The effect of acute exercise on calcium and bone metabolism: the role of acid-base influences

Abstract

Exercise and bone health has been a focus of intense research in recent years. It is generally accepted that exercise can produce favourable bone adaptations when the stimulus produces sufficient mechanical stress to elicit a cellular response. However, exercise that does not produce adequate mechanical strain, e.g., endurance exercise, appears to stimulate a chronic maladaptation manifesting in reduced bone mineral density and strength. Ultimately, this has been associated with the greater prevalence and risk of stress fractures in endurance athletes. Current available evidence has shown that the increased bone breakdown following acute endurance exercise is largely dependent on calcium metabolism. It appears that exercise stimulates a progressive decrease in ionised calcium (Ca2+) and subsequent increase parathyroid hormone (PTH),which stimulates bone breakdown to restore calcium homeostasis. The precise aetiology of the exercise-induced decrease in Ca2+ remains elusive. The aim of this thesis was to investigate the acute bone and calcium metabolism response to varying exercise and experimental conditions to assess the role acid-base regulation of ionised calcium.

Three independent laboratory studies were performed: Study one utilised acute hypoxic exercise to observe if/how respiratory alkalosis affected Ca2+ and subsequent increase in PTH and bone breakdown. Hypoxia was also selected as an experimental condition as recent evidence has demonstrated a potentially direct negative effect on bone metabolism and structure. Results demonstrated that acute hypoxic exercise exerts no direct effect on bone metabolism, but that it may attenuate an exercise-induced increase in PTH via a reduction in phosphate. Study two investigated the effect of exercise intensity, prescribed at physiological landmarks, on calcium metabolism and PTH. Data from study two revealed that both Ca2+ and PTH changed but these effects were intensity dependent, whereby, exercise below the gas exchange threshold resulted in no temporal changes. Exercise above the gas exchange threshold did elicit a biphasic temporal response. Furthermore, study two identified that pH could account for the intensity-dependency of Ca2+ but not its temporal profile. Study three examined whether high-intensity intermittent exercise and the ingestion of the buffer/alkalising agent, sodium bicarbonate, influenced the calcium metabolism response. It was found that sodium bicarbonate significantly reducedCa2+, which appeared to attenuate a decrease in PTH. Moreover, Ca2+ was shown to flux with intermittent high intensity exercise, which was significantly correlated with potassium, possibly suggesting muscle as a source of calcium sequestering during exercise. This thesis provides further insight into the characteristics of the calcium and parathyroid hormone response to exercise, while exploring the role of acid-base influences. In summary, acid-base regulation of calcium accounted for the differences between exercise intensity and part of the temporal response. All studies demonstrated a significant negative relationship between pH and Ca2+. However, Ca2+ was not exclusively regulated by acid-base alterations, but rather seems to be linked to the contractile process during exercise.

Date of Award	Jun 2022
Original language	English
Sponsors	Department for the Economy
Supervisor	Conor McClean (Supervisor), Sonyia McFadden (Supervisor) & Andrea McNeilly (Supervisor)