Adolescent physical activity trajectories and later non-communicable disease risk factors: A systematic review of...

To systematically examine the associations between adolescent physical activity (PA) trajectories and the development of non-communicable disease (NCD) risk factors, and to identify key mediating pathways, including fat mass and inflammation.

Systematic review of longitudinal studies.

Five electronic databases (PubMed, Embase, Scopus, Ovid Medline, and Web of Science) were searched for longitudinal studies assessing PA trajectories in adolescents (10-19 years) and subsequent NCD risk factors. Eligible studies included at least two time points of PA measurement and reported cardiovascular, metabolic, anthropometric, or inflammatory outcomes. Risk of bias was assessed using the ROBINS-E tool. Due to methodological heterogeneity, findings were synthesized narratively.

Ten longitudinal studies comprising 20,133 adolescent participants were included, with follow-up periods ranging from 4 to 25 years. Most studies identified declining PA trajectories across adolescence. Lower PA was consistently associated with adverse anthropometric outcomes, including higher BMI and increased obesity risk (OR = 0.50-0.67 for higher PA). Cardiovascular outcomes, particularly blood pressure, showed inverse associations with PA, while sedentary time was positively associated with risk. Metabolic outcomes indicated increased insulin resistance and impaired glucose regulation among low or declining PA groups (e.g., OR = 1.20 for hyperinsulinemia). Inflammatory markers, including C-reactive protein, were elevated with greater sedentary exposure. Fat mass emerged as a central mediator, accounting for 30-77% of the associations between PA and inflammatory outcomes. Even light-intensity PA demonstrated protective effects. Mid-adolescence (∼15 years) was identified as a critical period for trajectory-related risk.

Adolescent PA trajectories are important determinants of later cardiometabolic health. Declining activity patterns contribute to NCD risk through complex pathways involving adiposity and inflammation. Interventions targeting sustained or increased PA, particularly during mid-adolescence, and reducing sedentary behaviour may mitigate long-term disease risk.