scholarly journals Nicotinamide riboside supplementation does not alter whole‐body or skeletal muscle metabolic responses to a single bout of endurance exercise

2021 ◽  
Author(s):  
Ben Stocks ◽  
Stephen P. Ashcroft ◽  
Sophie Joanisse ◽  
Linda C. Dansereau ◽  
Yen Chin Koay ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Whole Body ◽  
Metabolic Responses ◽  
Nicotinamide Riboside ◽  
Single Bout

scholarly journals Nicotinamide Riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise

2020 ◽  
Author(s):  
Ben Stocks ◽  
Stephen P. Ashcroft ◽  
Sophie Joanisse ◽  
Yasir S. Elhassan ◽  
Gareth G. Lavery ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Endurance Exercise ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Endurance Capacity ◽  
Similar Response ◽  
Transcriptional Responses ◽  
Nicotinamide Riboside ◽  
Exercise Induced

AbstractOral supplementation of the NAD+ precursor Nicotinamide Riboside (NR) has been reported to increase Sirtuin (SIRT) signalling, mitochondrial biogenesis and endurance capacity in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study aimed to assess the effect of 7-day NR supplementation on exercise-induced transduction and transcriptional responses in skeletal muscle of young, healthy, recreationally active human volunteers. In a double-blinded, randomised, counter-balanced, crossover design, eight male participants (age: 23 ± 4 years, VO2peak: 46.5 ± 4.4 mL·kg-1·min-1) received one week of NR or cellulose placebo (PLA) supplementation (1000 mg·d-1) before performing one hour of cycling at 60% Wmax. Muscle biopsies were collected prior to supplementation and pre-, immediately and three-hours post-exercise from the medial vastus lateralis, whilst venous blood samples were collected throughout the trial. Global acetylation, auto-PARylation of PARP1, acetylation of p53Lys382 and MnSODLys122 were unaffected by NR supplementation or exercise. Exercise led to an increase in AMPKThr172 (1.6-fold), and ACCSer79 (4-fold) phosphorylation, in addition to an increase in PGC-1α (∼5-fold) and PDK4 (∼10-fold) mRNA expression, however NR had no additional effect on this response. There was also no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Finally, NR supplementation blunted the exercise induced activation of skeletal muscle NNMT mRNA expression, but had no effect on mRNA expression of NMRK1, NAMPT or NMNAT1, which were not significantly affected by NR supplementation or exercise. In summary, one week of NR supplementation does not augment skeletal muscle signal transduction pathways implicated in mitochondrial adaptation to endurance exercise.

scholarly journals Effects of 10 Days of Endurance Exercise Training on the Suppression of Whole Body and Regional Lipolysis by Insulin1

2000 ◽  
Vol 85 (4) ◽  
pp. 1498-1504
Author(s):  
R. C. Hickner ◽  
S. B. Racette ◽  
E. F. Binder ◽  
J. S. Fisher ◽  
W. M. Kohrt
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Premenopausal Women ◽  
Whole Body ◽  
Obese Women ◽  
Endurance Exercise Training ◽  
Before And After ◽  
Basal Plasma

The aim of this study was to evaluate in premenopausal women (10 sedentary obese women) the effects of 10 days of exercise on the suppression of whole body and regional lipolysis by insulin. Lipolysis was determined using 2H5-glycerol infusion and microdialysis of sc adipose tissue during a two-stage hyperinsulinemic-euglycemic clamp [10 (LO) and 20 (MO) mU/m·min]. Microdialysis probes were positioned in abdominal and femoral sc adipose tissue to monitor interstitial glycerol and blood flow. Basal plasma glycerol was 86.7 ± 17.0 and 100.3 ± 19.8 μmol/L before and after training, respectively (P < 0.05). Plasma glycerol was suppressed to a greater extent after [to 47 ± 5% (LO) and 42 ± 5% (MO) of basal] than before [to 62 ± 8% (LO) and 55 ± 8% (MO) of basal] training. The rate of appearance of glycerol was suppressed to 49 ± 7% and 40 ± 5% of basal during LO and to 38 ± 5% and 30 ± 4% of basal during MO (P < 0.05) before and after training, respectively. There were no differences in the suppression of lipolysis in abdominal as well as femoral sc adipose tissue as evidenced by similar reductions in dialysate glycerol levels before and after training in each of these tissues. The results indicate that the antilipolytic response to insulin can be improved through endurance exercise training. Intraabdominal adipose tissue or skeletal muscle may be the site of improved antilipolytic response to insulin after training, as improvement was not evident in abdominal or femoral sc adipose tissue.

scholarly journals Contrasting effects of exercise, AICAR, and increased fatty acid supply on in vivo and skeletal muscle glucose metabolism

2008 ◽  
Vol 104 (2) ◽  
pp. 363-370 ◽  
Author(s):  
C. Rantzau ◽  
M. Christopher ◽  
F. P. Alford
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Acute Exercise ◽  
Maximal Oxygen Consumption ◽  
Whole Body ◽  
Metabolic Responses ◽  
Glycolytic Flux ◽  
Glucose Turnover ◽  
Moderate Exercise

The increased energy required for acute moderate exercise by skeletal muscle (SkM) is derived equally from enhanced fatty acid (FA) oxidation and glucose oxidation. Availability of FA also influences contracting SkM metabolic responses. Whole body glucose turnover and SkM glucose metabolic responses were determined in paired dog studies during 1) a 30-min moderate exercise (maximal oxygen consumption of ∼60%) test vs. a 60-min low-dose 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) infusion, 2) a 150-min AICAR infusion vs. modest elevation of FA induced by a 150-min combined intralipid-heparin (IL/hep) infusion, and 3) an acute exercise test performed with vs. without IL/hep. The exercise responses differed from those observed with AICAR: plasma FA and glycerol rose sharply with exercise, whereas FA fell and glycerol was unchanged with AICAR; glucose turnover and glycolytic flux doubled with exercise but rose only by 50% with AICAR; SkM glucose-6-phosphate rose and glycogen content decreased with exercise, whereas no changes occurred with AICAR. The metabolic responses to AICAR vs. IL/hep differed: glycolytic flux was stimulated by AICAR but suppressed by IL/hep, and no changes in glucose turnover occurred with IL/hep. Glucose turnover responses to exercise were similar in the IL/hep and non-IL/hep, but SkM lactate and glycogen concentrations rose with IL/hep vs. that shown with exercise alone. In conclusion, the metabolic responses to acute exercise are not mimicked by a single dose of AICAR or altered by short-term enhancement of fatty acid supply.

scholarly journals Calcineurin activates interleukin-6 transcription in mouse skeletal muscle in vivo and in C2C12 myotubes in vitro

2010 ◽  
Vol 298 (1) ◽  
pp. R198-R210 ◽  
Author(s):  
David L. Allen ◽  
Jill J. Uyenishi ◽  
Allison S. Cleary ◽  
Ryan S. Mehan ◽  
Sarah F. Lindsay ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Exercise ◽  
Binding Sites ◽  
Promoter Activity ◽  
Wheel Running ◽  
Mrna Levels ◽  
Dna Binding Sites ◽  
Single Bout

Expression of the cytokine interleukin-6 (IL-6) by skeletal muscle is hugely increased in response to a single bout of endurance exercise, and this appears to be mediated by increases in intracellular calcium. We examined the effects of endurance exercise on IL-6 mRNA levels and promoter activity in skeletal muscle in vivo, and the role of the calcium-activated calcineurin signaling pathway on muscle IL-6 expression in vivo and in vitro. IL-6 mRNA levels in the mouse tibialis anterior (TA) were increased 2–10-fold by a single bout of treadmill exercise or by 3 days of voluntary wheel running. Moreover, an IL-6 promoter-driven luciferase transgene was activated in TA by both treadmill and wheel-running exercise and by injection with a calcineurin plasmid. Exercise also increased muscle mRNA expression of the calcineurin regulatory gene MCIP1, as did treatment of C2C12 myotubes with the calcium ionophore A23187. Cotransfection of C2C12 myotubes with a constitutively active calcineurin construct significantly increased while cotransfection with the calcineurin inhibitor CAIN inhibited activity of a mouse IL-6 promoter-reporter construct. Cotransfection with a myocyte enhancer-factor-2 (MEF-2) expression construct increased basal IL-6 promoter activity and augmented the effects of calcineurin cotransfection, while cotransfection with the MEF-2 antagonist MITR repressed calcineurin-activated IL-6 promoter activity in vitro. Surprisingly, cotransfection with a dominant-negative form of another calcineurin-activated transcription factor, nuclear factor activator of T cells (NFAT), greatly potentiated both basal and calcineurin-stimulated IL-6 promoter activity in C2C12 myotubes. Mutation of the MEF-2 DNA binding sites attenuated, while mutation of the NFAT DNA binding sites potentiated basal and calcineurin-activated IL-6 promoter activity. Finally, CREB and C/EBP were necessary for basal IL-6 promoter activity and sufficient to increase IL-6 promoter activity but had minimal roles in calcineurin-activated IL-6 promoter activity. Together, these results suggest that IL-6 transcription in skeletal muscle cells can be activated by a calcineurin-MEF-2 axis which is antagonized by NFAT.

scholarly journals High-fat diet impairs the effects of a single bout of endurance exercise on glucose transport and insulin sensitivity in rat skeletal muscle

Metabolism ◽  
2007 ◽  
Vol 56 (12) ◽  
pp. 1719-1728 ◽  
Author(s):  
Satsuki Tanaka ◽  
Tatsuya Hayashi ◽  
Taro Toyoda ◽  
Taku Hamada ◽  
Yohei Shimizu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Transport ◽  
Endurance Exercise ◽  
High Fat Diet ◽  
High Fat ◽  
Rat Skeletal Muscle ◽  
Single Bout

scholarly journals Nicotinamide riboside supplementation to improve skeletal muscle mitochondrial health and whole‐body glucose homeostasis: does it actually work in humans?

2020 ◽  
Vol 598 (4) ◽  
pp. 619-620
Author(s):  
Jean‐Philippe Leduc‐Gaudet ◽  
Maude Dulac ◽  
Olivier Reynaud ◽  
Marie‐Belle Ayoub ◽  
Gilles Gouspillou
Keyword(s):  
Skeletal Muscle ◽  
Glucose Homeostasis ◽  
Whole Body ◽  
Nicotinamide Riboside
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