NUTRITION & EXERCISE TO IMPROVE PROTEIN METABOLISM & PREVENT SARCOPENIA IN AGING
NUTRITION & EXERCISE TO IMPROVE PROTEIN METABOLISM & PREVENT SARCOPENIA IN AGING
批准号:
7952172
负责人:
Elena Volpi
金额:
$0.21万
依托单位国家:
美国
项目类别:
财政年份:
2009
资助国家:
美国
项目状态:
已结题
起止时间:
2009-04-01 至 2009-07-31
关键词:
AcuteAgeBlood VesselsCaloric RestrictionChronicClinical ResearchComputer Retrieval of Information on Scientific Projects DatabaseDevelopmentExerciseFrail ElderlyFundingGoalsGrantInjuryInstitutionInterventionMeasuresMetabolicMethodologyMuscleMuscle ProteinsNutritionalObesityPerformancePerfusionPlayProtein BiosynthesisResearchResearch PersonnelResourcesRiskRoleSourceSupplementationTestingTranslatingUltrasonographyUnited States National Institutes of Healthdiabeticdisabilityfallsfrailtyimprovedmuscle formnutritionpreventprotein metabolismsarcopeniasedentarystable isotope
中文摘要
这个子项目是许多研究子项目中的一个
由NIH/NCRR资助的中心赠款提供的资源。子项目和
研究者(PI)可能从另一个NIH来源获得了主要资金,
因此可以在其他CRISP条目中表示。所列机构为
研究中心,而研究中心不一定是研究者的研究机构。
老年人残疾的一个根本原因和促成因素是肌肉质量和力量的非自愿损失(肌肉减少症),这最终会降低功能,从而增加福尔斯的风险和受伤的脆弱性。我们的一般假设是,营养因素和不活动在肌肉减少症的发展中起着重要作用。因此,包括营养操作和/或锻炼在内的针对年龄的长期干预可能有助于减少、稳定甚至逆转肌肉质量和力量随年龄的损失。我们的目标是确定可以急剧增加肌肉蛋白质合成的特定干预措施是否也可以有效地转化为老年久坐者肌肉质量和/或性能的增加,从而防止虚弱和促进身体独立。为此,我们将使用稳定同位素方法来测量肌肉蛋白质代谢和对比增强超声来测量肌肉灌注,以确定治疗的急性效应是否可以预测其对肌肉质量和功能的慢性影响。此外,我们还将确定慢性治疗是否会导致代谢和/或血管适应,这可能解释肌肉质量和功能的测量变化。如果我们证实这种类型的补充剂可以有效地改善久坐的老年受试者的肌肉质量和力量,那么不仅可以在虚弱的老年人中测试有效的补充剂,而且还可以在热量限制是必要的或可取的情况下,以及身体虚弱是潜在风险的情况下(例如,老年肥胖和/或糖尿病受试者、肌肉减少性肥胖)。
英文摘要
This subproject is one of many research subprojects utilizing the
resources provided by a Center grant funded by NIH/NCRR. The subproject and
investigator (PI) may have received primary funding from another NIH source,
and thus could be represented in other CRISP entries. The institution listed is
for the Center, which is not necessarily the institution for the investigator.
A fundamental cause of and contributor to disability in older people is the involuntary loss of muscle mass and strength (sarcopenia), which eventually reduces function , thus increasing risk of falls and vulnerability to injury. Our general hypothesis is that nutritional factors and inactivity play significant roles in the development of sarcopenia. Thus, age-specific prolonged interventions including nutritional manipulations and/or exercise may help to reduce, stabilize, or even reverse the loss of muscle mass and strength with age. Our goal is to establish if specific interventions that can acutely increase muscle protein synthesis can also effectively translate into increased muscle mass and/or performance in older sedentary people, thus preventing frailty and promoting physical independence. To this end we will use stable isotope methodologies to measure muscle protein metabolism and contrast enhanced ultrasound to measure muscle perfusion, in order to determine if the treatments' acute effects can predict their chronic impact on muscle mass and function. Furthermore, we will also determine if chronic treatment leads to metabolic and/or vascular adaptations that may explain the measured changes in muscle mass and function. If we confirm that this type of supplementation can effectively improve muscle mass and strength in sedentary older subjects, it will be possible to test efficient supplements not only in frail elderly, but also in cases where caloric restriction is necessary or desirable, and where physical frailty is a potential risk (e.g., older obese and/or diabetic subjects, sarcopenic obesity).
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