C M Swanson1, W M Kohrt2, P Wolfe3, K P Wright4,5, S A Shea6,7, S W Cain8,9,10, M Munch11,12, N Vujović8,9, C A Czeisler8,9, E S Orwoll13, O M Buxton8,9,14. 1. Division of Endocrinology, Metabolism and Diabetes, University of Colorado, 12801 E. 17th Ave. Mail Stop 8106, Aurora, CO, 80045, USA. Christine.Swanson@UCDenver.edu. 2. Division of Geriatric Medicine, University of Colorado Anschutz Medical Campus, and Eastern Colorado VA Geriatric, Research, Education, and Clinical Center, Aurora, CO, USA. 3. Department of Biostatistics and Informatics, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO, USA. 4. Division of Endocrinology, Metabolism and Diabetes, University of Colorado, 12801 E. 17th Ave. Mail Stop 8106, Aurora, CO, 80045, USA. 5. Department of Integrative Physiology, University of Colorado Boulder, Boulder, CO, USA. 6. Oregon Institute of Occupational Health Sciences, Oregon Health & Science University, Portland, OR, USA. 7. OHSU-PSU School of Public Health, Portland, OR, USA. 8. Sleep Health Institute, Division of Sleep and Circadian Disorders, Departments of Medicine and Neurology, Brigham and Women's Hospital, Boston, MA, USA. 9. Division of Sleep Medicine, Harvard Medical School, Boston, MA, USA. 10. Monash Institute of Cognitive and Clinical Neurosciences, School of Psychological Sciences, Monash University, Clayton, VIC, 3800, Australia. 11. Institute of Physiology, Charité University Medicine Berlin, Berlin, Germany. 12. Sleep/Wake Research Centre, Massey University Wellington Campus, Wellington, New Zealand. 13. Division of Endocrinology and Bone and Mineral Unit, Oregon Health & Science University, Portland, OR, USA. 14. Department of Biobehavioral Health, Pennsylvania State University, University Park, State College, PA, USA.
Abstract
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.
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.
Entities:
Keywords:
Bone formation; Bone loss; Circadian disruption; P1NP; Sleep restriction
Authors: Christine M Swanson; Wendy M Kohrt; Orfeu M Buxton; Carol A Everson; Kenneth P Wright; Eric S Orwoll; Steven A Shea Journal: Metabolism Date: 2017-12-09 Impact factor: 8.694
Authors: Orfeu M Buxton; Milena Pavlova; Emily W Reid; Wei Wang; Donald C Simonson; Gail K Adler Journal: Diabetes Date: 2010-06-28 Impact factor: 9.461
Authors: Christine M Swanson; Steven A Shea; Wendy M Kohrt; Kenneth P Wright; Sean W Cain; Mirjam Munch; Nina Vujović; Charles A Czeisler; Eric S Orwoll; Orfeu M Buxton Journal: J Clin Endocrinol Metab Date: 2020-07-01 Impact factor: 5.958
Authors: Christine M Swanson; Prajakta Shanbhag; Emma J Tussey; Corey A Rynders; Kenneth P Wright; Wendy M Kohrt Journal: Calcif Tissue Int Date: 2022-02-08 Impact factor: 4.000