Abstract
The complexity of the adaptive response of diabetics to intense exercise is still poorly understood. To optimize exercise interventions in diabetics, the chronology of inflammatory mediators in muscle and the signaling involved in muscle hypertrophy/atrophy must be understood. Herein, we studied the kinetic inflammatory profile and cellular signaling pathways modulated by physical exhaustion after the induction of type 1 diabetes by streptozotocin in rats. Soleus muscle samples were obtained from diabetic and control groups at the following moments: baseline (no exercise); immediately after exhaustive exercise; and at 2 h, 24 h, 48 h, and 72 h after a treadmill exhaustive exercise. Kinetic production of cytokines and kinetic activation of proteins related to muscle synthesis (p70S6K and Akt) and degradation (GSK3, MuRF1, and MAFbx) were measured in the soleus muscle. We observed that the muscle TNF-α (0.9-fold; p = 0.0007), IL-1β (0.8-fold; p = 0.01), IL-6 (0.8-fold; p = 0.0013), L-selectin (1.0-fold; p = 0.0019), and CINC-2α/β (0.9-fold; p = 0.04) levels were higher in almost all stages of the study in the diabetic animals compared with the control group. Our data showed that exhaustive exercise decreased MAFbx expression in diabetic animals compared to the control group in a time-dependent manner. The decreased activation ratios of MAFbx were followed by a decrease in TNF-α, IL-1β, and IL-6 levels. p70S6k phosphorylation was also decreased in the diabetic group compared to the control group after physical exhaustion. Regarding the activation of proteins related to muscle synthesis and degradation, we found that the alterations induced by exhaustive exercise in the diabetic rats might involve pathways related to synthesis and muscle breakdown. Moreover, after an exhaustive exercise session, the recovery of the inflammatory response in the diabetic animals was slower than that in the control rats while the return of inflammatory cytokines to baseline levels was more effective in the diabetic animals.
Highlights
The benefits of exercise as adjuvant therapy in the management of all diabetes types need to be constantly emphasized
This research was the first to demonstrate the levels of tumor necrosis factor (TNF)-α, IL-6, IL-1β, L-selectin, VEGF, and cytokineinduced neutrophil chemo-attractants (CINC)-3α/β in the soleus muscle from diabetic rats before exercise, IA exhaustive exercise and at 2 h, 24 h, and 48 h after exercise
We noted that 2 h after exhaustive exercise, the diabetic animals presented elevated levels of muscle TNF-α, IL-1β, IL-6, L-selectin, and CINC
Summary
The benefits of exercise as adjuvant therapy in the management of all diabetes types need to be constantly emphasized. Data on the time required by diabetic patients or animals with streptozotocin-induced diabetes to recover without risks from exercise-induced tissue damage are lacking (Bortolon et al, 2012). Such data are important because inflammation induced by intense physical activity may be detrimental to the health and muscle structure of patients with diabetes. The hypertrophic effects of Akt are modulated partly by stimulating protein synthesis pathways downstream of GSK3β and mTOR (Schiaffino and Mammucari, 2011), whereas the muscle-specific ubiquitin ligases MAFbx and MuRF1 are important for activating muscle atrophy. Few pharmacological targets have been provided in diabetic muscle atrophy studies, and information about postexercise inflammatory management in diabetic muscle is relevant since both hypertrophy and atrophy depend on the inflammatory state generated by exercise (Schiaffino and Mammucari, 2011; Bonaldo and Sandri, 2013)
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