Running-Related Biomechanical Risk Factors for Overuse Injuries in Distance Runners: A Systematic Review Considering Injury Specificity and the Potentials for Future Research.

BACKGROUND: Running overuse injuries (ROIs) occur within a complex, partly injury-specific interplay between training loads and extrinsic and intrinsic risk factors. Biomechanical risk factors (BRFs) are related to the individual running style. While BRFs have been reviewed regarding general ROI risk, no systematic review has addressed BRFs for specific ROIs using a standardized methodology. OBJECTIVE: To identify and evaluate the evidence for the most relevant BRFs for ROIs determined during running and to suggest future research directions. DESIGN: Systematic review considering prospective and retrospective studies. (PROSPERO_ID: 236,832). DATA SOURCES: PubMed. Connected Papers. The search was performed in February 2021. ELIGIBILITY CRITERIA: English language. Studies on participants whose primary sport is running addressing the risk for the seven most common ROIs and at least one kinematic, kinetic (including pressure measurements), or electromyographic BRF. A BRF needed to be identified in at least one prospective or two independent retrospective studies. BRFs needed to be determined during running. RESULTS: Sixty-six articles fulfilled our eligibility criteria. Levels of evidence for specific ROIs ranged from conflicting to moderate evidence. Running populations and methods applied varied considerably between studies. While some BRFs appeared for several ROIs, most BRFs were specific for a particular ROI. Most BRFs derived from lower-extremity joint kinematics and kinetics were located in the frontal and transverse planes of motion. Further, plantar pressure, vertical ground reaction force loading rate and free moment-related parameters were identified as kinetic BRFs. CONCLUSION: This study offers a comprehensive overview of BRFs for the most common ROIs, which might serve as a starting point to develop ROI-specific risk profiles of individual runners. We identified limited evidence for most ROI-specific risk factors, highlighting the need for performing further high-quality studies in the future. However, consensus on data collection standards (including the quantification of workload and stress tolerance variables and the reporting of injuries) is warranted.

Glucagon-Like Peptide-1 Receptor Agonism Improves Nephrotoxic Serum Nephritis by Inhibiting T-Cell Proliferation.

Glucagon-like peptide (GLP)-1 analogs such as liraglutide improved albuminuria in patients with type 2 diabetes in large randomized controlled trials. One of the suspected mechanisms is the anti-inflammatory potential of GLP-1 receptor (Glp1r) agonism. Thus, the anti-inflammatory action of Glp1r agonism was tested in a nondiabetic, T-cell-mediated murine model of nephrotoxic serum nephritis (NTS). The role of Glp1r in NTS was evaluated by using Glp1r-/- mice or C57BL/6 mice treated with liraglutide. In vitro, murine T cells were stimulated in the presence of liraglutide or vehicle. Glp1r-/- mice displayed increased renal infiltration of neutrophils and T cells after induction of NTS. Splenocyte proliferation and TH1 cytokine transcription were increased in spleen and lymph nodes of Glp1r-/- mice. Liraglutide treatment significantly improved the renal outcome of NTS in C57BL/6 mice by decreasing renal infiltration and proliferation of T cells, which resulted in decreased macrophage infiltration. In vitro, T cells stimulated in the presence of liraglutide showed decreased proliferation of TH1 and TH17 cells. Liraglutide blocked glycolysis in T cells and decreased their Glut1 mRNA expression. Together, Glp1r agonism protects mice from a T-cell-dependent glomerulonephritis model by inhibition of T-cell proliferation, possibly by interacting with their metabolic program. This mechanism may explain in part the renoprotective effects of Glp1r agonism in diabetic nephropathy.