RESUMO
Obesity has a complex multifactorial etiology and is characterized by excessive accumulation of adipose tissue. Visceral adipose tissue has deleterious effects on health because it secretes large amounts of inflammatory cytokines. Nutritional calorie restriction associated with strength training may be useful in managing chronic systemic inflammation. This study aimed to evaluate the acute effect of a single strength-training session on plasma adipokine levels in sedentary, overweight, and obese young men. This study included twelve men (Age: [34.95 â± â9.77] years; Height: [174.16 â± â3.66] centimeter [cm]; Weight: [97.83 â± â12.87] kilogram (kg); body mass index [BMI]: [32.30 â± â4.51] kg/m2), who performed a single strength training session. The strength training protocol consisted of 4 sets of 12 repetitions in the following six exercises, 45° leg press, bench press, leg extension, machine row, leg curl, and shoulder press. Blood samples were collected before, immediately after, and 1-h subsequent after strength training. The plasma levels of resistin and leptin were measured. A significant decrease in resistin levels were found 1 âh after the strength training session if compared to levels before the training session (pre-[before] [2 390 â± â1 199] picograms per milliliter [pg/mL] vs post-1 h [1-h subsequent] [1 523 â± â798],6 âpg/mL, p â= â0.002 8). The plasma leptin levels did not differ at any time point. In conclusion, a very well controlled single session of strength training significantly decreased the plasma levels of resistin without altering the concentration of leptin in overweight and obese individuals. This effect, at least in part, supports the benefits of exercise by reducing the low grade inflammation and insulin resistance in obesity.
RESUMO
AIMS: The renin-angiotensin system (RAS) is a dual system with two opposite arms: i) the classical one formed by the angiotensin converting enzyme (ACE), angiotensin (Ang) II and angiotensin type 1 (AT1) receptors; ii) the counter-regulatory arm consisting of ACE2, Ang-(1-7) and Mas receptor. Physical exercise can modulate this system, however, only animal studies have compared the effects of different intensity protocols on the RAS. No data with humans were provided. Therefore, we investigated the acute effect of two protocols of isowork aerobic exercise [High-Intensity Interval Exercise (HIIE) and Moderate-Intensity Continuous Exercise (MICE)] in plasma and urinary levels of RAS components in physically active men. MAIN METHODS: The HIIE protocol included a 5-minute warm-up cycling at 60-70% of heart rate peak (HRp) intensity followed by 10 sets of 30 s above 90% with 1 min of recovery and 3 min of cool down. The MICE protocol was performed at a constant power corresponding to 60-70% of HRp and finalized at the same total work of HIIE. Blood and urine samples were collected before and after the protocols. Plasma and urinary levels of ACE, ACE2, Ang-(1-7) and Ang II were analyzed by enzyme-linked immunoassay. KEY FINDINGS: While the HIIE protocol significantly increased urinary levels of ACE and plasma levels of ACE2, the MICE protocol elevated urinary concentrations of ACE2 and of Ang-(1-7). A greater increase of urine concentrations of Ang-(1-7) occurred in the MICE if compared with the HIIE protocol. SIGNIFICANCE: Aerobic physical exercise acutely increases the activity of the counter-regulatory RAS axis, mostly the MICE protocol.