Introduction: Recent investigations suggest that acute exercise decreases Ca²⁺, subsequently stimulating parathyroid hormone (PTH) and bone breakdown (Townsend et al., 2016; Kohrt et al., 2018). It has been suggested the exercise-induced decrease of Ca²⁺ may contribute to the low bone mineral density phenomenon observed in many endurance athletes (Duckham et al., 2012; Scofield and Hecht, 2012). The aim of this study was to investigate the effect of exercise intensity, and the associated acid-base changes, on Ca²⁺ and PTH. 

Methods: Twelve healthy males (n = 12) completed a three-arm, randomised-counterbalanced design experiment. Physiological thresholds and associated workloads were identified from a maximal cardiopulmonary exercise test. Participants completed 30-minutes (or until volitional fatigue) of cycle exercise below gas exchange threshold (GET), above GET, or 10W above the estimated critical power (Above RCP). Blood samples were taken every 5 minutes for 35 minutes, or until volitional fatigue. Ca²⁺ and pH were analysed using an i-STAT point of care device and EG7+ cartridge system. PTH was analysed using ELICA. Data were analysed using linear mixed effects models and omnibus ANOVAs of fixed terms (R Core Team, 2020).

Results: Exercise produced a biphasic intensity-dependent Ca²⁺ response to exercise (F (12, 189.83) = 3.45, p <.001). Exercise below GET did not alter Ca²⁺ when referenced to baseline (M_diff = -0.01–0.02 mmol⋅L^-1, SE = 0.01, p > 0.05), but exercise above GET (including above RCP) significantly increased Ca²⁺, peaking at 10-minutes (M_diff = 0.04–0.07, SE = 0.01, p < 0.001). Plasma-volume adjusted PTH (PTH_Adj) was significantly decreased in the initial 10-minutes of exercise above GET/RCP (M_diff = -15.81 – -10.61 , SE = 3.30, p < 0.001). Ca²⁺ decreased throughout the remainder of exercise above GET and RCP, returning to baseline concentrations. PTH_Adj mirrored Ca²⁺’s response: PTH_Adj increased from 10 minutes above GET and above RCP, but was only significantly greater than baseline following above GET exercise (M_diff = 30.93, SE= 3.38, t(189.33) = 9.14, p < 0.001). Introducing pH as a covariate in the Ca²⁺ model (b = -0.27, SE = 0.06, t(189.30) = -4.11, p < 0.001) removed significant interactions at 5 and 10-minutes between exercise below GET and above RCP. However, pH could not account for all Ca²⁺ variation, as the main effect of time (F (7, 191.77) = 13.85, p < 0.001), and its interaction with condition (F (12, 190.17) = 4.37, p < 0.001), remained significant. Pooled concentrations of PTH_Adj were negatively associated with Ca2+ (R = -0.6, p < 0.001). 

Conclusion: These findings suggest GET may act as an intensity threshold for eliciting significant biphasic response in Ca²⁺ and PTH_Adj. pH may explain the intensity-dependency of Ca²⁺ during exercise, likely due to the physiochemical competitive binding model (Pedersen, 1972; Fogh-Andersen et al., 1993). However, pH could not account for the entirety of Ca²⁺’s temporal response, suggesting other exercise-mediated effects may play a role in calcium regulation. It appears Ca²⁺ is important for mediating PTH response to exercise, but that other exercise-induced responses may also influence PTH and subsequent bone metabolism.