Bone: an acute buffer of plasma sodium during exhaustive exercise?

Both hyponatremia and osteopenia separately have been well documented in endurance athletes. Although bone has been shown to act as a "sodium reservoir" to buffer severe plasma sodium derangements in animals, recent data have suggested a similar function in humans. We aimed to explore if acute changes in bone mineral content were associated with changes in plasma sodium concentration in runners participating in a 161 km mountain footrace. Eighteen runners were recruited. Runners were tested immediately pre- and post-race for the following main outcome measures: bone mineral content (BMC) and density (BMD) via dual-energy X-ray absorptiometry (DEXA); plasma sodium concentration ([Na+]p), plasma arginine vasopressin ([AVP]p), serum aldosterone concentration ([aldosterone]s), and total sodium intake. Six subjects finished the race in a mean time of 27.0±2.3 h. All subjects started and finished the race with [Na+]p within the normal range (137.7±2.3 and 136.7±1.6 mEq/l, pre- and post-race, respectively). Positive correlations were noted between change (Δ; post-race minus pre-race) in total BMC (grams) and [Na+]p (mEq/l) (r=0.99; p<0.0001), and between total sodium intake (mEq/kg) and %Δ lumbar spine BMD (r=0.94; p<0.001). Change in [aldosterone]s was positively correlated with: rate of total sodium intake (r=0.84; p<0.05); Δ total BMC (r=0.82; p<0.05); and Δ [Na+]p (r=0.88; p<0.05). No significant pre- to post-race mean differences were noted in BMC or BMD. Robust associations between Δ BMC and Δ [Na+]p suggest that sodium status and bone density may be inter-related during endurance exercise and should be considered in future investigations of athletic osteopenia.