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The time-dependency of bone response to exercise might partly be explained by the interaction between vitamin D and exercise.
Thus, further studies aimed at investigating whether the use of a myostatin inhibitor or BMP treatment can restore the bone response to exercise of PPARβ−/− mice are warranted.
However, the function of PPARβ on bone formation, particularly bone modeling, and its role in the bone response to exercise is yet to be elucidated.
Previous findings suggest that bone response to exercise is slower at the femoral neck than at the trochanter region [ 24, 28, 30, 31].
We hypothesize that the lack of periosteal bone response to exercise in PPARβ−/− may be attributed to lower muscle contraction in these mice because muscle stimulation is not involved in the bone response to direct mechanical loading.
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Conversely, Bennell et al. (2002), who compared 5 weeks old female rats with 17 weeks old female rats, concluded that age does not influence the bone response to treadmill exercise.
Postn KO mice have low bone mass, a minimal bone formation response to exercise and axial compression and increased bone fatigue damage in response to loading.
These observations therefore indicate an altered muscle and bone anabolic response to exercise in the absence of PPARβ.
Children display a high bone turnover rate and a more pronounced change in bone mass in response to exercise training than later in life.
There are many studies on prescriptive exercise regimes but the interventions were aimed at studying bone density in response to exercise interventions, not physical activity uptake behaviour.
Other studies in rats comparing the responses to resistance [12] and treadmill exercise [13] found increased bone formation in response to exercise in aged animals when directly compared with young adults.
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