Purpose of review In this article, we review sarcopenia in chronic kidney disease (CKD). We aim to present how definitions of sarcopenia from the general population may pertain to those with CKD, its assessment by clinicians and emerging therapies for sarcopenia in CKD. For this review, we limit our description and recommendations to patients with CKD who are not on dialysis. Recent findings Poorer parameters of lean mass, strength and physical function are associated with worsening patient-centered outcomes such as limiting mobility, falls and mortality in CKD; however, the magnitude of these associations are different in those with and without CKD. Sarcopenia in CKD is a balance between skeletal muscle regeneration and catabolism, which are both altered in the uremic environment. Multiple pathways are involved in these derangements, which are briefly reviewed. Differences between commonly used terms cachexia, frailty, protein-energy wasting, dynapenia and sarcopenia are described. Therapeutic options in predialysis CKD are not well studied; therefore, we review exercise options and emerging pharmacological therapies. Summary Sarcopenia, now with its own International Classification of Diseases, 10th Revision (ICD-10) code, is of importance clinically and should be accounted for in research studies in patients with CKD. Multiple therapies for sarcopenia are in development and will hopefully be available for our patients in the future.
This CGS provides recommendations to assist physical therapists in the identification and management of fall risk in older community-dwelling adults.
Objective. To evaluate the evidence for patellar taping and bracing in the management of chronic knee pain. Methods. Randomized or quasi-randomized studies assessing patellar taping or bracing effects on chronic knee pain were sourced from 7 electronic databases (to November 2006), and assessed using the Physiotherapy Evidence Database scale. Weighted mean differences were determined, and pooled estimates of taping and bracing effects were obtained using random-effects models. Results. Of 16 eligible trials, 13 investigated patellar taping or bracing effects in individuals with anterior knee pain, and 3 investigated taping effects in individuals with knee osteoarthritis (OA). The methodologic quality of the taping studies was significantly higher than the bracing studies (mean ؎ SD 4.8 ؎ 2.1 versus 2.8 ؎ 0.8; P < 0.05). On a 100-mm scale, tape applied to exert a medially-directed force on the patella decreased chronic knee pain compared with no tape by 16.1 mm (95% confidence interval [95% CI] ؊22.2, ؊10.0; P < 0.001) and sham tape by 10.9 mm (95% CI ؊18.4, ؊3.4; P < 0.001). For anterior knee pain and OA, medially-directed tape decreased pain compared with no tape by 14.7 mm (95% CI ؊22.8, ؊6.9; P < 0.001) and 20.1 mm (95% CI ؊26.0, ؊14.3; P < 0.001), respectively. There was disputable evidence from low-quality studies for patellar bracing benefits. Conclusion. There was evidence that tape applied to exert a medially-directed force on the patella produces a clinically meaningful change in chronic knee pain. There was limited evidence to demonstrate the efficacy of patellar bracing. These outcomes were limited by the presence of high heterogeneity between study outcomes and significant publication bias.
Static task intensity–endurance time (ET) relationships (e.g. Rohmert's curve) were first reported decades ago. However, a comprehensive meta-analysis to compare experimentally-observed ETs across bodily regions has not been reported. We performed a systematic literature review of ETs for static contractions, developed joint-specific power and exponential models of the intensity–ET relationships, and compared these models between each joint (ankle, trunk, hand/grip, elbow, knee, and shoulder) and the pooled data (generalised curve). 194 publications were found, representing a total of 369 data points. The power model provided the best fit to the experimental data. Significant intensity-dependent ET differences were predicted between each pair of joints. Overall, the ankle was most fatigue-resistant, followed by the trunk, hand/grip, elbow, knee and finally the shoulder was most fatigable. We conclude ET varies systematically between joints, in some cases with large effect sizes. Thus, a single generalised ET model does not adequately represent fatigue across joints. Statement of Relevance Rohmert curves have been used in ergonomic analyses of fatigue, as there are limited tools available to accurately predict force decrements. This study provides updated endurance time–intensity curves using a large meta-analysis of fatigue data. Specific models derived for five distinct joint regions should further increase prediction accuracy.
Overall, older adults were able to sustain relative-intensity tasks significantly longer or with less force decay than younger adults (effect size=0.49). However, this age-related difference was present only for sustained and intermittent isometric contractions, whereas this age-related advantage was lost for dynamic tasks. When controlling for contraction type, the additional modifiers played minor roles. Identifying muscle endurance capabilities in the older adult may provide an avenue to improve functional capabilities, despite a clearly established decrement in peak torque.
Skeletal muscle atrophy and impaired muscle function are associated with lower health-related quality of life, and greater disability and mortality risk in those with chronic kidney disease (CKD). However, the pathogenesis of skeletal dysfunction in CKD is unknown. We used a slow progressing, naturally occurring, CKD rat model (Cy/+ rat) with hormonal abnormalities consistent with clinical presentations of CKD to study skeletal muscle signaling. The CKD rats demonstrated augmented skeletal muscle regeneration with higher activation and differentiation signals in muscle cells (i.e. lower Pax-7; higher MyoD and myogenin RNA expression). However, there was also higher expression of proteolytic markers (Atrogin-1 and MuRF-1) in CKD muscle relative to normal. CKD animals had higher indices of oxidative stress compared to normal, evident by elevated plasma levels of an oxidative stress marker, 8-hydroxy-2' -deoxyguanosine (8-OHdG), increased muscle expression of succinate dehydrogenase (SDH) and Nox4 and altered mitochondria morphology. Furthermore, we show significantly higher serum levels of myostatin and expression of myostatin in skeletal muscle of CKD animals compared to normal. Taken together, these data show aberrant regeneration and proteolytic signaling that is associated with oxidative stress and high levels of myostatin in the setting of CKD. These changes likely play a role in the compromised skeletal muscle function that exists in CKD.
There is growing interest in the interaction between skeletal muscle and bone, particularly at the genetic and molecular levels. However, the genetic and molecular linkages between muscle and bone are achieved only within the context of the essential mechanical coupling of the tissues. This biomechanical and physiological linkage is readily evident as muscles attach to bone and induce exposure to varied mechanical stimuli via functional activity. The responsiveness of bone cells to mechanical stimuli, or their absence, is well established. However, questions remain regarding how muscle forces applied to bone serve to modulate bone homeostasis and adaptation. Similarly, the contributions of varied, but unique, stimuli generated by muscle to bone (such as low-magnitude, high-frequency stimuli) remains to be established. The current article focuses upon the mechanical relationship between muscle and bone. In doing so, we explore the stimuli that muscle imparts upon bone, models that enable investigation of this relationship, and recent data generated by these models.
Klotho is a powerful longevity protein that has been linked to the prevention of muscle atrophy, osteopenia, and cardiovascular disease. Similar anti-aging effects have also been ascribed to exercise and physical activity. While an association between muscle function and Klotho expression has been previously suggested from longitudinal cohort studies, a direct relationship between circulating Klotho and skeletal muscle has not been investigated. In this paper, we present a review of the literature and preliminary evidence that, together, suggests Klotho expression may be modulated by skeletal muscle activity. Our pilot clinical findings performed in young and aged individuals suggest that circulating Klotho levels are upregulated in response to an acute exercise bout, but that the response may be dependent on fitness level. A similar upregulation of circulating Klotho is also observed in response to an acute exercise in young and old mice, suggesting that this may be a good model for mechanistically probing the role of physical activity on Klotho expression. Finally, we highlight overlapping signaling pathways that are modulated by both Klotho and skeletal muscle and propose potential mechanisms for cross-talk between the two. It is hoped that this review will stimulate further consideration of the relationship between skeletal muscle activity and Klotho expression, potentially leading to important insights into the well-documented systemic anti-aging effects of exercise.
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