Author(s): DING, K., LIANG, C., HE, J., Institution: CHINA INSTITUTE OF SPORT SCIENCE, Country: CHINA, Abstract-ID: 581

INTRODUCTION:
Age-related declines in cardiorespiratory fitness are a key physiological hallmark of aging and are closely associated with reduced physical function and quality of life in older adults. Exercise training is widely recommended to promote healthy aging; however, its role in intervening in age-related physiological decline and the underlying mechanisms remain insufficiently understood. Peak oxygen uptake (VO2peak) is a central indicator of cardiorespiratory fitness and a potential mechanistic link between exercise training and functional health outcomes. This study examined whether improvements in VO2peak mediate the effects of exercise training on physical quality of life in older adults, providing longitudinal mechanistic evidence for exercise as an intervention targeting age-related functional decline.
METHODS:
Forty community-dwelling older adults were allocated to an exercise training group (n = 20) or a control group (n = 20). The exercise group completed 3 months of supervised combined aerobic and resistance training, while the control group maintained their usual lifestyle. VO2peak and health-related quality of life were assessed before and after the intervention, with the Physical Component Summary (PCS) score derived from the SF-36 questionnaire. Linear mixed-effects models were used to examine group-by-time interaction effects, with intervention effects evaluated after adjusting for age, sex, body mass index (BMI), and other relevant covariates. Pearson correlation analysis and causal mediation analysis based on changes (Delta) in VO2peak and PCS were subsequently conducted. Nonparametric bootstrap procedures with 5000 resamples were applied to estimate mediation effects and corresponding confidence intervals.
RESULTS:
Significant group-by-time interactions were found for VO2peak and PCS (p < 0.01), with greater improvements in the exercise group. Delta VO2peak was positively correlated with Delta PCS (r = 0.69, p < 0.001). Mediation analysis indicated that Delta VO2peak significantly mediated the effect of exercise on PCS (ACME = 2.92, 95% CI: 0.81-5.43, p = 0.008), accounting for approximately 39% of the total effect (total effect = 7.49, p < 0.001). The direct effect of exercise remained significant (ADE = 4.56, p = 0.004).
CONCLUSION:
Using a controlled longitudinal design, this study provides mechanistic evidence that exercise training can intervene in age-related functional decline by improving VO2peak, which in turn contributes to better physical quality of life in older adults. Beyond enhancing cardiorespiratory fitness levels, the findings suggest that structured exercise training may modify the age-related trajectory of cardiorespiratory fitness decline. VO2peak therefore represents not only a key outcome of exercise training, but also a modifiable physiological pathway through which exercise may influence functional aging.