Abstract
Advancing age is associated with bone loss and an increased risk of osteoporosis. Exercise training improves bone metabolism and peripheral nerve regeneration, and may play a critical role in osteogenesis and increase in skeletal nerve fiber density. In this study, the potential positive role of aerobic exercise training in bone metabolism and skeletal nerve regeneration was comprehensively evaluated in 14-month-old male C57BL/6 mice. The mice were divided into two groups: no exercise (non-exercise group) and 8-weeks of aerobic exercise training (exercise group), with six mice in each group. Dual-energy X-ray absorptiometry and micro-computed tomography showed that femoral and tibial bone parameters improved after aerobic exercise training. Greater skeletal nerve fiber density was also observed in the distal femoral and proximal tibial periostea, measured and analyzed by immunofluorescence staining and confocal microscopy. Pearson correlation analysis revealed a significant association between skeletal nerve densities and trabecular bone volume/total volume ratios (distal femur; R2 = 0.82, p < 0.05, proximal tibia; R2 = 0.59, p = 0.07) in the exercise group; while in the non-exercise group no significant correlation was found (distal femur; R2 = 0.10, p = 0.54, proximal tibia; R2 = 0.12, p = 0.51). Analysis of archival microarray database confirmed that aerobic exercise training changed the microRNA profiles in the mice femora. The differentially expressed microRNAs reinforce the role of aerobic exercise training in the osteogenic and neurogenic potential of femora and tibiae. In conclusion, 8-weeks of aerobic exercise training positively regulate bone metabolism, an effect that paralleled a significant increase in skeletal nerve fiber density. These findings suggest that aerobic exercise training may have dual utility, both as a direct stimulator of bone remodeling and a positive regulator of skeletal nerve regeneration.
Highlights
Advancing age is a well-known irreversible risk factor for bone loss and increased fracture risk associated with osteoporosis (Aspray and Hill, 2019)
The differences were not statistically significant, body mass was slightly lower after exercise training compared to baseline in the exercise group, FIGURE 2 | Aerobic exercise training demonstrates greater proximal tibial bone mineral density (BMD), bone mineral content (BMC), trabecular bone microarchitecture, and cortical bone perimeter
Osteoporosis is a devastating age-related metabolic disease associated with low BMD, BMC, reduced bone volume and bone microstructure caused by dysfunctional/dysregulated bone remodeling, leading to increased fracture risk (Aspray and Hill, 2019)
Summary
Advancing age is a well-known irreversible risk factor for bone loss and increased fracture risk associated with osteoporosis (Aspray and Hill, 2019). Exercise is a renowned non-pharmacological intervention that effectively improves bone metabolism by stimulating bone adaptation to mechanical force (Santos et al, 2017). Exercise-induced mechanical force stimulates mechano-sensors and osteocytes, which control bone remodeling by regulating osteoblast and osteoclast differentiation (Klein-Nulend and Bakker, 2007) and stimulating osteoprotegerin, which inhibits osteoclastogenesis (Regard et al, 2012). Exercise has several indirect effects, such as enhancing bone vascular function and blood flow. These alter the osteoblast and osteoclast differentiation via the nitric oxide (NO)-mediated pathway (Dominguez et al, 2010; Stabley et al, 2014). Exercise training has been shown to protect against peripheral neuropathy in diabetic (Kluding et al, 2012) and chemotherapy-induced (Park et al, 2015) peripheral neuropathy models
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