Maharaj, Arun

The purpose of this study was to determine if maximal aerobic exercise promotes
BDNF expression in obese individuals. Plasma levels and the expression of BDNF in
PBMCs were examined. 22 participants (10 obese, 12 non-obese) completed a V02max
treadmill test and blood was obtained pre, post, and 1 and 2 hours into exercise recovery.
Plasma and PBMCs were isolated and analyzed for BDNF via ELISA and Western blot
techniques. A significant effect for time was observed for plasma BDNF (P= <0.00 1 ).
Additionally, A significant group-by-time interaction was found from pre-to-RIH for
BDNF expression in PBMCs (P= 0.046). Further, significant correlations were found
between BMI and waist circumference (r= .91, P< 0.001), WHR (r= .51, P= 0.002) and
Pre-to-RlH ratio (r=0.58, P=0.008). Young obese subject's BDNF response to maximal
exercise was consistent with previous studies. Post-exercise BDNF expressed in PBMCs
were significantly higher than rest suggesting immunological-neuroprotective
interactions in the CNS.

The secular issue of obesity has been linked to increased inflammatory mediators, such as calprotectin (S100A8/A9). This study examined the effect of acute aerobic exercise on plasma calprotectin response in obese and normal-weight subjects and its relationship with inflammatory cytokine (IL-6). All subjects (11 obese and 10 normal-weight) performed 30 minutes of treadmill exercise at 75% maximal oxygen consumption (VO2max). Blood samples were collected prior to, immediately following exercise, and one hour after exercise. Our results showed higher baseline levels of calprotectin in obese subjects than normal-weight subjects. While acute aerobic exercise increased an elevation in calprotectin and IL-6, no difference was found between two groups. Furthermore, a positive relationship was observed between calprotectin area-under-the curve “with respect to increase” (AUCi) and IL-6 AUCi, even after controlling for cardiorespiratory fitness (VO2max). Our results support previous finding that IL-6 may potentially regulate calprotectin expression in skeletal muscle during exercise.

Pentraxin 3 (PTX3) has been demonstrated as a vital biomarker for chronic inflammatory diseases. Decreased plasma PTX3 has been observed in obese populations. However, no studies have examined the impact of obesity on PTX3 reactivity to exercise. Therefore, our study sought to investigate PTX3 plasma response to maximal exercise in obese and normal-weight subjects, and its relationship with insulin sensitivity. Twenty-one subjects (9 obese and 12 normal-weight) were recruited. Plasma PTX3, insulin, and glucose levels were measured before and following exercise. While our results showed lower resting PTX3 levels in obese subjects, exercise elicited similar elevations in PTX3 and insulin sensitivity in both groups. Furthermore, PTX3 area-under-curve (AUC) was correlated with glucose AUC, even when controlled for body mass index and fitness level. These findings suggest that glucose may potentially regulate PTX3 response to exercise. Further investigation is needed to verify the impact of substrate utilization on exercise-induced PTX3 elevation.