Abstract
The purpose of this study was to verify the effects of overtraining (OT) on insulin, inflammatory and gluconeogenesis signaling pathways in the livers of mice. Rodents were divided into control (CT), overtrained by downhill running (OTR/down), overtrained by uphill running (OTR/up) and overtrained by running without inclination (OTR). Rotarod, incremental load, exhaustive and grip force tests were used to evaluate performance. Thirty-six hours after a grip force test, the livers were extracted for subsequent protein analyses. The phosphorylation of insulin receptor beta (pIRbeta), glycogen synthase kinase 3 beta (pGSK3beta) and forkhead box O1 (pFoxo1) increased in OTR/down versus CT. pGSK3beta was higher in OTR/up versus CT, and pFoxo1 was higher in OTR/up and OTR versus CT. Phosphorylation of protein kinase B (pAkt) and insulin receptor substrate 1 (pIRS–1) were higher in OTR/up versus CT and OTR/down. The phosphorylation of IκB kinase alpha and beta (pIKKalpha/beta) was higher in all OT protocols versus CT, and the phosphorylation of stress-activated protein kinases/Jun amino-terminal kinases (pSAPK-JNK) was higher in OTR/down versus CT. Protein levels of peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha) and hepatocyte nuclear factor 4alpha (HNF-4alpha) were higher in OTR versus CT. In summary, OTR/down improved the major proteins of insulin signaling pathway but up-regulated TRB3, an Akt inhibitor, and its association with Akt.
Highlights
High intensity and volume exercise sessions are generally used during training programs to disrupt cellular homeostasis, induce overcompensation and improve physical performance
Pereira et al [3] verified that mice subjected to an eightweek overtraining (OT) protocol based on eccentric exercise (EE) presented nonfunctional overreaching (NFOR) and increased the protein levels of interleukin–6 (IL–6), myostatin and tumor necrosis factor-alpha (TNF-alpha) in skeletal muscle samples as well as serum levels of IL–6 [4]
Eight-week-old C57BL/6 mice were divided into four groups: control (CT; sedentary mice; n = 18), overtrained by downhill running (OTR/down; performed the OT protocol based on downhill running; n = 18), overtrained by uphill running (OTR/up; performed the OT protocol based on uphill running; n = 18) and overtrained by running without inclination (OTR; performed the OT protocol based on running without inclination; n = 18)
Summary
High intensity and volume exercise sessions are generally used during training programs to disrupt cellular homeostasis, induce overcompensation and improve physical performance. The optimal training adaptations require adequate periods of recovery because high-load exercise sessions may lead to temporary performance decreases and acute fatigue [1]. According to Meussen and coworkers [2], FOR occurs after an increased training load and is characterized by a short-term performance decrement without severe psychological symptoms or other lasting negative symptoms. After days of recovery, FOR eventually leads to an improvement in performance. Athletes who do not respect this recovery period may experience NFOR, a performance decrement that may be reversed after weeks or months of recovery and may be related to psychological and hormonal disturbances. Pereira et al [3] verified that mice subjected to an eightweek overtraining (OT) protocol based on eccentric exercise (EE) presented NFOR and increased the protein levels of interleukin–6 (IL–6), myostatin and tumor necrosis factor-alpha (TNF-alpha) in skeletal muscle samples as well as serum levels of IL–6 [4]
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