To investigate the relationship among PA, BMD, and body composition in both obese individuals and athletes, our study employed QUS to measure BMD. Although the WHO designates DXA as the gold standard for diagnosing osteoporosis,[
20] stand-alone QUS is not recommended for initiating treatment decisions or for follow-up assessments. Additionally, QUS may not be suitable for screening early postmenopausal women for low axial or peripheral BMD. [
21] Nevertheless, calcaneal QUS has been shown to effectively predict proximal femoral BMD in middle-aged and elderly populations, as well as lumbar BMD in women. As a screening method for osteoporosis, calcaneal QUS demonstrates good specificity, making it a viable option as a prescreening tool. This approach could potentially reduce the need for DXA screenings, particularly in resource-limited settings, by identifying patients at low risk of fractures that do not require further screening, thereby reserving DXA for those at the highest risk.[
22] It is known that BMD tends to decrease after reaching peak bone mass due to the complex interplay of factors including changes in sex hormones, nutrition, and mechanical loading on bones. Modifiable behaviors such as smoking, dietary choices, and PA significantly contribute to the development of osteoporosis in older adults.[
23] Physical inactivity, particularly due to prolonged bed rest or exposure to reduced gravity, can alter bone turnover and mineral homeostasis.[
11] PA has been shown to promote bone health, aligning with previous studies that report varying effects of PA on BMD in females and males. However, in obese populations, the relationship between BMD and PA often appears to be nonsignificant.[
24] In contrast to these findings, our study suggests that BMD increases with higher levels of PA (r=0.284,
P=0.023), although the weak correlation may be attributed to the limited number of participants. Historically, obesity has been associated with improved bone integrity, leading to suggestions of an osteoprotective effect. However, more recent evidence indicates that obesity may also correlate with poor bone quality and a heightened risk of fractures. [
25] The association between obesity and fracture risk is complex and appears to vary by skeletal site, with potential differences between men and women.[
26] The risks of hip and wrist fracture were reduced by 25% (N=8; relative risk [RR], 0.75; 95% confidence interval [CI], 0.62-0.91;
P=0.003; I
2=95%) and 15% (N=2 studies; RR, 0.85; 95% CI, 0.81-0.88), respectively, while ankle fracture risk was increased by 60% (N=2 studies; RR, 1.60; 95% CI, 1.52-1.68) in postmenopausal women with obesity compared with those without obesity.[
27] Conversely, high BMI was associated with an increased risk of humerus and elbow fractures. Furthermore, although numerous studies consistently report higher areal BMD in individuals with obesity, it seems that altered bone quality may play a significant role in determining fracture risk within this population.[
28] Osteoporosis did not significantly increase the odds of ankle fractures thus, suffering an ankle fracture does not automatically warrant further osteoporosis assessment. These data suggest that mechanical factors may be more important than bone density in determining ankle fractures in obese individuals. Similarly, the extra fat mass near the hip could play an important role in hip fracture protection in obese individuals.[
29] Several studies have been published showing a positive association between obesity and bone health. [
30] The scientific literature shows how weight bearing increases bone density by acting also at the cellular level. Studies conducted on animals show that osteocytes are particularly sensitive to biomechanical stress. They die by apoptosis in the absence of loading, while when the shear stress signal is picked up by the osteocytes, they do not undergo apoptosis, and their secretion of sclerostin is suppressed. At the same time, the action of the osteoclasts is repressed, and osteoblastic differentiation is stimulated. [
31-
38] In addition, the increase in BMD that has been found in obesity also seems to be linked to the action of estrogens. It is widely demonstrated that estrogens have an important effect on bone metabolism, stimulating bone formation and reducing its resorption.[
23] Even though a wide literature shows that a higher BMD is correlated with obesity in part of BMI our findings reveal that this association is not significant.[
39] After adjusting for body weight and BMI, we observed a negative association between BMD and BMI. In our study, BMD showed a significant positive correlation with PA, a negative correlation with BMI and visceral fat, and no significant association with body composition metrics such as fat mass, lean mass, and BMR. These results suggest that maintaining a higher level of PA could be beneficial for preventing future risks of osteoporosis. Moreover, our study confirms that among various body composition variables and baseline anthropometric characteristics, BMI and visceral fat consistently serve as significant negative independent contributors to BMD in both athletes and obese groups aged 18 to 30 years. A study comparing athletes involved in high-impact sports indicated that these athletes maintained adequate BMD for their chronological age (Z-score≥−2.0). Moreover, a significant difference in BMD was observed when comparing the athletes to the obese group (
P=0.018). This study underscores the importance of addressing PA and body composition in mitigating osteoporosis risk, particularly among the obese population. Notably, no correlation between lean mass and BMD was found. Given the association of obesity with higher mortality and increased risks of cardiovascular disease, diabetes, cancer, and BMD our study focused on assessing fat mass, lean mass, and visceral fat instead of BMI to better understand their correlation.