Positive effects of total recovery period on anti- and pro-inflammatory cytokines are not linked to performance re-establishment in overtrained mice

Rocha, Aristides Almeida; Pinto, Ana P.; Pereira, Bruno; Kohama, Eike B.; Morais, Gustavo P.; Vicente, Larissa G. de; Pauli, José Rodrigo; Cintra, Dennys Esper; Ropelle, Eduardo R.; Moura, Leandro Pereira de; Filho, Hugo Tourinho; Silva, Adelino Sánchez Ramos da

doi:10.1016/j.cyto.2018.01.005

Cited by 3 publications

(2 citation statements)

References 25 publications

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“…Carmichael et al 17 demonstrated that intracerebroventricular (ICV) injections of IL‐1β decreased the time to exhaustion and wheel‐running activity 17 . Although the present study did not evaluate interleukins in the brain tissue or serum, previous investigations using the same downhill running‐based overtraining protocol described an increase in these proinflammatory cytokines 4,16,18,19 …”

Section: Discussionmentioning

confidence: 55%

“…17 Although the present study did not evaluate interleukins in the brain tissue or serum, previous investigations using the same downhill running-based overtraining protocol described an increase in these proinflammatory cytokines. 4,16,18,19 The OT/Rapa group had higher glucose at two times (before and after the ILT test). In contrast, the OT and AER groups had lower glucose, corroborating a previous study.…”

Section: Discussionmentioning

confidence: 92%

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Chronic rapamycin treatment decreases hepatic IL‐6 protein, but increases autophagy markers as a protective effect against the overtraining‐induced tissue damage

Pinto

Rocha

Marafon

et al. 2022

Clin Exp Pharma Physio

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Regular endurance exercise is a non‐pharmacological strategy to protect the liver against diseases. Conversely, exercise may be harmful when excessive, the so‐called overtraining. As expected, mice who underwent an overtraining protocol presented higher levels of proinflammatory cytokines in the serum and liver. Based on the relationship among overtraining, inflammation and mammalian target of rapamycin complex 1 (mTORC1) upregulation, the present study verified if animals submitted to an overtraining protocol, but with inhibition of the mTOR pathway via rapamycin injections could mitigate the liver and serum inflammation. Once autophagy can be linked to the improvement of hepatic dysfunction, we also investigated if the inhibition of mTORC1 by rapamycin can improve hepatic autophagy. The animals were randomized into four groups: control (CT; sedentary mice), overtraining by downhill running (OT; mice submitted to the downhill running‐based overtraining protocol), overtraining by downhill running with chronic administration of rapamycin (OT/Rapa; mice submitted to the downhill running‐based overtraining protocol with intraperitoneal injections of rapamycin) and aerobic (AER; submitted to aerobic training protocol). The serum and liver of the animals were used for biochemical analysis, reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR) and immunoblotting. The main results are (a) OT and OT/Rapa protocols decreased the performance; (b) the protein levels of interleukin 6 (IL‐6) were higher for the OT group; the OT/Rapa group reduced the autophagic genes, increased the microtubule‐associated protein light chain 3 II/I (LC3II/LC3I) protein ratio and decreased the sequestosome 1 (SQSTM1) protein. In conclusion, rapamycin appears efficiently to increase the autophagy proteins and decrease IL‐6 protein in the liver of overtraining mice.

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 92%

Chronic rapamycin treatment decreases hepatic IL‐6 protein, but increases autophagy markers as a protective effect against the overtraining‐induced tissue damage

Pinto

Rocha

Marafon

et al. 2022

Clin Exp Pharma Physio

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The proinflammatory effects of chronic excessive exercise

et al. 2019

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Pathophysiology of exercise-induced muscle damage and its structural, functional, metabolic, and clinical consequences

Stožer¹,

Vodopivc²,

Bombek

2020

Physiol Res

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Extreme or unaccustomed eccentric exercise can cause exercise-induced muscle damage, characterized by structural changes involving sarcomere, cytoskeletal, and membrane damage, with an increased permeability of sarcolemma for proteins. From a functional point of view, disrupted force transmission, altered calcium homeostasis, disruption of excitation-contraction coupling, as well as metabolic changes bring about loss of strength. Importantly, the trauma also invokes an inflammatory response and clinically presents itself by swelling, decreased range of motion, increased passive tension, soreness, and a transient decrease in insulin sensitivity. While being damaging and influencing heavily the ability to perform repeated bouts of exercise, changes produced by exercise-induced muscle damage seem to play a crucial role in myofibrillar adaptation. Additionally, eccentric exercise yields greater hypertrophy than isometric or concentric contractions and requires less in terms of metabolic energy and cardiovascular stress, making it especially suitable for the elderly and people with chronic diseases. This review focuses on our current knowledge of the mechanisms underlying exercise-induced muscle damage, their dependence on genetic background, as well as their consequences at the structural, functional, metabolic, and clinical level. A comprehensive understanding of these is a prerequisite for proper inclusion of eccentric training in health promotion, rehabilitation, and performance enhancement.

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Positive effects of total recovery period on anti- and pro-inflammatory cytokines are not linked to performance re-establishment in overtrained mice

Cited by 3 publications

References 25 publications

Chronic rapamycin treatment decreases hepatic IL‐6 protein, but increases autophagy markers as a protective effect against the overtraining‐induced tissue damage

Chronic rapamycin treatment decreases hepatic IL‐6 protein, but increases autophagy markers as a protective effect against the overtraining‐induced tissue damage

The proinflammatory effects of chronic excessive exercise

Pathophysiology of exercise-induced muscle damage and its structural, functional, metabolic, and clinical consequences

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