Abstract
PurposeRac1 and its downstream target PAK1 are novel regulators of insulin and exercise-induced glucose uptake in skeletal muscle. However, it is not yet understood how different training intensities affect the expression of these proteins. Therefore, we studied the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on Rac1 and PAK1 expression in fast-type (gastrocnemius, GC) and slow-type (soleus, SOL) muscles in rats after HIIT and MICT swimming exercises.MethodsThe mRNA expression was determined using qPCR and protein expression levels with reverse-phase protein microarray (RPPA).ResultsHIIT significantly decreased Rac1 mRNA expression in GC compared to MICT (p = 0.003) and to the control group (CON) (p = 0.001). At the protein level Rac1 was increased in GC in both training groups, but only the difference between HIIT and CON was significant (p = 0.02). HIIT caused significant decrease of PAK1 mRNA expression in GC compared to MICT (p = 0.007) and to CON (p = 0.001). At the protein level, HIIT increased PAK1 expression in GC compared to MICT and CON (by ∼17%), but the difference was not statistically significant (p = 0.3, p = 0.2, respectively). There were no significant differences in the Rac1 or PAK1 expression in SOL between the groups.ConclusionOur results indicate that HIIT, but not MICT, decreases Rac1 and PAK1 mRNA expression and increases the protein expression of especially Rac1 but only in fast-type muscle. These exercise training findings may reveal new therapeutic targets to treat patients with metabolic diseases.
Highlights
Muscle contractions increase glucose uptake (GU) via GLUT4 mediated mechanisms (Sahlin, 1990; Warburton et al, 2006)
high-intensity interval training (HIIT) group showed significantly lower related C3 botulinum toxin substrate 1 (Rac1) mRNA expression in GC compared to moderate-intensity continuous training (MICT) (p = 0.003) or to CON (p = 0.001) (Figure 1A)
The similar trend was seen in SOL, but the difference was only seen between HIIT and CON (p = 0.04) (Figure 1C)
Summary
Muscle contractions increase glucose uptake (GU) via GLUT4 (glucose transporter type 4) mediated mechanisms (Sahlin, 1990; Warburton et al, 2006). Incompletely elucidated but recent studies indicate that in addition to insulinstimulated GU, Rac1/PAK1 signaling seems to play an important role in contraction-mediated GU (Sylow et al, 2013b, 2016). The consecutive cytoskeleton remodeling and translocation of GLUT4 to the cell membrane increases GU into the muscle (Tunduguru et al, 2017). Recent data suggest that Rac is required for skeletal muscle GU in both insulin- and exercise-mediated signaling (Sylow et al, 2013a,b). Disturbances in the function of Rac signaling have been observed in insulin resistance in both human and mice (Sylow et al, 2013a), but the effects of different exercise training intensities on the expression of PAK1 and Rac remain sparsely characterized
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