Age-related differences in the loss and recovery of serial sarcomere number following disuse atrophy in rats.

IF 5.3 2区 医学 Q2 CELL BIOLOGY
Avery Hinks, Geoffrey A Power
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引用次数: 0

Abstract

Background: Older adults exhibit a slower recovery of muscle mass following disuse atrophy than young adults. At a smaller scale, muscle fibre cross-sectional area (i.e., sarcomeres in parallel) exhibits this same pattern. Less is known, however, about age-related differences in the recovery of muscle fibre length, driven by increases in serial sarcomere number (SSN), following disuse. The purpose of this study was to investigate age-related differences in SSN adaptations and muscle mechanical function during and following muscle immobilization. We hypothesized that older adult rats would experience a similar magnitude of SSN loss during immobilization, however, take longer to recover SSN than young following cast removal, which would limit the recovery of muscle mechanical function.

Methods: We casted the plantar flexors of young (8 months) and old (32 months) male rats in a shortened position for 2 weeks, and assessed recovery during 4 weeks of voluntary ambulation. Following sacrifice, legs were fixed in formalin for measurement of soleus SSN and physiological cross-sectional area (PCSA) with the un-casted soleus acting as a control. Ultrasonographic measurements of pennation angle (PA) and muscle thickness (MT) were conducted weekly. In-vivo active and passive torque-angle relationships were constructed pre-cast, post-cast, and following 4 weeks of recovery.

Results: From pre- to post-cast, young and older adult rats experienced similar decreases in SSN (-20%, P < 0.001), muscle wet weight (-25%, P < 0.001), MT (-30%), PA (-15%, P < 0.001), and maximum isometric torque (-40%, P < 0.001), but there was a greater increase in passive torque in older (+ 180%, P < 0.001) compared to young adult rats (+ 68%, P = 0.006). Following cast removal, young exhibited quicker recovery of SSN and MT than old, but SSN recovered sooner than PA and MT in both young and old. PCSA nearly recovered and active torque fully recovered in young adult rats, whereas in older adult rats these remained unrecovered at ∼ 75%.

Conclusions: This study showed that older adult rats retain a better ability to recover longitudinal compared to parallel muscle morphology following cast removal, making SSN a highly adaptable target for improving muscle function in elderly populations early on during rehabilitation.

大鼠废用性肌萎缩后序列肌节数量的损失和恢复与年龄有关。
背景:老年人在肌肉废用性萎缩后,肌肉质量的恢复速度比年轻人慢。在较小的范围内,肌肉纤维横截面积(即平行的肌节)也表现出同样的模式。然而,对于肌肉纤维长度在废用后的恢复方面与年龄有关的差异(由序列肌节数(SSN)的增加驱动),人们却知之甚少。本研究的目的是调查肌肉固定期间和之后 SSN 适应性和肌肉机械功能与年龄相关的差异。我们假设,老年大鼠在固定期间会经历类似程度的 SSN 损失,但在拆除石膏后,SSN 的恢复时间要长于年轻大鼠,这将限制肌肉机械功能的恢复:方法:我们将幼年(8 个月)和老年(32 个月)雄性大鼠的跖屈肌以缩短姿势固定 2 周,并在 4 周的自主活动中评估其恢复情况。大鼠牺牲后,将腿固定在福尔马林中,测量比目鱼肌SSN和生理横截面积(PCSA),以未固定的比目鱼肌作为对照。每周对五点角(PA)和肌肉厚度(MT)进行超声波测量。在铸造前、铸造后和恢复 4 周后,构建了体内主动和被动扭矩-角度关系:结果:从浇铸前到浇铸后,年轻成年大鼠和老年成年大鼠的 SSN 下降幅度相似(-20%,P 结论:从浇铸前到浇铸后,年轻成年大鼠和老年成年大鼠的 SSN 下降幅度相似:这项研究表明,与平行肌肉形态相比,老年大鼠在拆除石膏后仍能保持较好的纵向肌肉形态恢复能力,这使得 SSN 成为一个适应性很强的目标,可在康复早期改善老年人群的肌肉功能。
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来源期刊
Skeletal Muscle
Skeletal Muscle CELL BIOLOGY-
CiteScore
9.10
自引率
0.00%
发文量
25
审稿时长
12 weeks
期刊介绍: The only open access journal in its field, Skeletal Muscle publishes novel, cutting-edge research and technological advancements that investigate the molecular mechanisms underlying the biology of skeletal muscle. Reflecting the breadth of research in this area, the journal welcomes manuscripts about the development, metabolism, the regulation of mass and function, aging, degeneration, dystrophy and regeneration of skeletal muscle, with an emphasis on understanding adult skeletal muscle, its maintenance, and its interactions with non-muscle cell types and regulatory modulators. Main areas of interest include: -differentiation of skeletal muscle- atrophy and hypertrophy of skeletal muscle- aging of skeletal muscle- regeneration and degeneration of skeletal muscle- biology of satellite and satellite-like cells- dystrophic degeneration of skeletal muscle- energy and glucose homeostasis in skeletal muscle- non-dystrophic genetic diseases of skeletal muscle, such as Spinal Muscular Atrophy and myopathies- maintenance of neuromuscular junctions- roles of ryanodine receptors and calcium signaling in skeletal muscle- roles of nuclear receptors in skeletal muscle- roles of GPCRs and GPCR signaling in skeletal muscle- other relevant aspects of skeletal muscle biology. In addition, articles on translational clinical studies that address molecular and cellular mechanisms of skeletal muscle will be published. Case reports are also encouraged for submission. Skeletal Muscle reflects the breadth of research on skeletal muscle and bridges gaps between diverse areas of science for example cardiac cell biology and neurobiology, which share common features with respect to cell differentiation, excitatory membranes, cell-cell communication, and maintenance. Suitable articles are model and mechanism-driven, and apply statistical principles where appropriate; purely descriptive studies are of lesser interest.
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