Levinger Itamar, Brennan-Speranza Tara C, Jerums George, Stepto Nigel K, Serpiello Fabio R, McConell Glenn K, Anderson Mitchell, Hare David L, Byrnes Elizabeth, Ebeling Peter R, Seeman Ego
Clinical Exercise Science Research Program, Institute of Sport, Exercise and Active Living (ISEAL), Victoria University , Melbourne, Victoria, Australia ; Australian Institute of Musculoskeletal Science, North West Academic Centre, The University of Melbourne, Western Health , Melbourne, Victoria, Australia.
Department of Physiology, Bosch Institute for Medical Research, University of Sydney , Sydney, New South Wales, Australia.
Bonekey Rep. 2015 Aug 26;4:731. doi: 10.1038/bonekey.2015.100. eCollection 2015.
Bone remodelling markers (BRMs) are suppressed following a glucose load and during glucose infusion. As exercise increases indices of bone health and improves glucose handling, we hypothesised that, at rest, hyperinsulinaemic-euglycaemic clamp will suppress BRMs in obese men and that exercise prior to the clamp will prevent this suppression. Eleven obese nondiabetic men (age 58.1±2.2 years, body mass index=33.1±1.4 kg m(-2) mean±s.e.m.) had a hyperinsulinaemic-euglycaemic clamp (HEC) at rest (Control) and 60 min post exercise (four bouts × 4 min cycling at 95% of hazard ratiopeak). Blood samples were analysed for serum insulin, glucose, bone formation markers, total osteocalcin (tOC) and procollagen type 1 N-terminal propeptide (P1NP), and the bone resorption marker, β-isomerised C-terminal telopeptides (β-CTx). In the control trial (no exercise), tOC, P1NP and β-CTx decreased with HEC by >10% compared with baseline (P<0.05). Fasting serum glucose, but not insulin, tended to correlate negatively with the BRMs (β range -0.57 to -0.66, p range 0.051-0.087). β-CTx, but not OC or P1NP, increased within 60 min post exercise (∼16%, P<0.01). During the post-exercise HEC, the glucose infusion rate was ∼30% higher compared with the no exercise trial. Despite this, BRMs were only suppressed to a similar extent as in the control session (10%). HEC suppressed BRMs in obese men. Exercise did not prevent this suppression of BRMs by HEC but improved glucose handling during the trial. It remains to be tested whether an exercise intervention of longer duration may be able to prevent the effect of HEC on bone remodelling.
葡萄糖负荷后及葡萄糖输注期间，骨重塑标志物（BRMs）会受到抑制。由于运动可提高骨骼健康指标并改善葡萄糖代谢，我们推测，在静息状态下，高胰岛素正常血糖钳夹会抑制肥胖男性的BRMs，而在钳夹前进行运动会预防这种抑制作用。11名肥胖非糖尿病男性（年龄58.1±2.2岁，体重指数=33.1±1.4 kg·m⁻²，均值±标准误）在静息状态下（对照组）和运动后60分钟（4组，每组4分钟，以危险比峰值的95%进行骑行）接受了高胰岛素正常血糖钳夹（HEC）。对血样进行分析，检测血清胰岛素、葡萄糖、骨形成标志物、总骨钙素（tOC）和I型前胶原N端前肽（P1NP），以及骨吸收标志物β-异构化C端肽（β-CTx）。在对照试验（无运动）中，与基线相比，HEC使tOC、P1NP和β-CTx降低超过10%（P<0.05）。空腹血清葡萄糖而非胰岛素，与BRMs呈负相关趋势（β范围为-0.57至-0.66，p范围为0.051至0.087）。运动后60分钟内，β-CTx升高（约16%，P<0.01），而OC或P1NP未升高。在运动后HEC期间，葡萄糖输注速率比无运动试验高约30%。尽管如此，但BRMs仅被抑制至与对照试验相似的程度（1
