Exercise training favors increased insulin-stimulated glucose uptake in skeletal muscle in contrast to adipose tissue: a randomized study using FDG PET imaging

Physical exercise increases peripheral insulin sensitivity, but regional differences are poorly elucidated in humans. We investigated the effect of aerobic exercise training on insulin-stimulated glucose uptake in five individual femoral muscle groups and four different adipose tissue regions, using dynamic (femoral region) and static (abdominal region) 2-deoxy-2-[18F]fluoro-d-glucose (FDG) PET/CT methodology during steady-state insulin infusion (40 mU·m−2·min−1). Body composition was measured by dual X-ray absorptiometry and MRI. Sixty-one healthy, sedentary [V̇o2max 36(5) ml·kg−1·min−1; mean(SD)], moderately overweight [BMI 28.1(1.8) kg/m2], young [age: 30(6) yr] men were randomized to sedentary living (CON; n = 17 completers) or moderate (MOD; 300 kcal/day, n = 18) or high (HIGH; 600 kcal/day, n = 18) dose physical exercise for 11 wk. At baseline, insulin-stimulated glucose uptake was highest in femoral skeletal muscle followed by intraperitoneal visceral adipose tissue (VAT), retroperitoneal VAT, abdominal (anterior + posterior) subcutaneous adipose tissue (SAT), and femoral SAT ( P < 0.0001 between tissues). Metabolic rate of glucose increased similarly (∼30%) in the two exercise groups in femoral skeletal muscle (MOD 24[9, 39] μmol·kg−1·min−1, P = 0.004; HIGH 22[9, 35] μmol·kg−1·min−1, P = 0.003) (mean[95% CI]) and in five individual femoral muscle groups but not in femoral SAT. Standardized uptake value of FDG decreased ∼24% in anterior abdominal SAT and ∼20% in posterior abdominal SAT compared with CON but not in either intra- or retroperitoneal VAT. Total adipose tissue mass decreased in both exercise groups, and the decrease was distributed equally among subcutaneous and intra-abdominal depots. In conclusion, aerobic exercise training increases insulin-stimulated glucose uptake in skeletal muscle but not in adipose tissue, which demonstrates some interregional differences.

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Insulin-resistant subjects have normal angiogenic response to aerobic exercise training in skeletal muscle, but not in adipose tissue

Physiological Reports ◽

10.14814/phy2.12415 ◽

2015 ◽

Vol 3 (6) ◽

pp. e12415 ◽

Cited By ~ 11

Author(s):

R. Grace Walton ◽

Brian S. Finlin ◽

Jyothi Mula ◽

Douglas E. Long ◽

Beibei Zhu ◽

...

Keyword(s):

Skeletal Muscle ◽

Adipose Tissue ◽

Exercise Training ◽

Aerobic Exercise ◽

Aerobic Exercise Training ◽

Angiogenic Response ◽

Insulin Resistant

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Endurance exercise training-responsive miR-19b-3p improves skeletal muscle glucose metabolism

Nature Communications ◽

10.1038/s41467-021-26095-0 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Julie Massart ◽

Rasmus J. O. Sjögren ◽

Brendan Egan ◽

Christian Garde ◽

Magnus Lindgren ◽

...

Keyword(s):

Skeletal Muscle ◽

Glucose Metabolism ◽

Exercise Training ◽

Aerobic Exercise ◽

Glucose Uptake ◽

Human Skeletal Muscle ◽

Muscle Cells ◽

Skeletal Muscle Cells ◽

Aerobic Exercise Training ◽

Human Skeletal Muscle Cells

AbstractSkeletal muscle is a highly adaptable tissue and remodels in response to exercise training. Using short RNA sequencing, we determine the miRNA profile of skeletal muscle from healthy male volunteers before and after a 14-day aerobic exercise training regime. Among the exercise training-responsive miRNAs identified, miR-19b-3p was selected for further validation. Overexpression of miR-19b-3p in human skeletal muscle cells increases insulin signaling, glucose uptake, and maximal oxygen consumption, recapitulating the adaptive response to aerobic exercise training. Overexpression of miR-19b-3p in mouse flexor digitorum brevis muscle enhances contraction-induced glucose uptake, indicating that miR-19b-3p exerts control on exercise training-induced adaptations in skeletal muscle. Potential targets of miR-19b-3p that are reduced after aerobic exercise training include KIF13A, MAPK6, RNF11, and VPS37A. Amongst these, RNF11 silencing potentiates glucose uptake in human skeletal muscle cells. Collectively, we identify miR-19b-3p as an aerobic exercise training-induced miRNA that regulates skeletal muscle glucose metabolism.

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Skeletal Muscle Insulin Resistance: Roles of Fatty Acid Metabolism and Exercise

Physical Therapy ◽

10.2522/ptj.20080018 ◽

2008 ◽

Vol 88 (11) ◽

pp. 1279-1296 ◽

Cited By ~ 87

Author(s):

Lorraine P Turcotte ◽

Jonathan S Fisher

Keyword(s):

Insulin Resistance ◽

Skeletal Muscle ◽

Fatty Acid ◽

Exercise Training ◽

Aerobic Exercise ◽

Glucose Uptake ◽

Muscle Cells ◽

Aerobic Exercise Training ◽

Muscle Insulin Resistance ◽

Skeletal Muscle Insulin Resistance

The purpose of this review is to provide information about the role of exercise in the prevention of skeletal muscle insulin resistance, that is, the inability of insulin to properly cause glucose uptake into skeletal muscle. Insulin resistance is associated with high levels of stored lipids in skeletal muscle cells. Aerobic exercise training decreases the amounts of these lipid products and increases the lipid oxidative capacity of muscle cells. Thus, aerobic exercise training may prevent insulin resistance by correcting a mismatch between fatty acid uptake and fatty acid oxidation in skeletal muscle. Additionally, a single session of aerobic exercise increases glucose uptake by muscle during exercise, increases the ability of insulin to promote glucose uptake, and increases glycogen accumulation after exercise, all of which are important to blood glucose control. There also is some indication that resistance exercise may be effective in preventing insulin resistance. The information provided is intended to help clinicians understand and explain the roles of exercise in reducing insulin resistance.

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Relationship between intermuscular adipose tissue infiltration and myostatin before and after aerobic exercise training

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00030.2018 ◽

2018 ◽

Vol 315 (3) ◽

pp. R461-R468 ◽

Cited By ~ 11

Author(s):

Adam R. Konopka ◽

Christopher A. Wolff ◽

Miranda K. Suer ◽

Matthew P. Harber

Keyword(s):

Skeletal Muscle ◽

Adipose Tissue ◽

Exercise Training ◽

Aerobic Exercise ◽

Exercise Capacity ◽

Muscle Function ◽

Aerobic Exercise Training ◽

Skeletal Muscle Function ◽

Intermuscular Adipose Tissue ◽

Before And After

Intermuscular adipose tissue (IMAT) is associated with impaired skeletal muscle contractile and metabolic function. Myostatin and downstream signaling proteins such as cyclin-dependent kinase 2 (CDK2) contribute to the regulation of adipose and skeletal muscle mass in cell culture and animals models, but this relationship remains incompletely understood in humans. The purpose of this study was to determine if the infiltration of IMAT was associated with skeletal muscle myostatin and downstream proteins before and after 12 wk of aerobic exercise training (AET) in healthy older women (OW; 69 ± 2 yr), older men (OM; 74 ± 3 yr), and young men (YM; 20 ± 1 yr). We found that the infiltration of IMAT was correlated with myostatin and phosphorylated CDK2 at tyrosine 15 [P-CDK2(Tyr15)]. IMAT infiltration was greater in the older subjects and was associated with lower skeletal muscle function and exercise capacity. After 12 wk of AET, there was no change in body weight. Myostatin and P-CDK2(Tyr15) were both decreased after AET, and the reduction in myostatin was associated with decreased IMAT infiltration. The decrease in myostatin and IMAT occurred concomitantly with increased exercise capacity, skeletal muscle size, and function after AET. These findings demonstrate that the reduction in IMAT infiltration after AET in weight stable individuals was accompanied by improvements in skeletal muscle function and exercise capacity. Moreover, the association between myostatin and IMAT was present in the untrained state and in response to exercise training, strengthening the potential regulatory role of myostatin on IMAT.

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