To our knowledge, this is the first and largest survey to examine the prevalence and the independent and joint associations of sleep duration and different intensities of PA with T2D. The current study highlights the high prevalence of T2D in the LPA and short sleep groups. Short sleep duration (< 6 hours/day), rather than long sleep duration (> 8 hours/day), was identified as a risk factor for T2D. Additionally, VPA serves as a protective factor in reducing the risk of T2D associated with sleep disorders.
Higher levels of PA intensity were associated with a lower prevalence of T2D [27]. The benefits of MVPA are well established and it is recognized and recommended by guidelines as a robust preventive factor for T2D [28]. Consequently, both the public and researchers may focus more on MVPA, potentially overlooking the independent effects of MPA. This tendency could result in insufficient attention to the independent effects of MPA in research and public health recommendations. An analysis of PA intensity in this study revealed that VPA has a negative association with T2D prevalence, while MPA has no association with T2D. The results indicate that MPA can not serve as a protective factor against the risk of T2D.
The findings of this study further reinforced the widely recognized association between short sleep duration and an increased risk of T2D [10]. However, in contrast to existing findings [10], this study found no significant association between prolonged sleep duration and T2D. The inconsistent findings may be attributed to potential biases in self-reported sleep data, as participants might have overestimated their actual sleep duration, thus influencing the study outcomes. In fact, prolonged sleep duration is typically positively associated with an increased risk of T2D [29]. Prolonged sleep can potentially disrupt the body's circadian rhythm and metabolic processes, thereby affecting insulin sensitivity and glucose homeostasis [30]. Furthermore, prolonged sleep is often accompanied by extended bed rest and sedentary behavior, as well as sleep fragmentation, all of which are behavioral risk factors for the development of T2D [31, 32]. This suggests that the measurement of sleep duration should rely more on objective assessments.
To our knowledge, this is the first study to systematically examine the joint association between sleep duration, PA and T2D. LPA demonstrated a certain protective effect when combined with normal sleep duration, suggesting that even lower-intensity activity, when coupled with good sleep habits, can moderately reduce the risk of T2D. However, the protective effect of prolonged sleep duration was not significant in the LPA group, which may reflect the detrimental impact of excessive sleep, such as the potential association between oversleeping and metabolic abnormalities [33]. Conversely, MPA did not exhibit a significant risk-reducing effect in this study, particularly in the short and long sleep duration groups. VPA showed a significant protective effect across all sleep duration groups, with the effect being most pronounced when combined with prolonged sleep. Taken together, these results suggest that high levels of PA (> 3000 MET minutes/week) may protect short sleepers from developing T2D.
Short sleep duration is positively associated with T2D. Lifestyle interventions aimed at increasing PA levels may help mitigate this excess risk. These findings on the protective effect of increasing PA for short sleepers against T2D are largely consistent with existing evidence. For instance, evidence from cohort studies has indicated that VPA can help mitigate the inflammatory effects induced by short sleep duration [34]. Cross-sectional studies have found that among individuals with short sleep duration, those with higher levels of PA have a lower risk of developing diabetes or insulin resistance compared to their age-matched counterparts [35]. A previous small-sample experimental study (n = 10) found that PA can partially protect sleep-deprived men from a decline in insulin sensitivity [36]. The present study provides direct and robust evidence supporting the hypothesis that achieving 3000 MET-minutes/week of PA may help reduce the excessive risk of T2D in individuals with short sleep duration.
This study has several notable strengths. First, the large sample size of 16,735 participants and the detailed epidemiological profile allowed for high-quality data analysis and accurate estimation of the exposure-disease relationship. Furthermore, the study not only focused on sleep duration but also distinguished between different intensities of PA (e.g., light, moderate, and vigorous), providing more detailed and specific health recommendations. However, the study has some limitations. Sleep duration and PA intensity were primarily obtained through self-reported questionnaires, which may introduce recall bias or social desirability bias, potentially affecting data accuracy. Furthermore, PA was estimated in intervals, which may have led to overestimation or underestimation of activity duration. In addition. the specific timing of measurements also limited the collection of blood samples, preventing the inclusion of key variables such as blood glucose levels as covariates. Finally, as PA intensity was presented in interval form, the optimal dose of PA matched to sleep duration could not be determined.