Longitudinal Changes in Fat and Lean Mass: Comparisons between 3D-Infrared and Dual-Energy X-ray Absorptiometry Scans in Athletes

International Journal of Exercise Science 15(4): 1587-1599, 2022. The low cost and portability of three-dimensional (3D) infrared body scanners make them an attractive tool for body composition measurement in athletes. The main purpose of this study was to compare total body fat percentage (BF%) and total lean mass (LM in kg), in a cohort of collegiate athletes, using a 3D infrared body scanner versus a dual energy x-ray absorptiometry (DXA) scanner. Phase I was a pre-season cross-sectional analysis of 61 (39 male) athletes while Phase II was a longitudinal subset analysis of 38 (27 male) student-athletes who returned to the laboratory for post-season scans (Post minus pre-season change). Both the 3D and DXA scans were performed within 20-minutes of one another in the same room, wearing the same clothing. Paired t-tests were used to compare the mean values (BF% and LM) between measurement devices with estimated effects size calculated using Cohen’s d. Data reported as mean±SD. Mean difference (DXA minus 3D) in LM were significantly higher using the 3D scan (5.84 ± 3.55kg; p \u3c 0.001; d = 0.90) compared to the DXA scan, while significantly underestimating BF% (-4.57 ± 4.67%; p \u3c 0.001; d = 1.6) in Phase I analyses. In Phase II analyses, significant differences in the change (post-season minus pre-season change) values were found between methods for LM (4.45 ± 5.04; p \u3c 0.001; d = 0.90), while BF% (-0.41 ± 2.06; p= 0.223; d = 0.2) showed no significant differences. In summary, the 3D and DXA scan values for LM and BF% were not interchangeable in cross-sectional nor longitudinal body composition analyses in collegiate athletes. Close agreement was only observed in longitudinal analyses of BF% and requires further validation with larger cohorts

Cytoprotective pathways in the vascular endothelium. Do they represent a viable therapeutic target?

The vascular endothelium is a critical interface, which separates the organs from the blood and its contents. The endothelium has a wide variety of functions and maintenance of endothelial homeostasis is a multi-dimensional active process, disruption of which has potentially deleterious consequences if not reversed. Vascular injury predisposes to endothelial apoptosis, dysfunction and development of atherosclerosis. Endothelial dysfunction is an end-point, a central feature of which is increased ROS generation, a reduction in endothelial nitric oxide synthase and increased nitric oxide consumption. A dysfunctional endothelium is a common feature of diseases including rheumatoid arthritis, systemic lupus erythematosus, diabetes mellitus and chronic renal impairment. The endothelium is endowed with a variety of constitutive and inducible mechanisms that act to minimise injury and facilitate repair. Endothelial cytoprotection can be enhanced by exogenous factors such as vascular endothelial growth factor, prostacyclin and laminar shear stress. Target genes include endothelial nitric oxide synthase, heme oxygenase-1, A20 and anti-apoptotic members of the B cell lymphoma protein-2 family. In light of the importance of endothelial function, and the link between its disruption and the risk of atherothrombosis, interest has focused on therapeutic conditioning and reversal of endothelial dysfunction. A detailed understanding of cytoprotective signalling pathways, their regulation and target genes is now required to identify novel therapeutic targets. The ultimate aim is to add vasculoprotection to current therapeutic strategies for systemic inflammatory diseases, in an attempt to reduce vascular injury and prevent or retard atherogenesis