Effects Of Age-Muscle Strength, Body Composition, Health

随着年龄的增长，力量的丧失会在成年后缓慢发生。大多数研究都集中在老年人身上发生了什么。然而，初级过程在更早的年龄就开始了。在年轻和中年工人中，早期的损失会导致与工作相关的伤害，对于一些职业来说，会导致工作表现。年龄相关性力量丧失的原因是多方面的。研究的重点是与年龄相关的肌肉损失，也就是所谓的骨质疏松症，而骨质疏松症主要在肌肉质量和力量变化最明显的老年人中进行研究，到50岁时，个人平均失去了10%的最大力量。虽然骨质疏松症显然是力量丧失的一个主要因素，但还有其他因素导致最大功能的变化。要了解骨质疏松症，还需要研究其他因素。我们的目标是了解力量损失的时间过程、造成力量损失的因素、老年人和年轻人运动反应的不同程度，以及可能影响力量损失的激励因素和替代运动计划的形式。我们使用了几种不同的方法来解决这些问题。 首先是使用巴尔的摩老龄化纵向研究(BLSA)的描述性研究。这些研究的重点是通过检查整个成年人的寿命及其对功能和寿命的影响来描述随着年龄增长而发生的肌肉力量、质量和身体功能方面的特征损失。我们以前已经证明，考虑到年龄、体力活动和肌肉质量，肌肉力量的下降和肌肉力量的变化率是男性死亡率的独立贡献者。我们进一步表明，肌肉力量和运动速度是进一步独立的促进骨骼形成的因素，有助于长寿。这些观察表明，中枢神经系统的过程有助于骨质疏松症对长寿的重要性。 其次，与马里兰大学的合作者合作，我们正在研究与肌肉肥大和力量有关的基因贡献。我们已经确定了几个基因，这些基因决定了我们拥有多少肌肉和力量的遗传方面。例如，我们报告了IGF-II基因与肌肉力量有关，但与肌肉质量无关。这与死亡率数据是一致的，在死亡率数据中，肌肉质量和肌肉力量对预后有共同和不同的影响。此外，我们还发现IL6和CNTF基因对体成分有一定的影响，而身体成分对骨质疏松症有影响。同样，男性外显子1中较长的雄激素受体重复与较高的睾酮水平和较高的脱脂质量水平相关。 第三是干预研究，以改变力量和肌肉质量变化的时间进程。在以前的工作中，我们证明了年轻和老年受试者对阻力训练的运动反应非常相似。然而，虽然不同年龄的人对力量训练的反应可能相似，但以基因表达和身体成分变化为代表的肌肉反应有明显的差异。我们一直对运动干预的替代策略感兴趣。与劳拉·塔尔博特博士一起，我们研究了两种可供选择的运动策略，使用的是膝骨性关节炎患者。首先是神经肌肉电刺激(NMES)，这是一种使用电刺激器被动激活膝关节伸肌的方法。我们测试了一种方案，该方案在更低的力水平下使用NMES，以使刺激更容易接受(即更少或没有疼痛)，并将膝骨性关节炎患者受伤的可能性降至最低。NMES组使用便携式电肌肉刺激器，在12周内逐渐增加等长收缩强度，最高可达他们最大自愿力量的20%-40%。我们发现，在这种被动活动的反应下，肌肉力量增加了，治疗后膝关节疼痛立即减少(尽管不是持久的效果)。第二种方法是使用家庭计步器驱动的激励计划，结果是改善了行走，增加了膝关节伸肌力量，并适度改善了功能。我们目前正处于一项研究的规划阶段，该研究旨在检查肌肉刺激的使用是否可以积极影响膝关节以下截肢手术后因战争而造成的创伤的康复过程。在恢复和康复过程中，创伤性截肢后股四头肌肌力下降。NMES可以提供一种被动的运动形式，可以在这段时间内保持力量。

Age associated losses of strength occur slowly over the adult lifespan. Most research has focused on what occurs in the elderly. However, the primary processes start at a much earlier age. In young and middle-aged workers, the early losses contribute to work related injuries and for some occupations, job performance. The causes of age related strength losses are multifactoral. Research has focused on age-associated loss of muscle that has been referred to as sarcopenia, While sarcopenia has been mainly studied in the elderly where the greatest changes in muscle mass and strength manifest, by age 50 the average individual has lost 10% of their maximal strength. While sarcopenia is clearly a major factor in strength loss, there are other contributors to the changes in maximal function. To understand sarcopenia these other factors need to be studied. Our goal is to understand the time course of strength loss, factors that contribute to the loss, the degree to which the exercise response differs between old and young individuals, and the forms of motivators and alternative exercise programs that might impact on the losses. We have used several different approaches to address these issues. First are descriptive studies using the Baltimore Longitudinal Study of Aging (BLSA). These studies focus on describing the characteristic losses that occur in muscle strength mass, and physical functioning that occur with aging by examining the entire adult lifespan and their impact on function and longevity. We have previously demonstrated that declining muscle strength and rate of change of muscle strength are independent contributors to mortality in men when considering age, physical activity and muscle mass. We have further shown that muscle power, and speed of movement are further independent sarcopenic factors that contribute to longevity. The observations suggest that central nervous system processes are contributing to the importance of sarcopenia on longevity. Second, working with collaborators at the University of Maryland, we are examining genetic contributions related to muscle hypertrophy and strength. We have identified several genes that contribute to the inherited aspects of how much muscle and strength we have. As an example, we reported that IGF-II genotype is related to muscle strength but not muscle mass. This is consistent with the mortality data, where muscle mass and muscle strength have common and different effects on outcome. Also, we found that IL6 and CNTF genotype had some influence on body composition which impacts on sarcopenia. Likewise, longer androgen receptor repeat in exon 1 in men is associated with higher testosterone blood levels and with greater levels of fat free mass. Third are intervention studies to alter the time course of strength and muscle mass changes. In previous work we demonstrated that the exercise response to resistive training is very similar in young and old subjects. However, while the response to strength training may be similar by age, there are clear differences in muscle responsiveness as represented by gene expression, and body compostion change differences. We have been interested in alternative strategies for exercise intervention. With Dr. Laura Talbot, we have examined two alternative exercise strategies using subjects with osteoarthritis of the knee. First was neuromuscular electrostimulation (NMES), a passive activation of the knee extensor muscles using an electric stimulator. We tested a protocol that used NMES at much lower force levels, to make the stimulation more acceptable (i.e. with less or no pain), and to minimize the likelihood of injury in individuals with osteoarthritis of the knee. The NMES group used a portable electrical muscle stimulator to incrementally increase the intensity of isometric contraction over 12 weeks up to 20-40% of their maximal voluntary strength. We found an increase in muscle strength in response to this passive activity, and a decline in knee pain immediately following the treatment (though not a sustained effect). The second approach was to use home based pedometer driven motivational program resulted in improved walking, increased knee extensor strength, and modest functional improvements. We are currently in the planning stages of a study to examine whether the use of electromyostimulation can positively impact the course of recovery from traumatic war-related below the knee amputation. During recovery and rehabilitation, quadriceps muscle strength declines following traumatic amputation. NMES may offer a passive form of exercise that can maintain strength during this time period.