0098 Chronic Sleep Restriction Results in Abnormal Bone Development in Adolescent Rats

Abstract Introduction Adolescence is often plagued by years of inadequate sleep at a time when nearly half of the adult skeletal mass is accrued and peak bone mass is attained. Previously we reported that chronic sleep restriction (SR) in adult male rats causes strikingly abnormal bone health. The purpose of this study was to test our hypothesis that SR results in abnormal bone development. Methods Chronic SR in juvenile rats from 42–60 d of age was produced by a validated modification of the Bergmann-Rechtschaffen paradigm with ambulation controls (AC). For five-day periods, sleep time was protected for 4 hours/day to model late bedtimes and early awakenings on schooldays, with a 35% sleep reduction for the rest of the time. Between five-day SR periods, sleep was undisturbed for 48 hours to model weekend catch-up sleep. Harvested femurs were studied for bone integrity by biomechanical testing (males and females, SR vs AC, N=3-4/sex/grp) and bone quality by micro-CT (male SR vs AC, N=4/grp). To investigate recovery, other male rats were studied at 90 and 120 d of age (N=5-6/grp) after chronic SR during 42–60 d of age. Results Chronic SR resulted in weak femurs, indicated by a 21% decrease in work to failure by three-point bending [N=7-8/grp pooled sexes, SR: 57 (SD 14); AC: 72 (SD 13) mJ, P< 0.02)]. By sex, there was a 23% decreased work to failure in male SR juveniles (P< 0.03) and a nonsignificant 17% decrease in female SR juveniles vs AC, but no differences in fat or lean body mass, leg muscle masses or femoral length. Trabeculae were decreased in number [SR vs AC, 1.9 (SD 0.4) and 2.4 (SD 0.4) /mm, P< 0.05] with increased spacing [SR vs AC, 552 (SD 122) and 419 (SD 66) µm, P=0.05]. In post-SR rats aged to 90 and 120 d, femoral work to failure was decreased by >44% (P< 0.004, P< 0.03 respectively). Conclusion Chronic SR during adolescence results in abnormal bone development with deficits that persist into adulthood. Failure to achieve peak bone mass or maintain bone in adolescence is known to significantly affect the progression to osteopenia/osteoporosis in later life. Support (if any)