11/02/2023
The relationships between acute changes in markers of bone formation and resorption in response to LEA and long-term bone health are unclear. Sustained and localized acceleration of bone remodeling may play a role in the pathogenesis of bone stress injury in athletes [82, 83]. However, bone (re)modeling markers are typically measured systemically and, therefore, any change in the balance of such markers does not necessarily reflect a change in bone remodeling at a specific site. Accordingly, prospective research has shown no significant differences in bone (re)modeling markers between athletes and military recruits who suffered a stress fracture and those who did not [84, 85]. It is commonly reported that a reduction in bone resorption leads to long-term bone accrual; however, in an individual bone remodeling unit, resorptive osteoclast cells initiate the remodeling cycle and precede bone formation [86]. Thus, suppression of resorption might actually inhibit adaptation [87]. Although the acute effects of LEA on bone (re)modeling markers cannot yet be interpreted in terms of long-term bone health, it is reasonable to assume that preventing the acute effects from occurring would be beneficial given that evidence suggests the long-term effect of LEA is detrimental to bone structure, strength and stress injury risk.