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Eccentric exercise leads to performance decrease and insulin signaling impairment.

Bruno C Pereira1, José R Pauli, Claudio T De Souza

  • 11School of Physical Education and Sport of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, BRAZIL; 2Sport Sciences Course, Faculty of Applied Sciences, State University of Campinas, Limeira, São Paulo, BRAZIL; and 3Exercise Biochemistry and Physiology Laboratory Postgraduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciuma, Santa Catarina, BRAZIL.

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Summary
This summary is machine-generated.

Overtraining using eccentric exercise impairs insulin signaling in mouse skeletal muscle, increasing inflammatory markers like IKK, SAPK/JNK, and SOCS3. This suggests overtraining negatively affects muscle adaptation and metabolic function.

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Area of Science:

  • Exercise Physiology
  • Molecular Biology
  • Biochemistry

Background:

  • Overtraining syndrome (OTS) is a complex condition affecting athletes, characterized by decreased performance and physiological maladaptations.
  • Eccentric exercise (EE) places unique stress on muscle fibers, potentially influencing metabolic and inflammatory pathways differently than concentric or isometric contractions.
  • Understanding the molecular mechanisms underlying OTS is crucial for developing effective prevention and recovery strategies.

Purpose of the Study:

  • To investigate the impact of an overtraining (OT) protocol, specifically utilizing eccentric exercise (EE) sessions, on insulin and inflammatory signaling pathways.
  • To analyze the protein expression and phosphorylation status of key molecules involved in insulin sensitivity and inflammation within skeletal muscles of mice subjected to OT.
  • To elucidate the molecular consequences of EE-induced overtraining on muscle adaptation.

Main Methods:

  • Swiss mice were allocated into three groups: control (sedentary), trained (aerobic protocol), and overtrained (OT protocol).
  • Performance was assessed using incremental load and exhaustive tests before and after the 8-week exercise interventions.
  • Skeletal muscles (extensor digitorum longus and soleus) were collected post-exercise for protein analysis via immunoblotting to quantify signaling pathway components.

Main Results:

  • Overtraining significantly reduced insulin receptor beta (pIRbeta) phosphorylation in both EDL and soleus muscles.
  • Insulin receptor substrate 1 (pIRS-1) and protein kinase B (pAkt) phosphorylation were decreased in overtrained mice compared to controls and trained groups.
  • Elevated levels of IκB kinase (pIKKalpha/beta), stress-activated protein kinases/Jun amino-terminal kinases (pSAPK/JNK), and suppressor of cytokine signaling 3 (SOCS3) were observed in overtrained mice.

Conclusions:

  • The eccentric exercise-based overtraining protocol negatively impacts insulin signaling pathways in mouse skeletal muscle.
  • Overtraining induced by EE leads to increased inflammatory markers, including IKK, SAPK/JNK, and SOCS3.
  • These molecular changes suggest that EE-induced overtraining impairs muscle's ability to respond to insulin and promotes an inflammatory state.