scholarly journals Skeletal muscle oxidative function in vivo and ex vivo in athletes with marked hypertrophy from resistance training

2013 ◽  
Vol 114 (11) ◽  
pp. 1527-1535 ◽  
Author(s):  
Desy Salvadego ◽  
Rossana Domenis ◽  
Stefano Lazzer ◽  
Simone Porcelli ◽  
Jörn Rittweger ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Mass ◽  
Body Mass ◽  
Mitochondrial Respiration ◽  
Ex Vivo ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Vastus Lateralis Muscle ◽  
Oxidative Function

Oxidative function during exercise was evaluated in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (RTA; body mass 102.6 ± 7.3 kg, mean ± SD) and 11 controls (CTRL; body mass 77.8 ± 6.0 kg). Pulmonary O2 uptake (V̇o2) and vastus lateralis muscle fractional O2 extraction (by near-infrared spectroscopy) were determined during an incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercise. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers obtained by biopsy. Quadriceps femoris muscle cross-sectional area, volume (determined by magnetic resonance imaging), and strength were greater in RTA vs. CTRL (by ∼40%, ∼33%, and ∼20%, respectively). V̇o2peak during CE was higher in RTA vs. CTRL (4.05 ± 0.64 vs. 3.56 ± 0.30 l/min); no difference between groups was observed during KE. The O2 cost of CE exercise was not different between groups. When divided per muscle mass (for CE) or quadriceps muscle mass (for KE), V̇o2 peak was lower (by 15–20%) in RTA vs. CTRL. Vastus lateralis fractional O2 extraction was lower in RTA vs. CTRL at all work rates, during both CE and KE. RTA had higher ADP-stimulated mitochondrial respiration (56.7 ± 23.7 pmol O2·s−1·mg−1 ww) vs. CTRL (35.7 ± 10.2 pmol O2·s−1·mg−1 ww) and a tighter coupling of oxidative phosphorylation. In RTA, the greater muscle mass and maximal force and the enhanced mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O2 diffusion. The net results are an enhanced whole body oxidative function at peak exercise and unchanged efficiency and O2 cost at submaximal exercise, despite a much greater body mass.

scholarly journals Japanese radio calisthenics prevents the reduction of skeletal muscle mass volume in people with type 2 diabetes

2020 ◽  
Vol 8 (1) ◽  
pp. e001027 ◽  
Author(s):  
Tomonori Kimura ◽  
Takuro Okamura ◽  
Keiko Iwai ◽  
Yoshitaka Hashimoto ◽  
Takafumi Senmaru ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Mass ◽  
High Intensity ◽  
Skeletal Muscle Mass ◽  
Whole Body ◽  
Therapeutic Exercises ◽  
The Difference

ObjectiveReduction of muscle mass and strength is an important treatment target for patients with type 2 diabetes. Recent studies have reported that high-intensity resistance training improves physical function; however, all patients found it difficult to perform high-intensity resistance training. Radio calisthenics, considered as therapeutic exercises to promote health in Japan, are simple exercises that can be performed regardless of age and help move the muscles and joints of the whole body effectively according to the rhythm of radio. We investigated the efficacy of radio calisthenics for muscle mass in patients with type 2 diabetes in this retrospective cohort study.Research design and methodsA total of 42 hospitalized patients with type 2 diabetes were recruited. The skeletal muscle mass index (SMI, kg/m2) was calculated as appendicular muscle mass (kg) divided by height squared (m2). We defined the change of SMI as the difference of SMI between the beginning and end of hospitalization.ResultsAmong 42 patients, 15 (11 men and 4 women) performed radio calisthenics. Body weights of both radio calisthenics exercisers and non-exercisers decreased during hospitalization. The change of SMI was significantly lesser in radio calisthenics exercisers than in non-exercisers (7.1±1.4 to 7.1±1.3, –0.01±0.09 vs 6.8±1.1 to 6.5±1.2, –0.27±0.06 kg/m2, p=0.016). The proportion of decreased SMI was 85.2% (23/27 patients) in non-radio calisthenics exercisers, whereas that in radio calisthenics exercisers was 46.7% (7/15 patients).ConclusionsRadio calisthenics prevent the reduction of skeletal muscle mass. Thus, radio calisthenics can be considered effective for patients with type 2 diabetes.

scholarly journals New records in aerobic power among octogenarian lifelong endurance athletes

2013 ◽  
Vol 114 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Scott Trappe ◽  
Erik Hayes ◽  
Andrew Galpin ◽  
Leonard Kaminsky ◽  
Bozena Jemiolo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Aerobic Capacity ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Endurance Athletes ◽  
Whole Body ◽  
Oxidative Enzymes ◽  
Vastus Lateralis Muscle ◽  
Peroxisome Proliferator ◽  
Mrna Targets

We examined whole body aerobic capacity and myocellular markers of oxidative metabolism in lifelong endurance athletes [ n = 9, 81 ± 1 yr, 68 ± 3 kg, body mass index (BMI) = 23 ± 1 kg/m2] and age-matched, healthy, untrained men ( n = 6; 82 ± 1 y, 77 ± 5 kg, BMI = 26 ± 1 kg/m2). The endurance athletes were cross-country skiers, including a former Olympic champion and several national/regional champions, with a history of aerobic exercise and participation in endurance events throughout their lives. Each subject performed a maximal cycle test to assess aerobic capacity (V̇o2max). Subjects had a resting vastus lateralis muscle biopsy to assess oxidative enzymes (citrate synthase and βHAD) and molecular (mRNA) targets associated with mitochondrial biogenesis [peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) and mitochondrial transcription factor A (Tfam)]. The octogenarian athletes had a higher ( P < 0.05) absolute (2.6 ± 0.1 vs. 1.6 ± 0.1 l/min) and relative (38 ± 1 vs. 21 ± 1 ml·kg−1·min−1) V̇o2max, ventilation (79 ± 3 vs. 64 ± 7 l/min), heart rate (160 ± 5 vs. 146 ± 8 beats per minute), and final workload (182 ± 4 vs. 131 ± 14 W). Skeletal muscle oxidative enzymes were 54% (citrate synthase) and 42% (βHAD) higher ( P < 0.05) in the octogenarian athletes. Likewise, basal PGC-1α and Tfam mRNA were 135% and 80% greater ( P < 0.05) in the octogenarian athletes. To our knowledge, the V̇o2max of the lifelong endurance athletes is the highest recorded in humans >80 yr of age and comparable to nonendurance trained men 40 years younger. The superior cardiovascular and skeletal muscle health profile of the octogenarian athletes provides a large functional reserve above the aerobic frailty threshold and is associated with lower risk for disability and mortality.

scholarly journals Metabolic phenotype of skeletal muscle in early critical illness

Thorax ◽  
2018 ◽  
Vol 73 (10) ◽  
pp. 926-935 ◽  
Author(s):  
Zudin A Puthucheary ◽  
Ronan Astin ◽  
Mark J W Mcphail ◽  
Saima Saeed ◽  
Yasmin Pasha ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Critical Illness ◽  
Muscle Mass ◽  
Mitochondrial Biogenesis ◽  
Vastus Lateralis ◽  
Metabolic Phenotype ◽  
Tumour Necrosis Factor Receptor ◽  
Vastus Lateralis Muscle ◽  
Atp Content ◽  
Mitochondrial Dna Copy Number

ObjectivesTo characterise the sketetal muscle metabolic phenotype during early critical illness.MethodsVastus lateralis muscle biopsies and serum samples (days 1 and 7) were obtained from 63 intensive care patients (59% male, 54.7±18.0 years, Acute Physiology and Chronic Health Evaluation II score 23.5±6.5).Measurements and main resultsFrom day 1 to 7, there was a reduction in mitochondrial beta-oxidation enzyme concentrations, mitochondrial biogenesis markers (PGC1α messenger mRNA expression (−27.4CN (95% CI −123.9 to 14.3); n=23; p=0.025) and mitochondrial DNA copy number (−1859CN (IQR −5557–1325); n=35; p=0.032). Intramuscular ATP content was reduced compared tocompared with controls on day 1 (17.7mmol/kg /dry weight (dw) (95% CI 15.3 to 20.0) vs. 21.7 mmol/kg /dw (95% CI 20.4 to 22.9); p<0.001) and decreased over 7 days (−4.8 mmol/kg dw (IQR −8.0–1.2); n=33; p=0.001). In addition, the ratio of phosphorylated:total AMP-K (the bioenergetic sensor) increased (0.52 (IQR −0.09–2.6); n=31; p<0.001). There was an increase in intramuscular phosphocholine (847.2AU (IQR 232.5–1672); n=15; p=0.022), intramuscular tumour necrosis factor receptor 1 (0.66 µg (IQR −0.44–3.33); n=29; p=0.041) and IL-10 (13.6 ng (IQR 3.4–39.0); n=29; p=0.004). Serum adiponectin (10.3 µg (95% CI 6.8 to 13.7); p<0.001) and ghrelin (16.0 ng/mL (IQR −7–100); p=0.028) increased. Network analysis revealed a close and direct relationship between bioenergetic impairment and reduction in muscle mass and between intramuscular inflammation and impaired anabolic signaling. ATP content and muscle mass were unrelated to lipids delivered.ConclusionsDecreased mitochondrial biogenesis and dysregulated lipid oxidation contribute to compromised skeletal muscle bioenergetic status. In addition, intramuscular inflammation was associated with impaired anabolic recovery with lipid delivery observed as bioenergetically inert. Future clinical work will focus on these key areas to ameliorate acute skeletal muscle wasting.Trial registration numberNCT01106300.

scholarly journals Resistance Training With Partial Blood Flow Restriction in a 99-Year-Old Individual: A Case Report

2021 ◽  
Vol 3 ◽  
Author(s):  
Maíra Camargo Scarpelli ◽  
João Guilherme Almeida Bergamasco ◽  
Estevan A. de Barros Arruda ◽  
Summer B. Cook ◽  
Cleiton Augusto Libardi
Keyword(s):  
Quality Of Life ◽  
Blood Flow ◽  
Resistance Training ◽  
Muscle Mass ◽  
Vastus Lateralis ◽  
Blood Flow Restriction ◽  
Vastus Lateralis Muscle ◽  
Timed Up And Go ◽  
Flow Restriction

In aging populations for which the use of high loads is contraindicated, low load resistance training associated with blood flow restriction (RT-BFR) is an alternative strategy to induce muscle mass gains. This study investigates the effects of RT-BFR on muscle mass, muscle function, and quality of life of a 99-year-old patient with knee osteoarthritis and advanced muscle mass deterioration. Training protocol consisted of 24 sessions of a unilateral free-weight knee extension exercise associated with partial blood flow restriction through a manometer cuff set at 50% of complete vascular occlusion pressure. We evaluated: cross-sectional area (CSA) and thickness (MT) of the vastus lateralis muscle by ultrasound; function through the Timed Up and Go (TUG) test; and quality of life (QoL) by the WHOQOL-bref, WHOQOL-OLD and WOMAC questionnaires. All tests were performed prior to the training period (Pre) and after the 12th (Mid) and 24th (Post) sessions. Changes were considered significant if higher than 2 times the measurement's coefficient of variation (CV). After 24 sessions, there was an increase of 12% in CSA and 8% in MT. Questionnaires scores and TUG values worsened from Pre to Mid and returned in Post. We consider RT-BFR a viable and effective strategy to promote muscle mass gains in nonagenarians and delay the decline in functionality and QoL associated with aging.

scholarly journals High Incomplete Skeletal Muscle Fatty Acid Oxidation Explains Low Muscle Insulin Sensitivity in Poorly Controlled T2D

2017 ◽  
Vol 103 (3) ◽  
pp. 882-889 ◽  
Author(s):  
Timothy P Gavin ◽  
Jacob M Ernst ◽  
Hyo-Bum Kwak ◽  
Sarah E Caudill ◽  
Melissa A Reed ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Fatty Acid Oxidation ◽  
Mitochondrial Respiration ◽  
Vastus Lateralis ◽  
Acid Oxidation ◽  
Vastus Lateralis Muscle ◽  
Intravenous Glucose ◽  
Mitochondrial Respiratory

Abstract Context Almost 50% of type 2 diabetic (T2D) patients are poorly controlled [glycated hemoglobin (HbA1c) ≥ 7%]; however, the mechanisms responsible for progressively worsening glycemic control are poorly understood. Lower skeletal muscle mitochondrial respiratory capacity is associated with low insulin sensitivity and the development of T2D. Objective We investigated if skeletal muscle insulin sensitivity (SI) was different between well-controlled T2D (WCD) and poorly controlled T2D (PCD) and if the difference was associated with differences resulting from mitochondrial respiratory function. Design Vastus lateralis muscle mitochondrial respiration, mitochondrial content, mitochondrial enzyme activity, and fatty acid oxidation (FAO) were measured. SI and the acute response to glucose (AIRg) were calculated by MINMOD analysis from glucose and insulin obtained during a modified, frequently sampled, intravenous glucose tolerance test. Results SI and AIRg were lower in PCD than WCD. Muscle incomplete FAO was greater in PCD than WCD and greater incomplete FAO was associated with lower SI and higher HbA1c. Hydroxyacyl-coenzyme A dehydrogenase expression and activity were greater in PCD than WCD. There was no difference in maximal mitochondrial respiration or content between WCD and PCD. Conclusion The current results suggest that greater skeletal muscle incomplete FAO in poorly controlled T2D is due to elevated β oxidation and is associated with worsening muscle SI.

Postprandial myofibrillar and whole body protein synthesis in young and old human subjects

1994 ◽  
Vol 267 (4) ◽  
pp. E599-E604 ◽  
Author(s):  
S. Welle ◽  
C. Thornton ◽  
M. Statt ◽  
B. McHenry
Keyword(s):  
Protein Synthesis ◽  
Lean Body Mass ◽  
Body Mass ◽  
Human Subjects ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Vastus Lateralis Muscle ◽  
Body Protein ◽  
Creatinine Excretion ◽  
Fractional Rate

Rates of incorporation of leucine (using L-[1-13C]leucine as a tracer) into myofibrillar and whole body proteins were determined in healthy old (> 60 yr old, n = 7) and young (< 30 yr old, n = 9) men and women who were fed small meals (4% of daily energy) every 30 min. There was no difference in whole body incorporation of leucine into proteins in the young (148 +/- 5 mumol.h-1.kg lean body mass-1, means +/- SE) and old groups (150 +/- 3 mumol.h-1.kg lean body mass-1). However, the fractional myofibrillar protein synthesis in the vastus lateralis muscle was 28% slower in the older group (0.063 +/- 0.004 vs. 0.088 +/- 0.003 %/h, P < 0.001). Extrapolation of these results to whole body myofibrillar synthesis (fractional rate x myofibrillar mass estimated by creatinine excretion) indicated that, in the older group, total myofibrillar synthesis was 43% slower (1.8 +/- 0.2 vs. 3.1 +/- 0.2 g/h, P < 0.01) and that their myofibrillar synthesis was a smaller portion of whole body protein synthesis (15 +/- 1 vs. 23 +/- 1%, P < 0.001). Compared with age-matched postabsorptive subjects, whole body protein synthesis was approximately 25% faster, and fractional myofibrillar synthesis was approximately 50% faster in these fed subjects, both young and old. We conclude that myofibrillar synthesis is slower in older subjects during both postabsorptive and postprandial conditions but that aging does not impair the stimulatory effect of feeding on protein synthesis.

scholarly journals Aberrant REDD1-mTORC1 responses to insulin in skeletal muscle from Type 2 diabetics

2015 ◽  
Vol 309 (8) ◽  
pp. R855-R863 ◽  
Author(s):  
David L. Williamson ◽  
Cory M. Dungan ◽  
Abeer M. Mahmoud ◽  
Jacob T. Mey ◽  
Brian K. Blackburn ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vastus Lateralis ◽  
Glycosylated Hemoglobin ◽  
Whole Body ◽  
Glucose Disposal ◽  
Control Group ◽  
Vastus Lateralis Muscle ◽  
Percent Change ◽  
Phosphorylated Akt

The objective of this study was to establish whether alterations in the REDD1-mTOR axis underlie skeletal muscle insensitivity to insulin in Type 2 diabetic (T2D), obese individuals. Vastus lateralis muscle biopsies were obtained from lean, control and obese, T2D subjects under basal and after a 2-h hyperinsulinemic (40 mU·m−2·min−1)-euglycemic (5 mM) clamp. Muscle lysates were examined for total REDD1, and phosphorylated Akt, S6 kinase 1 (S6K1), 4E-BP1, ERK1/2, and MEK1/2 via Western blot analysis. Under basal conditions [(-) insulin], T2D muscle exhibited higher S6K1 and ERK1/2 and lower 4E-BP1 phosphorylation ( P < 0.05), as well as elevations in blood cortisol, glucose, insulin, glycosylated hemoglobin ( P < 0.05) vs. lean controls. Following insulin infusion, whole body glucose disposal rates (GDR; mg/kg/min) were lower ( P < 0.05) in the T2D vs. the control group. The basal-to-insulin percent change in REDD1 expression was higher ( P < 0.05) in muscle from the T2D vs. the control group. Whereas, the basal-to-insulin percent change in muscle Akt, S6K1, ERK1/2, and MEK1/2 phosphorylation was significantly lower ( P < 0.05) in the T2D vs. the control group. Findings from this study propose a REDD1-regulated mechanism in T2D skeletal muscle that may contribute to whole body insulin resistance and may be a target to improve insulin action in insulin-resistant individuals.

Exercise increases phosphorylation of the putative mTORC2 activity readout NDRG1 in human skeletal muscle

2021 ◽  
Author(s):  
Jonas Roland Knudsen ◽  
Kaspar W Persson ◽  
Jaroslawna Meister ◽  
Christian Strini Carl ◽  
Steffen H Raun ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Ex Vivo ◽  
Vastus Lateralis ◽  
Published Data ◽  
Vastus Lateralis Muscle ◽  
Mouse Muscle ◽  
Exercise Induced ◽  
Stimulation Of

In mice, exercise is suggested to activate the mechanistic target of rapamycin complex 2 (mTORC2) in skeletal muscle, and mTORC2 is required for normal muscle glucose uptake during exercise. Whether this translates to human skeletal muscle and what signaling pathways facilitate the exercise-induced mTORC2 activation is unknown but important to determine given the important role of mTORC2 in metabolism. We herein tested the hypothesis that exercise increases mTORC2 activity in human skeletal muscle and investigated if β2-adrenergic receptor (AR) activation mediates exercise-induced mTORC2 activation. We examined several mTORC2 activity readouts (p-NDRG1 Thr346, p-Akt Ser473, p-mTOR S2481, and p-Akt Thr450) in human skeletal muscle biopsies after uphill walking or cycling exercise. In mouse muscles, we assessed mTORC2 activity readouts following acute activation of muscle β2-adrenergic or Gs signaling and during in vivo and ex vivo muscle contractions. Exercise increased phosphorylation of NDRG1 Thr346 in human soleus, gastrocnemius, and vastus lateralis muscle, without changing p-Akt Ser473, p-Akt Thr450, and p-mTOR Ser2481. In mouse muscle, stimulation of β2-adrenergic or Gs signaling and ex vivo contractions failed to increase p-NDRG1 Thr346, while in vivo contractions were sufficient to induce p-NDRG1 Thr346. In conclusion, the mTORC2 activity readout p-NDRG1 Thr346 is a novel exercise-responsive signaling protein in human skeletal muscle. Notably, contraction-induced p-NDRG1 Thr346 appears to require a systemic factor. Unlike exercise, and in contrast to published data obtained in cultured muscles cells, stimulation of β2-adrenergic signaling is not sufficient to trigger NDRG1 phosphorylation in mature mouse skeletal muscle.

Normal mammalian skeletal muscle and its phenotypic plasticity

2002 ◽  
Vol 205 (15) ◽  
pp. 2143-2152 ◽  
Author(s):  
Hans Hoppeler ◽  
Martin Flück
Keyword(s):  
Skeletal Muscle ◽  
Phenotypic Plasticity ◽  
Muscle Mass ◽  
Body Mass ◽  
Gene Transcription ◽  
Muscle Tissue ◽  
Vastus Lateralis ◽  
Scaling Factor ◽  
Mammalian Skeletal Muscle ◽  
Total Body Mass

SUMMARYSince muscle mass makes up such a high proportion of total body mass, there must have been considerable selective pressure to minimize the cost of maintenance and to maximize the functionality of muscle tissue for all species. Phenotypic plasticity of muscle tissue allows the species blueprint of muscle tissue to be modified to accommodate specific demands experienced by animals over their lifetime. In this review, we report the scaling of muscle structural compartments in a set of mammals spanning five orders of magnitude(17 g woodmice to 450 kg horses and steers). Muscle mass, muscle myofibrillar volume and sarcoplasmic space were found to represent similar relative quantities in all species studies (scaling factor close to unity). Mitochondrial volumes were found to be systematically smaller in larger animals (scaling factor 0.91) and closely related to the scaling of V̇O2max (0.92) and were tracked by the scaling of total capillary length (0.95). In this set of species, we therefore found that maximal metabolic rate and supporting structures did not scale to the 0.75 power of body mass as generally suggested. Muscle phenotypic plasticity is reasonably well characterized on a structural and functional basis, but we still know little about the signals that cause the changes in gene expression necessary for phenotypic changes in muscle. The molecular responses of human m. vastus lateralis to endurance exercise indicate that a single bout of exercise causes specific transient transcriptional adaptations that may gradually accumulate after their translation into the (structural) modifications seen with phenotypic plasticity. Metabolic and mechanical factors are recognized candidate factors for the control of exercise-induced gene transcription in muscle. Distinct protein kinases and transcription factors emerge as possible interfaces that integrate the mechanical (MAPKs and jun/fos) and metabolic (AMPK, HIF-1αand PPARα) stimuli into enhanced gene transcription in skeletal muscle.

scholarly journals Genes and biochemical pathways in human skeletal muscle affecting resting energy expenditure and fuel partitioning

2011 ◽  
Vol 110 (3) ◽  
pp. 746-755 ◽  
Author(s):  
Xuxia Wu ◽  
Amit Patki ◽  
Cristina Lara-Castro ◽  
Xiangqin Cui ◽  
Kui Zhang ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Expenditure ◽  
Vastus Lateralis ◽  
Resting Energy Expenditure ◽  
Whole Body ◽  
Cellular Respiration ◽  
Vastus Lateralis Muscle ◽  
Peptidase Activity ◽  
The Metabolic Syndrome ◽  
Resting Energy

Genes influencing resting energy expenditure (REE) and respiratory quotient (RQ) represent candidate genes for obesity and the metabolic syndrome because of the involvement of these traits in energy balance and substrate oxidation. We aim to explore the molecular basis for individual variation in REE and fuel partitioning as reflected by RQ. We performed microarray studies in human vastus lateralis muscle biopsies from 40 healthy subjects with measured REE and RQ values. We identified 2,392 and 1,115 genes significantly correlated with REE and RQ, respectively. Genes correlated with REE and RQ encompass a broad array of functions, including carbohydrate and lipid metabolism, gene expression, mitochondrial processes, and membrane transport. Microarray pathway analysis revealed that REE was positively correlated with upregulation of G protein-coupled receptor signaling (meet criteria/total genes: 65 of 283) involved in autonomic nervous system functions, including those receptors mediating adrenergic, dopamine, γ-aminobutyric acid (GABA), neuropeptide Y (NPY), and serotonin action (meet criteria/total genes: 46 of 176). Reduced REE was associated with an increase in genes participating in ubiquitin-proteasome-dependent proteolytic pathways (58 of 232). Serine-type peptidase activity (9 of 76) was positively correlated with RQ, while genes involved in the protein phosphatase type 2A complex (4 of 9), mitochondrial function and cellular respiration (38 of 315), and unfolded protein binding (19 of 97) were associated with reduced RQ values and a preference for lipid fuel metabolism. Individual variations in whole body REE and RQ are regulated by differential expressions of specific genes and pathways intrinsic to skeletal muscle.

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