The association among skeletal muscle phosphocreatine recovery, adiposity, and insulin resistance in children

Wells, Greg D.; Banks, Laura; Caterini, Jessica E.; Thompson, Sam; Noseworthy, Michael D.; Rayner, Tammy; Syme, Catriona; McCrindle, Brian W.; Hamilton, Jill

doi:10.1111/ijpo.12123

Cited by 6 publications

(3 citation statements)

References 24 publications

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“…Mitochondrial transmembrane potential, inorganic phosphate utilization (indicative of ATP synthase capacity), and the activities of respiratory chain complexes I-IV in subcutaneous white adipose tissue were all reduced in obese and type 2 diabetes mellitus patients compared to those in control subjects (Kraunsøe et al 2010;Chattopadhyay et al 2011). Obesity and insulin resistance were also associated with impaired bioenergetics following exercise in overweight-to-obese children (Slattery et al 2014;Wells et al 2017) and adults (Valkovič et al 2013), as evaluated via slower mitochondrial oxidative capacity recovery in the skeletal muscle. Type 2 diabetes mellitus patients with apparently normal cardiac function have impaired myocardial and skeletal muscle energy metabolism, with significantly lower phosphocreatine-to-ATP ratio (1.50 ± 0.11) than the healthy volunteers (2.30 ± 0.12) (Scheuermann-Freestone et al 2003).…”

Section: Cardiometabolic Diseases and Impaired Bioenergeticsmentioning

confidence: 99%

Impaired Bioenergetics in Clinical Medicine: A Target to Tackle

Ostojić

2017

Tohoku J. Exp. Med.

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Mitochondrial energy deficit is considered a key element of different clinical pathologies -from inherited disorders of energy metabolism to drug-induced mitochondrial toxicity, to cardiometabolic and neurodegenerative diseases. However, clinical manifestations of impaired bioenergetics are not easy to recognize, with patient-reported features usually include non-pathognomonic fatigue and weakness, or exercise intolerance, while specific lab tests are missing. Although it is not clear whether poor energetics is a primary deficit or a secondary consequence of specific disorders, improving mitochondrial viability remains a challenging task in both experimental and clinical medicine. In this review, biochemical and clinical evidence of energy deficits were reviewed, along with possible therapeutic options to tackle energy failure and restore bioenergetics.

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Section: Cardiometabolic Diseases and Impaired Bioenergeticsmentioning

confidence: 99%

Impaired Bioenergetics in Clinical Medicine: A Target to Tackle

Ostojić

2017

Tohoku J. Exp. Med.

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“…In this work, we investigated whether there was a difference in energy metabolism between the thigh and calves muscles due to the different fiber type composition. The detection of impaired energy metabolism in skeletal muscle is an important indicator of muscular disorders (e.g., Duchenne muscular dystrophy) [6]; also, it is an auxiliary diagnostic method for systemic metabolic diseases (e.g., adiposity and insulin resistance) [9] and cardiovascular diseases (e.g., chronic heart failure) [10]. The measurement by muscle biopsy is limited in application because it is invasive, localized and unrepeatable [2,11].…”

Section: Introductionmentioning

confidence: 99%

Different energy transfer efficiencies and buffering capabilities in quadriceps and calves muscles with low-load isotonic exercise detected by dynamic localized phosphorus-31 magnetic resonance spectroscopy

Chen

Yao

et al. 2019

Chin J Acad Radiol

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Aim Our aim was to investigate if there are differences in mitochondrial energy metabolism in working quadriceps and calves muscles by dynamic localized phosphorus-31 magnetic resonance spectroscopy. Materials and methods Phosphate metabolites of muscles were detected while subjects were in a state of rest, during exercise and recovery. The phosphocreatine (PCr), inorganic phosphate (Pi), adenosine triphosphate (ATP), PCr/Pi, PCr/ATP, pH, work/energy cost ratio (WE) and oxidative capacity were compared between muscles. Results The quadriceps had larger volume, heavier exercise load, greater WE, lower PCr and Pi concentration than calves muscles at rest. The PCr/Pi ratio of both muscles exhibited a sharp decline during exercise. PCr/ATP also had a downtrend in during exercise. Meanwhile, PCr/ATP of quadriceps during exercise was lower than that of calves muscles. The ATP concentration and pH value of quadriceps were decreased in end exercise compared to rest. And our results indicated that quadriceps had higher energy transfer efficiency and relatively poor energy buffering capability than calves muscles. The change in log(PCr) could adopt a linear fit model for both muscles at recovery. Conclusion Quadriceps had higher energy transfer efficiency and relatively poor energy buffering capability than calves muscles in mitochondrial energy metabolism partially accounts for different fiber type compositions.

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“…Assessing the high-energy phosphorus-containing metabolites within tissues using phosphorus-31 magnetic resonance spectroscopy ( 31 P-MRS), in conjunction with specifically designed exercise protocols, provides insight into the bioenergetic and mechanical function of skeletal muscle and furthers our understanding of exercise intolerance in pediatric cancer populations. [18][19][20][21][22] The objective of this study was to identify and quantify muscle metabolic limitations in childhood cancer patients compared with healthy controls using 31 P-MRS techniques. Understanding central and peripheral contributors to overall exercise capacity is critical for the development of evidence-based physical activity recommendations.…”

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confidence: 99%

Peripheral Skeletal Muscle Impairment in Children After Treatment for Leukemia and Lymphoma

White

West

Sabiston

et al. 2022

Journal of Pediatric Hematology/Oncology

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Exercise intolerance is a common adverse effect of childhood cancer, contributing to impaired health and well-being. While reduced aerobic fitness has been attributed to central cardiovascular deficiencies, the involvement of peripheral musculature has not been investigated. We studied peripheral muscle function in children following cancer treatment using noninvasive phosphorus-31 magnetic resonance spectroscopy. Ten acute lymphoblastic leukemia (ALL) and 1 lymphoma patient 8 to 18 years of age who completed treatment 6 to 36 months prior and 11 healthy controls participated in the study. Phosphorus-31 magnetic resonance spectroscopy was used to characterize muscle bioenergetics at rest and following an in-magnet knee-extension exercise. Exercise capacity was evaluated using a submaximal graded treadmill test. Both analysis of variance and Cohen d were used as statistical methods to determine the statistical significance and magnitude of differences, respectively, on these parameters between the patient and control groups. The patients treated for ALL and lymphoma exhibited lower anaerobic function (P = 0.14, d = 0.72), slower metabolic recovery (P = 0.08, d = 0.93), and lower mechanical muscle power (d = 1.09) during exercise compared with healthy controls. Patients demonstrated lower estimated VO 2peak (41.61 ± 5.97 vs. 47.71 ± 9.99 mL/ min/kg, P = 0.11, d = 0.76), lower minutes of physical activity (58.3 ± 35.3 vs. 114.8 ± 79.3 min, P = 0.12, d = 0.99) and higher minutes of inactivity (107.3 ± 74.0 vs. 43.5 ± 48.3 min, d = 1.04, P < 0.05). Children treated for ALL and lymphoma exhibit altered peripheral skeletal muscle metabolism during exercise. Both deconditioning and direct effects of chemotherapy likely contribute to exercise intolerance in this population.

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The association among skeletal muscle phosphocreatine recovery, adiposity, and insulin resistance in children

Cited by 6 publications

References 24 publications

Impaired Bioenergetics in Clinical Medicine: A Target to Tackle

Impaired Bioenergetics in Clinical Medicine: A Target to Tackle

Different energy transfer efficiencies and buffering capabilities in quadriceps and calves muscles with low-load isotonic exercise detected by dynamic localized phosphorus-31 magnetic resonance spectroscopy

Peripheral Skeletal Muscle Impairment in Children After Treatment for Leukemia and Lymphoma

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