CKD and Muscle Mitochondrial Energetics

Roshanravan, Baback; Kestenbaum, Bryan; Gamboa, Jorge L.; Jubrias, Sharon A.; Ayers, Ernest; Curtin, Lester R.; Himmelfarb, Jonathan; Boer, Ian H. de; Conley, Kevin E.

doi:10.1053/j.ajkd.2016.05.011

Cited by 44 publications

(50 citation statements)

References 10 publications

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“…***Denotes P < .001 vs healthy controls. Roshanravan and colleagues 54 reported an uncoupling of mitochondria within skeletal muscle determined using 31 P-MRS. D, Densitometry analysis of OXPHOS complex abundance.…”

Section: Discussionmentioning

confidence: 99%

Reductions in skeletal muscle mitochondrial mass are not restored following exercise training in patients with chronic kidney disease

et al. 2019

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Patients with chronic kidney disease (CKD) exhibit reduced exercise capacity, poor physical function and symptoms of fatigue. The mechanisms that contribute to this are not clearly defined but may involve reductions in mitochondrial function, mass and biogenesis. Here we report on the effect of non-dialysis dependent CKD (NDD-CKD) on mitochondrial mass and basal expression of transcription factors involved in mitochondrial biogenesis compared to a healthy control cohort (HC). In addition, we sought to investigate the effect of a 12-week exercise-training programme on these aspects of mitochondrial dysfunction in a NDD-CKD cohort.For the comparison between NDD-CKD and HC populations, skeletal muscle biopsies were collected from the vastus lateralis (VL) of n=16 non-dialysis dependent CKD patient's stage 3b-5 (NDD-CKD) and n=16 healthy controls matched for age, gender and physical activity (HC). To investigate the effect of exercise training, VL biopsies were collected from n=17 NDD-CKD patients before and after a 12-week exercise intervention that was comprised of aerobic exercise (AE) or a combination of aerobic exercise and resistance training (CE). Mitochondrial mass was analysed by citrate synthase activity and mitochondrial protein content by Porin expression, whilst the expression of transcription factors involved in mitochondrial biogenesis were quantified by real-time qPCR. NDD-CKD patients exhibited a significant reduction in mitochondrial mass when compared to HC, coupled to a reduction in PGC-1α, NRF-1, Nrf2, TFam, mfn2 and SOD1/2 gene expression. 12-weeks of exercise training resulted in a significant increase in PGC-1α expression in both groups, with no further changes seen across indicators of mitochondrial biogenesis. No significant changes in mitochondrial mass were observed in response to either exercise programme. NDD-CKD patients exhibit reduced skeletal muscle mitochondrial mass and gene expression of 1756 |

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Section: Discussionmentioning

confidence: 99%

Reductions in skeletal muscle mitochondrial mass are not restored following exercise training in patients with chronic kidney disease

et al. 2019

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“…The advent of non-invasive functional 31 Phosphorous Magnetic Resonance Spectroscopy ( 31 P MRS) and optical spectroscopy (OS) provides a window into early alterations of in-vivo muscle mitochondrial energetics among patients with kidney disease. Recently a study of non-diabetic patients with advanced CKD and preserved lower extremity physical performance demonstrated substantial reductions in coupling efficiency of muscle mitochondria defined by the amount of ATP (ATP flux ) generated per unit of oxygen consumption (O 2 uptake) (or P/O ratio) compared with healthy controls 20 (Figure 1). This lower mitochondrial coupling efficiency is primarily characterized by an increased consumption of oxygen to maintain ATP flux through the electron transport chain.…”

Section: Kidney Disease and Muscle Dysfunctionmentioning

confidence: 99%

Exercise and CKD: Skeletal Muscle Dysfunction and Practical Application of Exercise to Prevent and Treat Physical Impairments in CKD

Roshanravan

Gamboa

Wilund

2017

American Journal of Kidney Diseases

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181

190

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Patients with chronic kidney disease (CKD) experience substantial loss of muscle mass, weakness and poor physical performance. As kidney disease progresses, skeletal muscle dysfunction forms a common pathway for mobility limitation, loss of functional independence, and vulnerability to disease complications. Screening for those at high-risk of mobility disability by self-reported and objective measures of function is an essential first step in developing an interdisciplinary approach to treatment which includes rehabilitative therapies and counseling on physical activity. Exercise has beneficial effects on systemic inflammation, muscle and physical performance in CKD. Kidney health providers need to identify patient- and care delivery barriers to exercise in order to effectively counsel patients on physical activity. A thorough medical evaluation and assessment of baseline function using self-reported and objective function assessment is essential to guide an effective, individualized exercise prescription to prevent function decline in persons with kidney disease. This review focuses on the impact of kidney disease on skeletal muscle dysfunction in the context of the disablement process and reviews screening and treatment strategies that kidney health professionals can employ in clinical practice to prevent functional decline and disability.

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“…Low level of physical activity and skeletal muscle mass reduction in CKD patients are associated with sarcopaenia and higher risk of premature death . Several studies have demonstrated the importance of regular physical activity to prevent muscle loss, increase exercise capacity and improve the quality of life in CKD patients . In addition, exercise restores mitochondrial turnover and promotes a healthy mitochondrial pool that supports muscle preservation …”

Section: Exercise and Mitochondrial Function In Ckdmentioning

confidence: 99%

“…[84][85][86][87][88] Several studies have demonstrated the importance of regular physical activity to prevent muscle loss, increase exercise capacity and improve the quality of life in CKD patients. 43,84,[89][90][91][92] In addition, exercise restores mitochondrial turnover and promotes a healthy mitochondrial pool that supports muscle preservation. 93 In fact, muscle mitochondrial metabolic changes may be present in CKD patients with preserved physical performance and energy coupling (ie, mitochondrial efficiency), suggesting that altered mitochondrial metabolism in CKD might be of greater importance than differences in physical activity per se.…”

Section: Mitochondrial Function In Ckdmentioning

confidence: 99%

Bioactive food and exercise in chronic kidney disease: Targeting the mitochondria

Mafra

Gidlund

Borges

et al. 2018

Eur J Clin Investigation

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Chronic kidney disease (CKD), which affects 10%-15% of the population, associates with a range of complications-such as cardiovascular disease, frailty, infections, muscle and bone disorders and premature ageing-that could be related to alterations of mitochondrial number, distribution, structure and function. As mitochondrial biogenesis, bioenergetics and the dynamic mitochondrial networks directly or indirectly regulate numerous intra-and extracellular functions, the mitochondria have emerged as an important target for interventions aiming at preventing or improving the treatment of complications in CKD. In this review, we discuss the possible role of bioactive food compounds and exercise in the modulation of the disturbed mitochondrial function in a uraemic milieu.

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CKD and Muscle Mitochondrial Energetics

Cited by 44 publications

References 10 publications

Reductions in skeletal muscle mitochondrial mass are not restored following exercise training in patients with chronic kidney disease

Reductions in skeletal muscle mitochondrial mass are not restored following exercise training in patients with chronic kidney disease

Exercise and CKD: Skeletal Muscle Dysfunction and Practical Application of Exercise to Prevent and Treat Physical Impairments in CKD

Bioactive food and exercise in chronic kidney disease: Targeting the mitochondria

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