Few studies have examined exercise interventions in oldest-old women—that is, women aged 85 years and older—despite their high risk of experiencing functional decline and metabolic dysregulation. Thus, the present study investigated the effects of low-intensity aerobic and resistance training on functional fitness and selected metabolic biomarkers in this population.
This randomized controlled trial included women aged 85 years and older who were assigned to a control group (CG), an aerobic exercise group (AEG), or a resistance exercise group (REG). Both exercise groups completed 24 weeks of low-intensity training. Functional outcomes included handgrip strength, 30-s chair stand, 30-s arm curl, and 2-min step performance. Biological outcomes included adiponectin, high-sensitivity C-reactive protein (hs-CRP), fasting insulin, homeostatic model assessment for insulin resistance (HOMA-IR), and glucose. Intervention effects were evaluated using mixed-effects repeated-measures analyses including group, time, and group × time interaction.
Handgrip strength showed a significant group × time interaction, with a significant increase observed only in REG. Both exercise groups showed significant improvements in 30-s chair-stand, 30-s arm curl, and 2-min step performance relative to CG. Adiponectin increased significantly in both exercise groups, with the largest increase in REG. Fasting insulin and glucose were significantly lower in AEG and REG than in CG at 24 weeks, whereas hs-CRP and HOMA-IR did not show significant intervention effects.
Low-intensity aerobic and resistance training was found to improve multiple domains of functional fitness in oldest-old women. Favorable changes were also observed in selected metabolic biomarkers, including adiponectin, fasting insulin, and glucose. These functional and biomarker outcomes should be interpreted as parallel responses to the intervention rather than evidence of a direct relationship between functional improvements and biomarker changes. Low-intensity exercise may represent a feasible strategy for supporting functional capacity in women of very advanced age.
Sung-Wook Chun, Eun Jung Kim, N. An· European Review of Aging and...· 0 citations
BACKGROUND
Sarcopenia is a progressive muscle-wasting condition driven in part by chronic inflammation; however, the specific inflammatory mediators that contribute to functional decline in humans and their responses to exercise remain poorly defined.
METHODS
We analyzed public ribonucleic acid (RNA) datasets to identify inflammatory pathways associated with aging and exercise. Additionally, we validated candidate factors in older adults through 2 human studies. Complementary cellular and animal experiments were performed to dissect the mechanistic responses to muscle atrophy, injury, and exercise-mimetic therapies.
RESULTS
C-X-C motif chemokine ligand 2 (CXCL2) was identified as a prominent age-associated exercise-responsive inflammatory factor in human datasets. In older adults, plasma CXCL2 levels increased with sarcopenia severity and correlated with SPS-defined functional impairment (r = 0.6472, p = 0.0003). In the 48-week human intervention, structured exercise substantially improved strength, mobility, and endurance and markedly reduced circulating CXCL2 (p < 0.0001) and tumor necrosis factor-alpha (TNF-α) levels (p < 0.0001). In contrast, individuals in the non-exercise group exhibited progressive functional decline and increased cytokine levels. Moreover, Cxcl2 expression was upregulated in the skeletal muscles of aged mice and induced by muscle atrophy or injury (p = 0.0082). In contrast, exercise-mimetic stimulation and acute endurance exercise suppressed Cxcl2 expression (p = 0.0148, p = 0.0072). Importantly, blocking CXCL2-CXCR2 signaling attenuated dexamethasone-induced expression of the atrophy markers Fbxo32 (p = 0.0336, 0.0127, 0.0061) and Trim63 (p = 0.0296, 00160, 0.0042).
CONCLUSION
Human evidence from year-long clinical exercise interventions, supported by transcriptomic, cellular, and animal experiments, identified CXCL2 as a modifiable inflammatory mediator linking aging to muscle atrophy. Consistent suppression of CXCL2 by exercise and attenuation of atrophic signaling through CXCR2 inhibition highlights the CXCL2-CXCR2 axis as a promising target for mitigating sarcopenia.
Juyeon Lee, Sung-Wook Chun, Subin Choi et al.· Journal of Sport and Health...· 0 citations
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