Review Article

Influence of Acute and Chronic Exercise on Glucose Uptake

Table 3

Influence of exercise on glucose uptake-related signaling pathways in animal models.

ReferenceAnimals, Age, weekTraining modalityType of sportTraining frequencyAcute/chronic exerciseTraining intensityTissue & conditionTime since the last exercise bout, hChanges in glucose uptake-related molecular signaling

Treadway et al., 1989 [17]Male Sprague-Dawley ratsn.r.ETTreadmill running45 minAcute18 m/minInsulin stimulated muscleImmediately after exerciseNo effect on insulin binding, basal and insulin-stimulated receptor autophosphorylation, or basal and insulin-stimulated exogenous kinase activity

Goodyear et al., 1995 [18]Male Sprague-Dawley ratsn.r.ESContractionn.r.AcuteTraining duration, 500 ms; pulse rate, 100 Hz; duration, 0.1 ms at 1–3 VInsulin stimulated muscleImmediately after contraction phaseDecrease of insulin-stimulated tyrosine phosphorylation and PI3-kinase activity (20%), no effect of exercise without insulin

Sakamoto et al., 2002 [50]Male Sprague-Dawley ratsn.r.ESContractionn.r.AcuteTraining rate, 1/s; train duration, 500 ms; pulse rate, 100 Hz; duration, 0.1 ms at 2–5 VMuscleImmediately after contraction phaseIncrease of Akt Ser473 phosphorylation after 5 min (3-fold) and decrease to +23% after 30 min

Wojtaszewski et al., 1999 [51]Male muscle-specific insulin receptor knockout mice9-10ETTreadmill running60 minAcute22 m/min with 10% inclineInsulin stimulated muscleImmediately after exerciseIncrease of insulin-stimulated glucose transport without improvement of proximal insulin signaling, but increase of Akt phosphorylation (6.0-fold)

Castorena et al., 2014 [49]Male Wistar rats (LFD and HFD)n.r.ETSwimming4 × 30 minAcuten.r.Insulin stimulated muscleImmediately and 3 h after exercise phaseIncrease of AS160 immediately (2.0–2.5-fold) and after 3 h (3-fold, in LFD)

Bruss et al., 2005 [57]Male Wistar ratsn.r.ESContractionn.r.AcuteTraining rate, 2/min; training duration, 10 s; pulse rate, 100 Hz; duration, 0.1 ms at 2–5 VMuscleImmediately after contraction phaseIncrease of AS160 phosphorylation (3.7-fold)

Fujii et al., 2005 [97]Muscle-specific transgenic knockout of α2 subunits of AMPK mice10–16ESContraction10 minAcuteTraining rate, 1/min; training duration, 10 s; pulse rate, 100 Hz; duration, 0.1 ms at 100 VMuscleImmediately after contraction phaseNear normal glucose uptake (−13%) in KO mice

Jeppesen et al., 2013 [98]Muscle specific knockout of LKB1 mice16–20ETTreadmill running24 minAcute12.5 m/minMuscleImmediately after contraction phaseNormal glucose uptake in LKB1 deficient mice

Lefort et al., 2008 [99]Muscle-specific transgenic knockout of α2 subunits of AMPK micen.r.ESContraction2 minAcuteTraining rate, 1/s; training duration, 500 ms; pulse rate, 100 Hz; at 30 VMuscleImmediately after contraction phaseNo change of AMPK activity after contraction, but increase of glucose uptake by 50% compared to CON mice

Sakamoto et al., 2005 [100]Muscle specific knockout of LKB1 micen.r.ESContraction5 minAcuteTraining rate, 1/s; training duration, 200 ms; pulse rate, 50 Hz; duration, 0.1 ms at 2–5 VMuscleImmediately after contraction phaseReduced glucose uptake in LKB1 deficient mice

Thomson et al., 2008 [41]Fischer 344 × Brown Norway male rats32ESContraction22 minAcute10 sets 6 contractions for 3 sMuscleImmediately and 20, and 40 min after contraction phaseIncrease of AMPK activity and inhibition of mTOR signaling

Katta et al., 2009 [36]12 male lean normal Zucker rats, 12 male young obese Syndrome × Zucker rats10ESn.r.22 minAcute10 sets of 6 contractionsMuscleImmediately, 1 h and 3 h after exerciseIncrease of mTOR phosphorylation (Ser2448, 63%) and p70S6K (Thr389, 37%) compared to lean normal Zucker rats

Sylow et al., 2013 [101]Female C57BL/6 mice12–16ETTreadmill running50%–70% maximal running speed 30 minAcute16 m/min 
22 m/min
MuscleImmediately after exerciseIncrease of Rac1 activity by 44%/50%/100% after 40%/50%/70% of maximal speed

Witczak et al., 2007 [102]Female ICR mice8ESContraction15 minAcuten.r.Muscle45 min after contractionNo change in insulin-stimulated glucose uptake in calmodulin-binding domain-mutant mice, decrease of contraction-stimulated glucose uptake in calmodulin-binding domain-mutant mice

Witczak et al., 2010 [103]Female ICR mice6–8ESContraction10 minAcuteTraining rate, 1/min; training duration, 10 s; pulse rate, 100 pulses/s; duration, 0.1 ms; volts, 100 VMuscle45 min after contractionDecrease of contraction-induced muscle glucose uptake (30%)

Edgett et al., 2013 [46]Female Sprague-Dawley ratsn.r.ETTreadmill running120 minAcute15 m/min + 5 m/min every 5 minMuscleImmediately and 3 h after exerciseTime-dependent increase of mTOR mRNA by 44% after 180 min of recovery

Edgett et al., 2013 [46]Female Sprague-Dawley ratsn.r.ESContraction120 minChronic (7 days)n.r.MuscleImmediately and 3 h after exerciseIncrease of mTOR phosphorylation by 74% after 7 days of ES

Calegari et al., 2011 [31]20 male Wistar rats8ETTreadmill running5–60 minChronic (8 weeks)5 m/min–30 m/minPancreatic islets24 h after exerciseIncrease of AMPK phosphorylation (100%) and CaMKII phosphorylation (+50%)

Luo et al., 2013 [30]Male Sprague-Dawley rats18–20RTLadder climbing with weights3 × 10 repetitionsChronic (9 weeks)10% per week increase of additional weightMuscle48 h after exerciseIncrease of both total and phosphorylated AMPK compared to sedentary control

Ritchie et al., 2014 [53]Male wild-type (WT, C57BL/6J) mice, adiponectin knockout (AdKO, B6.129-Adipoqtm1Chan/J) mice12ETTreadmill running3 × 45–60 minChronic (8 weeks)20–32 m/minInsulin stimulated muscle48 h after exerciseIncrease in total AS160 phosphorylation from AdKO (44%) compared to WT mice (28%);  
no differences in total GLUT4 protein content

All changes given in the table were statistically significant; AMPK, AMP-activated protein kinase; AS160, Akt substrate of 160 kDa; Ca, calcium; CaMKII, Ca2+/calmodulin-dependent protein kinase 2; CON, controls; DIO, diet-induced obesity; ES, electrical stimulation; ET, endurance training; GLUT4, glucose transporter 4; HFD, high fed diet; LFD, low fed diet; LKB-1, liver kinase B1; mTOR, mammalian target of rapamycin (C1 complex 1 & C2 complex 2); n.r., not reported; PI3-K, phosphoinositide 3-kinase; Rac1, ras-related C3 botulinum toxin substrate 1; RT, resistance training; SK6, serine kinase 6; T2D, type 2 diabetes; TBC1D1, TBC1 domain family member 1.