Effects Of Age-Muscle Strength, Body Composition, Health

与年龄相关的力量损失在成年人的一生中缓慢发生。大多数研究都集中在老年人身上。然而，初级过程开始于更早的年龄。在青年和中年工人中，早期损失导致与工作有关的伤害，并对某些职业，工作表现。与年龄相关的强度损失的原因是多因素的。研究集中在与年龄相关的肌肉损失，被称为肌肉减少症，虽然肌肉减少症主要在肌肉质量和力量变化最大的老年人中进行研究，但到50岁时，平均个人已经失去了他们最大力量的10%。虽然肌肉减少症显然是力量损失的主要因素，但还有其他因素导致最大功能的变化。为了了解肌肉减少症，需要研究这些其他因素。我们的目标是了解力量损失的时间过程，导致损失的因素，老年人和年轻人之间运动反应的差异程度，以及可能影响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。这些研究的重点是描述肌肉力量质量发生的特征性损失，以及通过检查整个成人寿命及其对功能和寿命的影响而发生的身体功能老化。我们以前已经证明，在考虑年龄，体力活动和肌肉质量时，肌肉力量下降和肌肉力量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有助于长寿的独立的肌肉减少因素。这些观察结果表明，中枢神经系统的过程有助于肌肉减少症对长寿的重要性。 第二，我们与马里兰州大学的合作者合作，研究与肌肉肥大和力量有关的遗传贡献。我们已经确定了几个基因，有助于遗传方面的多少肌肉和力量，我们有。作为一个例子，我们报道了IGF-II基因型与肌肉力量有关，但与肌肉质量无关。这与死亡率数据一致，其中肌肉质量和肌肉力量对结果具有共同和不同的影响。同时发现IL 6和CNTF基因型对体成分有一定的影响，而体成分对肌少症有一定的影响。同样，男性雄激素受体外显子1中较长的重复序列与较高的睾酮血液水平和较高的去脂质量水平相关。 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，我们证明了抗阻训练的运动反应在年轻人和老年人中非常相似。然而，虽然对力量训练的反应可能因年龄而相似，但肌肉反应性存在明显差异，如基因表达和身体成分变化差异所示。我们一直对运动干预的替代策略感兴趣。劳拉塔尔博特博士，我们已经检查了两个替代运动策略与膝关节骨关节炎的主题。首先是神经肌肉电刺激（NMES），使用电刺激器被动激活膝伸肌。我们测试了一种方案，该方案在低得多的力水平下使用NMES，以使刺激更容易接受（即疼痛更少或没有疼痛），并最大限度地减少膝关节骨关节炎患者受伤的可能性。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的强度，达到其最大随意力量的20-40%。我们发现这种被动活动的肌肉力量增加，治疗后膝关节疼痛立即减少（尽管不是持续的效果）。第二种方法是使用基于家庭的计步器驱动的激励计划，导致改善行走，增加膝关节伸肌力量和适度的功能改善。我们目前正在计划一项研究，以检查使用肌电图刺激是否可以积极影响创伤性战争相关的膝盖以下截肢的恢复过程。在恢复和康复过程中，创伤性截肢后股四头肌肌力下降。NMES可以提供一种被动形式的锻炼，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.