Abstract
PurposeTo characterize the potential sexual dimorphism of bone in response to exercise.MethodsYoung male and female Wistar rats were either submitted to 12 weeks of exercise or remained sedentary. The training load was adjusted at the mid-trial (week 6) by the maximal speed test. A mechanical test was performed to measure the maximal force, resilience, stiffness, and fracture load. The bone structure, formation, and resorption were obtained by histomorphometric analyses. Type I collagen (COL I) mRNA expression and tartrate-resistant acid phosphatase (TRAP) mRNA expression were evaluated by quantitative real-time PCR (qPCR).ResultsThe male and female trained rats significantly improved their maximum speed during the maximal exercise test (main effect of training; p<0.0001). The male rats were significantly heavier than the females, irrespective of training (main effect of sex; p<0.0001). Similarly, both the weight and length of the femur were greater for the male rats when compared with the females (main effect of sex; p<0.0001 and p<0.0001, respectively). The trabecular volume was positively affected by exercise in male and female rats (main effect of training; p = 0.001), whereas the trabecular thickness, resilience, mineral apposition rate, and bone formation rate increased only in the trained males (within-sex comparison; p<0.05 for all parameters), demonstrating the sexual dimorphism in response to exercise. Accordingly, the number of osteocytes increased significantly only in the trained males (within-sex comparison; p<0.05). Pearson’s correlation analyses revealed that the COL I mRNA expression and TRAP mRNA expression were positively and negatively, respectively, related to the parameters of bone remodeling obtained from the histomorphometric analysis (r = 0.59 to 0.85; p<0.05).ConclusionExercise yielded differential adaptations with respect to bone structure, biomechanical proprieties, and molecular signaling in male and female rats.
Highlights
The notion that ‘‘senile osteoporosis is a pediatric disease’’ has been increasingly accepted [1,2,3]
Volumetric density remains constant during growth and similar in both sexes, whereas the bone mass content (BMC) is approximately 20% higher in males than in females at the end of puberty as their bones are larger [1]
According to Callewaert et al [8], androgen receptor and estrogen receptor-b signaling may attenuate the osteogenic response to mechanical strain in males and females, respectively, whilst estrogen receptor-a may stimulate the response of bone to mechanical strain in the female skeleton
Summary
The notion that ‘‘senile osteoporosis is a pediatric disease’’ has been increasingly accepted [1,2,3]. Differential bone plasticity in males and females may be rooted in the biologic properties of bone [1,8] In support of this concept, there is evidence suggesting sex-specific differences in the number of osteoprogenitor cells, hormone responses, and hormone regulation [9,10,11], which could potentially influence the normal growth of bone and its response to a given stimulus (e.g., dietary intervention, pharmacological treatment and physical activity). According to Callewaert et al [8], androgen receptor and estrogen receptor-b signaling may attenuate the osteogenic response to mechanical strain in males and females, respectively, whilst estrogen receptor-a may stimulate the response of bone to mechanical strain in the female skeleton These findings support the hypothesis that skeletal sexual dimorphism in response to exercise may exist
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