Abstract
We investigated whether an acute bout of moderate intensity exercise in the postprandial period attenuates the triglyceride and airway inflammatory response to a high-fat meal (HFM) compared to remaining inactive in the postprandial period. Seventeen (11 M/6 F) physically active (≥150 min/week of moderate-vigorous physical activity (MVPA)) subjects were randomly assigned to an exercise (EX; 60% VO2peak) or sedentary (CON) condition after a HFM (10 kcal/kg, 63% fat). Blood analytes and airway inflammation via exhaled nitric oxide (eNO) were measured at baseline, and 2 and 4 hours after HFM. Airway inflammation was assessed with induced sputum and cell differentials at baseline and 4 hours after HFM. Triglycerides doubled in the postprandial period (~113 ± 18%, P < 0.05), but the increase did not differ between EX and CON. Percentage of neutrophils was increased 4 hours after HFM (~17%), but the increase did not differ between EX and CON. Exhaled nitric oxide changed nonlinearly from baseline to 2 and 4 hours after HFM (P < 0.05, η 2 = 0.36). Our findings suggest that, in active individuals, an acute bout of moderate intensity exercise does not attenuate the triglyceride or airway inflammatory response to a high-fat meal.
Highlights
The prevalence of asthma has been on the rise, in obese individuals [1]
Recent studies confirm that saturated fatty acids activate macrophages in this signal transduction pathway via nuclear factor kappa B (NFκB), increasing the cytokines IL-8, IL6, and TNF-α from the airway cells as well as increasing the presence of pulmonary neutrophils [3]
Fat induced activation of NFκB occurs due to circulating nonesterified fatty acids (NEFA), as well as reactive oxygen species (ROS) [4]
Summary
The prevalence of asthma has been on the rise, in obese individuals [1]. T helper type 2 (TH2) activation causes airway eosinophilia in an acquired immune response via the JAK/STAT/Raf-1 signal transduction pathway [2]. Recent studies confirm that saturated fatty acids activate macrophages in this signal transduction pathway via nuclear factor kappa B (NFκB), increasing the cytokines IL-8, IL6, and TNF-α from the airway cells as well as increasing the presence of pulmonary neutrophils [3]. Toll-like receptor-4 (TLR4) can be activated by fatty acids and can activate NFκB [5] This inflammatory cascade results in an increase in inflammation in the airway via neutrophil influx and activation [6]. The burden of eosinophilic and neutrophilic inflammation present in asthma is reactive oxygen species (ROS) production and subsequent oxidative stress
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