Bone formation and resorption biological markers in cosmonauts during and after a 180-day space flight (Euromir 95)

TLDR

Long‑term spaceflight causes bone loss due to altered bone remodeling, mechanisms of which are not yet understood in humans. The study monitored serum and urinary bone turnover markers—including PTH, calcium, BAP, iBGP, PICP, CTX, and D‑Pyr—in cosmonauts before, during, and after a 180‑day mission to assess remodeling dynamics. During flight, PTH and bone formation markers fell while resorption markers rose, and after flight these trends reversed, revealing a microgravity‑induced uncoupling of bone remodeling that likely explains the observed bone loss.

Abstract

Long-term spaceflights induce bone loss as a result of profound modifications of bone remodeling, the modalities of which remain unknown in humans. We measured intact parathyroid hormone (PTH) and serum calcium; for bone formation, serum concentrations of bone alkaline phosphatase (BAP), intact osteocalcin (iBGP), and type 1 procollagen propeptide (PICP); for resorption, urinary concentrations (normalized by creatinine) of procollagen C-telopeptide (CTX), free and bound deoxypyridinoline (F and B D-Pyr), and Pyr in a 36-year-old cosmonaut (RTO), before (days -180, -60, and -15), during (from days 10 to 178, n = 12), and after (days +7, +15, +25, and +90) a 180-day spaceflight, in another cosmonaut (ASW) before and after the flight. Flight PTH tended to decrease by 48% and postflight PTH increased by 98%. During the flight, BAP, iBGP, and PICP decreased by 27%, 38%, and 28% respectively in CM1, and increased by 54%, 35%, and 78% after the flight. F D-Pyr and CTX increased by 54% and 78% during the flight and decreased by 29% and 40% after the flight, respectively. We showed for the first time in humans that microgravity induced an uncoupling of bone remodeling between formation and resorption that could account for bone loss.