Abstract

Exercise perturbs homeostasis, alters the levels of circulating mediators and hormones, and increases the demand by skeletal muscles and other vital organs for energy substrates. Exercise also affects bone and mineral metabolism, particularly calcium and phosphate, both of which are essential for muscle contraction, neuromuscular signaling, biosynthesis of adenosine triphosphate (ATP), and other energy substrates. Parathyroid hormone (PTH) is involved in the regulation of calcium and phosphate homeostasis. Understanding the effects of exercise on PTH secretion is fundamental for appreciating how the body adapts to exercise. Altered PTH metabolism underlies hyperparathyroidism and hypoparathyroidism, the complications of which affect the organs involved in calcium and phosphorous metabolism (bone and kidney) and other body systems as well. Exercise affects PTH expression and secretion by altering the circulating levels of calcium and phosphate. In turn, PTH responds directly to exercise and exercise-induced myokines. Here, we review the main concepts of the regulation of PTH expression and secretion under physiological conditions, in acute and chronic exercise, and in relation to PTH-related disorders.

Highlights

  • In highly trained elite cyclists sampled before the start, at mid race, and at the end of a 3-week stage race, after adjustment for plasma volume changes, 25-(OH)D, Parathyroid hormone (PTH), and total calcium remained stable, while fibroblast-growth factor 23 (FGF23) was increased by 50% and positively correlated with the indexes of metabolic effort and the decrease in serum phosphate, though only in the first half of the race [204], which was associated with increased bone resorption [205,206]

  • Calcium and phosphate metabolism is important for whole-body homeostasis; its dysregulation, because of altered PTH expression and/or secretion, manifests clinically with a wide range of abnormalities in which calcium and phosphate metabolism plays a role

  • This rise in circulating PTH concentrations seems to be dependent upon the effort spent with moderate-to-high intensity possibly prolonged exercise being more effective in inducing this elevation

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Summary

Introduction

Acute physical activity induces a hormone response that re-establishes homeostasis. The endocrine response to acute exercise occurs over multiple phases and its magnitude depends on the work volume and intensity. The homeostatic control of the two elements is important for physical activity and exercise performance. We report on recent research into PTH and PTH-dependent calcium-phosphate response to acute and chronic exercise. The terms physical activity, exercise, and training are often interchangeably and sometimes incorrectly used. Physical activity broadly refers to any bodily movement that is produced by skeletal muscles and that results in energy consumption. It is intrinsically associated with activities of daily living; except for involuntary actions, the amount of physical activity an individual performs is subjective. The force generated by the muscle exceeds the external resistance - Concentric: the muscle shortens

Physiology of PTH and Calcium-Phosphate Metabolism
Parathyroid Hormone and Calcium-Phosphate Homeostasis
The Kidney
Hypoparathyroidism
Hyperparathyroidism
Effects of Acute Exercise
Effects of Chronic Exercise and Training
Effects of PTH on Skeletal Muscle
IL-6 Family Cytokines
Myostatin
Irisin
Osteocalcin
Findings
Conclusions
Full Text
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