Combined respiratory muscle training and photobiomodulation improve systemic and tissue-specific redox homeostasis in a rat model of type 2 diabetes

AIMS: Oxidative stress plays a central role in the pathophysiology of type 2 diabetes and contributes to multiorgan dysfunction. Non-pharmacological strategies targeting redox imbalance may provide complementary benefits beyond glycemic control. This study investigated the effects of combined respiratory muscle training (RMT) and photobiomodulation (PBM) on systemic and tissue-specific redox homeostasis in an experimental model of type 2 diabetes. METHODS: Male rats were allocated into four groups: sedentary Sham (non-diabetic), Sham submitted to RMT combined with PBM, sedentary type 2 diabetes, and type 2 diabetes submitted to the RMT/PBM protocol. Type 2 diabetes was induced by a high-fat diet associated with low-dose streptozotocin. Interventions were performed five days per week for six weeks. Hematological and biochemical parameters were evaluated. Oxidative stress was assessed by lipid peroxidation (thiobarbituric acid reactive substances) and reactive oxygen species production (dichlorofluorescein), while antioxidant defenses were determined by superoxide dismutase activity and non-protein thiol levels in plasma and multiple tissues. RESULTS: In diabetic rats, the combined RMT/PBM protocol increased mean corpuscular hemoglobin concentration, reduced leukocyte and monocyte counts, and restored plasma protein levels. Oxidative damage was attenuated in plasma, diaphragm, lungs, and kidneys, while antioxidant defenses were enhanced, particularly in the diaphragm, heart, and kidneys. In normoglycemic rats, RMT/PBM also enhanced tissue antioxidant capacity, indicating preserved redox responsiveness. CONCLUSIONS: Combined RMT and PBM promote systemic and tissue-specific redox adaptations and improve hematological and biochemical parameters in diabetic rats. These findings support the potential of this combined intervention as a non-pharmacological strategy to mitigate oxidative dysfunction associated with type 2 diabetes.