Physical training, inflammation and bone integrity in elite female rowers
This study examined whether fluctuations in training load during an Olympic year lead to changes in mineral properties and factors that regulate bone (sclerostin (SOST), osteoprotegerin (OPG)), and receptor activator of nuclear factor kappa-B ligand (RANKL)) and energy metabolism (insulin-like growth factor-1 (IGF-1) and leptin), and inflammation (tumor necrosis factor-α (TNF-α)) in elite heavyweight female rowers. Blood samples were drawn from female heavy-weight rowers (n=15) (27.0±0.8y, 80.9±1.3 kg, 179.4±1.4 cm) at baseline (T1 – 45 weeks pre-Olympic Games) and following 7, 9, 20, 25 and 42 weeks (T1-6, respectively). Serum was analyzed by Multiplex assays (EMD Millipore, Toronto, CAN). Total weekly training load was recorded over the weeks prior to each time point. Bone mineral density (BMD) was measured by dual energy X-ray absorptiometry at T1 and T6. Total BMD increased significantly pre- to post-training (+1.6%). OPG, IGF-1, and leptin were not different across all time points. OPG/RANKL was significantly higher at both T4 and 5 compared to T1 and 2. High training load (T5) was associated with the highest TNF-α levels (2.1 pg/ml), and a parallel increase in SOST (993.1 pg/ml), while low training load (T6 - recovery) was associated with significantly lower TNF-α (1.5 pg/ml) and a parallel decrease in SOST (741.0 pg/ml). Leptin was a significant determinant of bone-mineral properties in these athletes. These results suggest exercise training can lead to an increase in OPG/RANKL, and training load periodization can control the inflammatory response associated with intense training, and combined with adequate caloric intake can preserve bone mineral integrity in elite female athletes.
Elite athletes, Bone Mineral Density, Sclerostin, Inflammation, Osteoclastogenesis
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