TIME COURSE CARDIOVASCULAR AND NEUROIMMUNE DYSFUNCTIONS IN A METABOLIC SYNDROME MODEL: IMPACT OF AEROBIC TRAINING

Abstract

This study analyzed the effects of aerobic exercise training (ET) in the time course of the dysfunctions observed in metabolic syndrome model (SHR + fructose overload). Animals were randomly distributed into two groups: hypertensive + fructose (HF) and hypertensive + fructose + ET (HFT). The fructose overload (100g/l) and the ET (treadmill 1h/d, 5d/wk) was initiated at 30 days of life, and the animals (n=6/group/time) were evaluated after 7, 15, 30 and 60 days. The ET (HFT group) induced an increase in baroreflex sensitivity for bradycardic response at 7 (100%), 15 (86%), 30 (76%) and 60 (74%) days of protocol and for tachycardia response (TR) in 7 (34%), 15 (31%) and 30 (49%) days of protocol as compared to sedentary group (HF). However, the ET did not attenuate the impairment in TR at 60 days of protocol. There was a reduction in the relation of TNF‐a/IL‐10 in fat tissue (40%) and IL‐1β in the spleen (30%) in the HFT group when compared to the HF group in 15 days of protocol. The nitrites in plasma were increased in HFT group as compared to HF group at 7 and 15 days of protocol. Regarding oxidative stress in plasma at 60 days of protocol, there was an increase in SOD activity (74%) and a decrease in lipid peroxidation (46%) and in protein oxidation (60%) in the HFT group when compared to the HF group. The ET reduced blood glucose (15%) and increased insulin sensitivity (31%) at the end of the protocol, although it did not alter blood triglycerides or blood pressure. Fructose consumption increased NFkB and p47 phox protein expression at day 60. However, aerobic exercise training was able to reduce NFkB at day 30 and 60, and p47 phox at day 60. In conclusion, the hemodynamic, autonomic, inflammatory and oxidative stress disorders seem to be time dependent in SHR with fructose overload. On the other hand, aerobic ET is effective in attenuate disorders in this model of metabolic syndrome.Support or Funding InformationFAPESP: 2018/17183‐4