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Kian Peng Goh, Hwei Yee Lee, Dawn Pingxi Lau, Wilma Supaat, Yiong Huak Chan and Angela Fang Yung Koh

Objectives:

The primary aims of the study were to examine the effect of resveratrol on skeletal muscle SIRT1 expression and energy expenditure in subjects with Type 2 diabetes mellitus (T2DM).

Background:

Animal and in vivo studies indicate that resveratrol increases SIRT1 expression that stimulates PGC1α activity. Subsequent upregulation of AMPK and GLUT4 expression are associated with improved insulin sensitivity in peripheral tissues.

Methods:

Ten subjects with T2DM were randomized in a double-blind fashion to receive 3g resveratrol or placebo daily for 12 weeks. Secondary outcomes include measures of AMPK, p-AMPK and GLUT4 expression levels, energy expenditure, physical activity levels, distribution of abdominal adipose tissue and skeletal muscle fiber type composition, body weight, HbA1c, plasma lipid subfraction, adiponectin levels, and insulin sensitivity.

Results:

There was a significant increase in both SIRT1 expression (2.01 vs. 0.86 arbitrary units [AU], p = .016) and p-AMPK to AMPK expression ratio (2.04 vs. 0.79 AU, p = .032) in the resveratrol group compared with the placebo group. Although the percentage of absolute change (8.6 vs. –13.9%, p = .033) and percentage of predicted resting metabolic rate (RMR; 7.8 vs. –13.9%, p = .013) were increased following resveratrol, there was a significant reduction in average daily activity (–38 vs. 43.2%, p = .028) and step counts (–39.5 vs. 11.8%, p = .047) when compared with placebo.

Conclusions:

In patients with T2DM, treatment with resveratrol regulates energy expenditure through increased skeletal muscle SIRT1 and AMPK expression. These findings indicate that resveratrol may have beneficial exercise-mimetic effects in patients with T2DM.

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Thomas W. Jones, Ian H. Walshe, David L. Hamilton, Glyn Howatson, Mark Russell, Oliver J. Price, Alan St Clair Gibson and Duncan N. French

Purpose:

To compare anabolic signaling responses to differing sequences of concurrent strength and endurance training in a fed state.

Methods:

Eighteen resistance-trained men were randomly assigned to the following experimental conditions: strength training (ST), strength followed by endurance training (ST-END), or endurance followed by strength training (END-ST). Muscle tissue samples were taken from the vastus lateralis before each exercise protocol, on cessation of exercise, and 1 h after cessation of strength training. Tissue was analyzed for total and phosphorylated (p-) signaling proteins linked to the mTOR and AMPK networks.

Results:

Strength-training performance was similar between ST, ST-END, and END-ST. p-S6k1 was elevated from baseline 1 h posttraining in ST and ST-END (both P < .05). p-4E-BP1 was significantly lower than baseline post-ST (P = .01), whereas at 1 h postexercise in the ST-END condition p-4E-BP1 was significantly greater than postexercise (P = .04). p-ACC was elevated from baseline both postexercise and 1 h postexercise (both P < .05) in the END-ST condition. AMPK, mTOR, p38, PKB, and eEF2 responded similarly to ST, ST-END, and END-ST. Signaling responses to ST, ST-END, and END were largely similar. As such it cannot be ascertained which sequence of concurrent strength and endurance training is most favorable in promoting anabolic signaling.

Conclusions:

In the case of the current study an acute bout of concurrent training of differing sequences elicited similar responses of the AMPK and mTOR networks.

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Laís Monteiro Rodrigues Loureiro, Caio Eduardo Gonçalves Reis and Teresa Helena Macedo da Costa

involved in the process of glycogen synthesis. Adenosine monophosphate-activated protein kinase (AMPK) is an enzyme responsible for the translocation of glucose transporter 4 (GLUT-4) to the cell membrane when activated by skeletal muscle contraction ( Mu et al., 2001 ; Stapleton et al., 1996 ). AMPK

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Erik A. Richter, Jørgen F.P. Wojtaszewski, Søren Kristiansen, Jens R. Daugaard, Jakob N. Nielsen, Wim Derave and Bente Kiens

In the present short review some factors affecting glucose utilization during exercise in skeletal muscle will be briefly described. Special focus will be put on the glucose transport step across the sarcolemma. Glucose transporters (GLUT4) are expressed at a surprisingly similar level in the different muscle fiber types in human skeletal muscle in contrast to findings in the rat. When working at the same absolute work load muscle glucose transport is decreased in trained compared with untrained muscle in part due to a decrease in GLUT4 translocation to the sarcolemma in trained muscle. However, when trained and untrained muscle are stressed severely by a workload taxing 100% of their peak oxygen uptake in a glycogen-depleted state, then glucose uptake is larger in trained than in untrained muscle and correlates with muscle GLUT4 content. Finally, the possible role of the AMP-activated protein kinase (AMPK) in regulating glucose uptake during exercise is discussed. It is indicated that at present no experiments definitively link activation of AMPK to activation of muscle glucose transport during exercise.

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Trent Stellingwerff, James P. Morton and Louise M. Burke

 al., 2005 ; Hulston et al., 2010 ; Morton et al., 2009 ; Yeo et al., 2008 ), given the rationale that glycogen concentration is a potent regular of key cell signaling kinases (e.g., AMPK, p38), transcription factors (e.g., p53, PPAR) and transcriptional coactivators, for example, PGC-1α ( Bartlett et

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Nicolas Berryman, Iñigo Mujika and Laurent Bosquet

inverse relationship between muscle fiber size and oxidative capacity. 1 At the molecular level, it was originally thought that the activation of the AMP-activated protein kinase (AMPK) by AT could inhibit the mammalian target of rapamycin (mTOR), which is activated by RT. 8 Consequently, this molecular

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Sabrina Skorski, Iñigo Mujika, Laurent Bosquet, Romain Meeusen, Aaron J. Coutts and Tim Meyer

intensified training phase. Ihsan et al 45 reported greater improvements in maximum oxygen consumption (VO 2 max) as well as maximum running velocity ( V max ) when CWI was regularly used after intense running bouts. The authors speculated that regular CWI applications might enhance p38 and AMPK activation

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Samuel G. Impey, Kelly M. Hammond, Robert Naughton, Carl Langan-Evans, Sam O. Shepherd, Adam P. Sharples, Jessica Cegielski, Kenneth Smith, Stewart Jeromson, David L. Hamilton, Graeme L. Close and James P. Morton

is not inhibited in human skeletal muscle despite prior activation of AMPK by high-intensity interval cycling . American Journal of Physiology-Endocrinology and Metabolism, 308 , 470 – 481 . doi:10.1152/ajpendo.00486.2014 10.1152/ajpendo.00486.2014 Apró , W. , Moberg , M. , Hamilton , D

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Andreas M. Kasper, Ben Crighton, Carl Langan-Evans, Philip Riley, Asheesh Sharma, Graeme L. Close and James P. Morton

-after-brazilian-mma-fighter-dies-while-cutting Bartlett , J. , Hwa Joo , C. , Jeong , T.S. , Louhelinen , J. , Cochran , A. , Gibala , M.J. , . . . Morton , J.P. ( 2012 ). Matched work high-intensity interval and continuous running induce similar increases in PGC-1α mRNA, AMPK, p38, and p53 phosphorylation in human skeletal muscle

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Louise M. Burke, John A. Hawley, Asker Jeukendrup, James P. Morton, Trent Stellingwerff and Ronald J. Maughan

activation of key cell signaling proteins (e.g., AMPK, p38, PPAR, PGC-1α), which achieve a coordinated upregulation of the nuclear and mitochondrial genomes (for review, see Bartlett et al., 2015 ; Hawley et al., 2018 ; Hearris et al., 2018 ; Impey et al., 2018 ). Over a chronic training period, this may