(54.6 ± 0.5 vs 54.9 ± 0.5 cm~2,p > 0.05)或股四头肌肌力(111.1 ± 2.0 vs 111.7 ± 2.0 Nm,p > 0.05)方面,非消费者和阿司匹林消费者之间没有差异。然而,阿司匹林使用者股四头肌(40.9 ± 0.3vs.44.4 ± 0.3Hounsfield单位[HU],p < 0.05)和腿肌(27.7 ± 0.4vs.33.2 ± 0.4 Hu,p < 0.05)的肌肉衰减(即密度)更高。这些横截面数据表明,长期服用阿司匹林并不影响与年龄相关的骨骼肌萎缩,但确实影响了70多岁老年人的骨骼肌组成。为了更好地了解慢性COX调节对衰老骨骼肌健康的影响,仍有必要进行前瞻性的纵向研究。阿司匹林是最常用的环氧合酶(COX)抑制剂和抗炎药物之一,已被证明可以阻断COX产生的人类骨骼肌炎症调节因子。考虑到老年人的炎症和肌肉质量之间的负相关,来自大规模衰老观察研究的数据可能会为阿司匹林在控制与年龄相关的骨骼肌萎缩中的作用提供洞察。这些横截面数据表明,长期服用阿司匹林并不影响与年龄相关的骨骼肌萎缩,但确实影响了70多岁老年人的骨骼肌组成。
Aspirin is one of the most commonly consumed cyclooxygenase (COX)‐inhibitors and anti‐inflammatory drugs and has been shown to block COX‐produced regulators of inflammation and aging skeletal muscle size. We used propensity score matching to compare skeletal muscle characteristics of individuals from the Health ABC study that did not consume aspirin or any other COX‐inhibiting drugs (non‐consumers, n = 497, 74 ± 3 year, 168 ± 9 cm, 75.1 ± 13.8 kg, 33.1 ± 7.4% body fat, 37% women, 34% black) to those that consumed aspirin daily (and not any other COX‐inhibiting drugs) and for at least 1 year (aspirin consumers, n = 515, 74 ± 3 year, 168 ± 9 cm, 76.2 ± 13.6 kg, 33.8 ± 7.1% body fat, 39% women, 30% black, average aspirin consumption: 6 year). Subjects were matched (p > 0.05) based on age, height, weight, % body fat, sex, and race (propensity scores: 0.33 ± 0.09 vs. 0.33 ± 0.09, p > 0.05). There was no difference between non‐consumers and aspirin consumers for computed tomography‐determined muscle size of the quadriceps (103.5 ± 0.9 vs. 104.9 ± 0.8 cm2, p > 0.05) or hamstrings (54.6 ± 0.5 vs. 54.9 ± 0.5 cm2, p > 0.05), or quadriceps muscle strength (111.1 ± 2.0 vs. 111.7 ± 2.0 Nm, p > 0.05). However, muscle attenuation (i.e., density) was higher in the aspirin consumers in the quadriceps (40.9 ± 0.3 vs. 44.4 ± 0.3 Hounsfield unit [HU], p < 0.05) and hamstrings (27.7 ± 0.4 vs. 33.2 ± 0.4 HU, p < 0.05). These cross sectional data suggest that chronic aspirin consumption does not influence age‐related skeletal muscle atrophy, but does influence skeletal muscle composition in septuagenarians. Prospective longitudinal investigations remain necessary to better understand the influence of chronic COX regulation on aging skeletal muscle health. Aspirin is one of the most commonly consumed cyclooxygenase (COX)‐inhibitors and anti‐inflammatory drugs and has been shown to block COX‐produced regulators of inflammation in human skeletal muscle. Considering the negative association between inflammation and muscle mass in older individuals, data from large scale observational studies of aging may provide insight into the role of aspirin in the control of age‐related skeletal muscle atrophy. These cross sectional data suggest that chronic aspirin consumption does not influence age‐related skeletal muscle atrophy, but does influence skeletal muscle composition in septuagenarians.
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