Background: Stress fractures are frequent injuries among athletes. In vitro, decreases in pH stimulate osteoclasts and inhibit osteoblasts. We hypothesized that exercise-induced lactacidosis stimulates osteoclasts and reduces osteoblast activity in vivo.
Methods: A total of 32 volunteers (MA, male athletes; MCo, male controls; female athletes; and female controls) performed three 60-min cycle ergometer tests at 75%, 95% and 110% of their individual anaerobic threshold (IAT). Blood was taken before and at 3 and 24 h after exercise. Osteocalcin (OC), pro-collagen type I N-terminal peptide (PINP), C-terminal telopeptides of collagen I (CTx) and tartrate-resistant acid phosphatase (TRAP) were measured.
Results: At 75% and 95% IAT, pH did not change. At 110% IAT, pH decreased in MA by 0.08 units (p=0.041) and in MCo by 0.03 units (p=0.017). The pH results were substantiated by circulating lactate concentrations. The bone resorption markers TRAP and CTx were not consistently modified by any of the exercise tests. Exercise at 75% decreased OC and PINP in all groups. Exercise at 95% and 110% did not induce homogeneous effects.
Conclusions: Anaerobic exercise does not systemically affect bone turnover, suggesting that exercise-induced acidosis is not involved in the pathogenesis of stress fractures.
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