Slusher, Aaron L.

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.

Obesity is associated with elevated levels of the pro-inflammatory cytokines
interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), contributing to systemic
insulin resistance. Fibroblast growth factor 21 (FGF21) is a vital metabolic and
inflammatory regulator, however circulating FGF21 concentrations are elevated in obese
individuals. Acute aerobic exercise increases systemic FGF21 in normal-weight
individuals, however the effect of acute aerobic exercise on plasma FGF21 response and
the relationships with inflammation (IL-6 and TNF-α), insulin resistance, and energy
expenditure in obese individuals is unknown. Following 30 minutes of treadmill running
at 75% VO2max, plasma FGF21 response, as indicated by area-under-the-curve “with
respect to increase” (AUCi) analyses, was attenuated in 12 obese compared to 12 normalweight
subjects. Additionally, FGF21 AUCi positively correlated with glucose AUCi,
total relative energy expenditure, and relative VO2max, suggesting that cardiorespiratory fitness levels may predict FGF21 response, contributing to the enhanced regulation of
glucose and energy metabolism.

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.