Attenuated fibroblast growth factor 21 response to acute aerobic exercise in obese individuals.

BACKGROUND AND AIM: Fibroblast growth factor 21 (FGF21) is positively associated with body mass index, potentially as a compensatory mechanism to mediate obesity related metabolic and inflammatory insult due to chronic low-grade elevations of the pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α). Therefore, FGF21 response in obese subjects and the associations with increased pro-inflammatory cytokines, insulin resistance, and energy utilization warrants investigation. METHODS AND RESULTS: Twenty four untrained subjects (12 obese and 12 normal-weight) performed 30 min of continuous submaximal aerobic exercise. Following exercise, obese subjects exhibited a blunted FGF21 response to exercise compared to normal-weight subjects as indicated by area-under-the-curves "with respect to increase" (AUCi) analyses (p = 0.005). Furthermore, while exercise-induced plasma FGF21 was not associated with any inflammatory cytokine (IL-6 and TNF-α) response, FGF21 AUCi was positively correlated with glucose AUCi (r = 0.495, p = 0.014), total relative energy expenditure (r = 0.562, p = 0.004), and relative maximal oxygen consumption (VO2max; r = 0.646, p = 0.001) in all subjects. CONCLUSION: Impaired cardiorespiratory fitness may influence the sensitivity of FGF21 response to acute exercise in obese individuals, potentially contributing to the attenuated metabolic response (e.g., glucose) and total exercise energy expenditure. Therefore, exercise training aimed at improving cardiorespiratory fitness and/or body composition may augment cardioprotective properties against obesity-associated CVD through enhanced FGF21 flux.

Brain-derived neurotrophic factor and substrate utilization following acute aerobic exercise in obese individuals.

Brain-derived neurotrophic factor (BDNF) serves as a vital regulator of neuronal proliferation and survival, and has been shown to regulate energy homeostasis, glucose metabolism and body weight maintenance. Elevated concentrations of plasma BDNF have been associated with obesity and type 2 diabetes mellitus. Acute aerobic exercise transiently increases circulating BDNF, potentially correcting obesity-related metabolic impairment. The present study aimed to compare acute aerobic exercise elicited BDNF responses in obese and normal-weight subjects. Furthermore, we aimed to investigate whether acute exercise-induced plasma BDNF elevations would be associated with improved indices of insulin resistance, as well as substrate utilization [carbohydrate oxidation (CHOoxi) and fat oxidation (FAToxi)]. Twenty-two healthy, untrained subjects [11 obese (four men and seven women; age = 22.91 ± 4.44 years; body mass index = 35.72 ± 4.17 kg/m(2)) and 11 normal-weight (five men and six women; age = 23.27 ± 2.24 years; body mass index = 21.89 ± 1.63 kg/m(2))] performed 30 min of continuous submaximal aerobic exercise at 75% maximal oxygen consumption. Our analyses showed that the BDNF response to acute aerobic exercise was similar in obese and normal-weight subjects across time (time: P = 0.015; group: P = not significant) and was not associated with indices of IR. Although no differences in the rates of CHOoxi and FAToxi were found between both groups, total relative energy expenditure was significantly lower in obese subjects compared to normal-weight subjects (3.53 ± 0.25 versus 5.59 ± 0.85; P < 0.001). These findings suggest that acute exercise-elicited BDNF elevation may not be sufficient to modulate indices of IR or the utilization of either carbohydrates or fats in obese individuals.