Isolated obesity resistance condition or associated with aerobic exercise training does not promote cardiac impairment

Abstract

Mechanisms involved in cardiac function and calcium (Ca 2+ ) handling in obese-resistant (OR) rats are still poorly determined. We tested the hypothesis that unsaturated high-fat diet (HFD) promotes myocardial dysfunction in OR rats, which it is related to Ca 2+ handling. In addition, we questioned whether exercise training (ET) becomes a therapeutic strategy. Male Wistar rats (n=80) were randomized to standard or HFD diets for 20 weeks. The rats were redistributed for the absence or presence of ET and OR: control (C; n=12), control + ET (CET; n=14), obese-resistant (OR; n=9), and obese-resistant + ET (ORET; n=10). Trained rats were subjected to aerobic training protocol with progressive intensity (55-70% of the maximum running speed) and duration (15 to 60 min/day) for 12 weeks. Nutritional, metabolic, and cardiovascular parameters were determined. Cardiac function and Ca 2+ handling tests were performed in isolated left ventricle (LV) papillary muscle. OR rats showed cardiac atrophy with reduced collagen levels, but there was myocardial dysfunction. ET was efficient in improving most parameters of body composition. However, the mechanical properties and Ca 2+ handling from isolated papillary muscle were similar among groups. Aerobic ET does not promote morphological and cardiac functional adaptation under the condition of OR.

Resistance to obesity prevents obesity development without increasing spontaneous physical activity and not directly related to greater metabolic and oxidative capacity

“…In addition to the incredible ability to resist the development of obesity, the OR model may have cardioprotective characteristics and protection against metabolic disorders, for example, lipotoxicity [ 1 ]. These characteristics were also observed in the current study, in which OR rats showed maintenance of glycemic control, normal insulin and improvement in the lipid profile evidenced by normal glycemic values during the glucose tolerance test and higher HDL values, indicating a probable cardioprotection.…”

“…In the study by Kleiner et al [ 38 ], using transgenic mice knockouts for PPARγ co-activator and gene transcription co-activator 1α (PGC1α), an important co-activator of mitochondrial biogenesis, demonstrate reduced oxidative capacity and insulin resistance [ 38 ]. As mentioned above, this seems to be one of the responses for the protective capacity of OR animals against the development of metabolic and cardiometabolic disorders [ 1 ].…”

“…Blood samples were collected at time 0, considered baseline condition, and after 30, 60, 90 and 120 minutes of glucose administration. Glucose tolerance in these animals was assessed by the area under the curve for glucose [ 1 ].…”

“…The BW was measured weekly, and the amount of body fat was determined by the sum of epididymal, retroperitoneal and visceral (mesenteric fat) fat deposits. AI was calculated by dividing the total body fat by the final body weight, multiplied by 100, as applied in the study by Cordeiro et al [ 1 ].…”

“…Resistance to Obesity (OR) is a growing research topic in the scientific community with a considerable increase in the number of publications in recent years [ 1 – 3 ]. However, the etiology of OR is still unknown in the literature, since its characterization was described more than three decades ago.…”