Effects of Exercise and Physical Interventions on Bone: Clinical Studies - Skeletal Aging and Osteoporosis: Biomechanics and Mechanobiology - page 246

Fig. 3 Hypothetical effects
of the disruption of calcium
homeostasis during exercise
on bone resorption

Sweating during exercise

Dermal calcium loss

Serum calcium

Stabilization of
serum calcium

PTH

Bone resorption

attenuates exercise-induced increases in inflammatory cytokines, such as IL-6,
which could activate bone resorption [ 64 ]. Further research will be needed to con-
firm the findings of this preliminary study and evaluate underlying mechanisms by
which NSAID use influences skeletal adaptations to exercise. Such research is of
high clinical significance because of the important role of exercise in the prevention
and treatment of osteoporosis and the widespread use of NSAIDs.

3.3.2 Disruption of Calcium Homeostasis During Exercise

Individuals who participate in weight-supported activities, such as cycling and
swimming, have often been observed to have BMD levels that are lower than those
of athletes who participate in weight-bearing activities [ 29 ]. This would not be
unexpected if, in general, weight-supported activities have less osteogenic
potential than weight-bearing activities. However, BMD levels of cyclists and
swimmers have sometimes been reported to be low even when compared with
normally active control subjects [ 12 , 14 , 70 ]. This suggests that the exercise may
be the cause of low BMD in some athletes. Indeed, a prospective study of
competitive road cyclists found that BMD declined over a year of training and
competition [ 3 ]. Total hip BMD decreased by 1.5%, a rate comparable to post-
menopausal bone loss, and was not explained by low calcium intake or changes in
body mass or composition. A prospective study of master cyclists also reported
that the rate of decline in BMD was greater in cyclists than in controls [ 71 ].
It is possible that disruptions in calcium homeostasis during exercise trigger
metabolic responses that lead to the loss of bone mineral. A working model for
this hypothesis (Fig. 3 ) portends that dermal calcium loss during exercise triggers
a decline in serum ionized calcium. Because serum calcium levels are well-
defended, the appropriate counter-regulatory response to a decline is an increase
in PTH, which can stabilize serum calcium levels by mobilizing skeletal calcium