Biomedical Engineering Reference
In-Depth Information
(i.e., via stimulation of bone resorption), enhancing intestinal calcium absorption,
and decreasing urinary calcium excretion. There is growing evidence to support
several steps of this conceptual model. Dermal calcium loss clearly increases
during prolonged and or vigorous exercise, and may be more than 100 mg/h
[
2
,
3
,
57
]. Exercise has been found to trigger a decline in serum calcium
[
2
,
55
,
56
] and an increase in PTH [
2
,
3
,
30
,
86
]. The decrease in serum calcium is
not a consistent finding, but may not be apparent at the end of exercise if counter-
regulatory mechanisms to prevent a decline in serum calcium are effective.
Finally, there is evidence that exercise can result in an acute increase in markers
of bone resorption [
2
,
30
,
86
]. Perhaps the most compelling evidence for the
biological plausibility of this cascade of events comes from a study in which
exercise was performed with or without calcium supplementation (i.e., calcium-
enriched water) before and during exercise [
30
]. In the absence of calcium sup-
plementation, exercise resulted in a 2- to 3-fold increase in serum PTH and a 48%
increase in serum C-terminal cross-linking telopeptide of type I collagen (CTX), a
marker of bone resorption. Calcium supplementation prevented the increases in
both PTH and CTX.
If the disruption in calcium homeostasis during exercise described in Fig.
3
occurs repeatedly during exercise training, this may contribute to the decline in
BMD that has been observed in cyclists during training and competition [
3
].
Further studies will be necessary to determine whether the decline in BMD can be
prevented by consuming calcium before and during exercise bouts. Although most
of the research on the disruption of calcium homeostasis during exercise has been
conducted on cyclists, it seems likely that it occurs during any exercise that is
sufficiently intense or prolonged to result in substantial dermal calcium loss.
It seems plausible that the net effect on BMD will depend on the relative activation
of both bone resorption (e.g., through an increase in PTH) and bone formation
during exercise. Under such a paradigm, the deleterious effects of disruptions in
calcium homeostasis would be more likely to adversely affect BMD in individuals
who participate in activities with a relatively low osteogenic potential (e.g.,
swimming) than in those with a relatively high osteogenic potential (e.g., soccer).
It is also important to recognize that, if dermal calcium loss during exercise is the
trigger for the metabolic cascade described in Fig.
3
, preclinical studies of rodents
will be of little use in advancing the understanding of these mechanisms.
4 Summary
The available evidence from prospective cohort and case-control studies suggests
that 3-4 h/week of physical activity can reduce the risk of hip fracture by 30-40%.
Activities such as walking, which are generally not adequate to stimulate an
increase in BMD when evaluated in intervention trials, may provide fracture
protection by preserving BMD and bone strength and/or by reducing risk of falls.
Follow-up evaluations from two small RCTs support the notion that exercise
Search WWH ::
Custom Search