We describe the time course of bone formation marker (P1NP) decline in men exposed to ~ 3 weeks of sleep restriction with concurrent circadian disruption. P1NP declined within 10 days and remained lower with ongoing exposure. These data suggest even brief exposure to sleep and circadian disruptions may disrupt bone metabolism. INTRODUCTION A serum bone formation marker (procollagen type 1 N-terminal, P1NP) was lower after ~ 3 weeks of sleep restriction combined with circadian disruption. We now describe the time course of decline. METHODS The ~ 3-week protocol included two segments: "baseline," ≥ 10-h sleep opportunity/day × 5 days; "forced desynchrony" (FD), recurring 28 h day (circadian disruption) with sleep restriction (~ 5.6-h sleep per 24 h). Fasted plasma P1NP was measured throughout the protocol in nine men (20-59 years old). We tested the hypothesis that PINP would steadily decline across the FD intervention because the magnitude of sleep loss and circadian misalignment accrued as the protocol progressed. A piecewise linear regression model was used to estimate the slope (β) as ΔP1NP per 24 h with a change point mid-protocol to estimate the initial vs. prolonged effects of FD exposure. RESULTS Plasma P1NP levels declined significantly within the first 10 days of FD ([Formula: see text] = - 1.33 μg/L per 24 h, p < 0.0001) and remained lower than baseline with prolonged exposure out to 3 weeks ([Formula: see text] = - 0.18 μg/L per 24 h, p = 0.67). As previously reported, levels of a bone resorption marker (C-telopeptide (CTX)) were unchanged. CONCLUSION Sleep restriction with concurrent circadian disruption induced a relatively rapid decline in P1NP (despite no change in CTX) and levels remained lower with ongoing exposure. These data suggest (1) even brief sleep restriction and circadian disruption can adversely affect bone metabolism, and (2) there is no P1NP recovery with ongoing exposure that, taken together, could lead to lower bone density over time.

中文翻译：

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快速抑制骨形成标志物以响应男性睡眠限制和昼夜节律紊乱。

我们描述了暴露于约 3 周睡眠限制并同时发生昼夜节律紊乱的男性骨形成标记物 (P1NP) 下降的时间过程。P1NP 在 10 天内下降，并随着持续暴露而保持较低水平。这些数据表明，即使是短暂的睡眠和昼夜节律紊乱也可能扰乱骨代谢。简介 在约 3 周的睡眠限制和昼夜节律紊乱后，血清骨形成标志物（1 型前胶原 N 末端，P1NP）较低。我们现在描述下降的时间过程。方法 ~ 3 周的方案包括两个部分：“基线”，≥ 10 小时睡眠机会/天 × 5 天；“强迫性不同步”(FD)，每天 28 小时反复出现（昼夜节律紊乱），睡眠受限（每 24 小时睡眠约 5.6 小时）。在整个方案中测量了九名男性（20-59 岁）的禁食血浆 P1NP。我们测试了 PINP 会在整个 FD 干预过程中稳步下降的假设，因为随着协议的进展，睡眠损失和昼夜节律失调的程度会增加。使用分段线性回归模型将斜率 (β) 估计为每 24 小时的 ΔP1NP，并使用中间协议的变化点来估计 FD 暴露的初始效应与长期效应。结果 在 FD 的前 10 天内，血浆 P1NP 水平显着下降（[公式：见正文] = - 1.33 μg/L 每 24 小时，p < 0.0001）并且随着暴露时间延长至 3 周（[公式：参见文本] = - 0.18 μg/L 每 24 小时，p = 0.67）。如前所述，骨吸收标记物（C-端肽（CTX））的水平没有变化。结论 睡眠限制与同时发生的昼夜节律紊乱导致 P1NP 相对快速下降（尽管 CTX 没有变化）并且水平随着持续暴露而保持较低水平。这些数据表明 (1) 即使是短暂的睡眠限制和昼夜节律紊乱也会对骨代谢产生不利影响，并且 (2) 持续暴露 P1NP 不会恢复，综合来看，随着时间的推移可能会导致骨密度降低。