Effects of aerobic exercise on lipid-effector molecules of the innate immune response

Abstract

Introduction: Consistent, moderate-to-vigorous-intensity exercise has been associated with a lower risk of upper respiratory tract infection (URI). However, the molecular basis for this apparent protection has not yet been fully resolved. Host-derived lipids such as cholesteryl esters (CE) have emerged as important effector molecules of innate defense against infections. Here, we compared antimicrobial CE in nasal fluid before and after moderate-to-vigorous exercise between active and inactive subjects.

Methods: Nasal fluid was collected from 14 healthy, recreationally active subjects (32 ± 11 yr, 7 men and 7 women) and 14 healthy, inactive subjects (25 ± 3 yr, 7 men and 7 women) before and after treadmill exercise at 70% heart rate reserve. Nasal fluid was analyzed for lysozyme, cholesteryl linoleate (CL), cholesteryl arachidonate (CA), and albumin (Alb) concentrations.

Results: Baseline concentrations (mean ± SEM, inactive vs active) of lysozyme (117.7 ± 31.1 vs 122.9 ± 15.5 μg·mL), CL + CA (15.3 ± 1.8 vs 26.2 ± 10.05 μg·mL), and Alb (156.6 ± 54.5 vs 126.9 ± 32.8 μg·mL) were similar to previously reported levels and did not differ significantly between study groups. However, postexercise, CL + CA concentration was significantly lower in inactive compared with active subjects (7.8 ± 1.5 vs 20.1 ± 4.8 μg·mL, P = 0.036) dropping below the antimicrobial effective range. Once adjusted to Alb concentrations, the changes were no longer significant, suggesting that plasma transudation accounted for the increased CA + CL concentration postexercise in the active group relative to the inactive group.

Conclusions: Moderate-to-vigorous aerobic exercise acutely decreases the antimicrobial CE response in inactive subjects but does not modify baseline levels of CE between active and inactive subjects. This suggests that compared with active individuals, inactive individuals may be at greater risk for upper respiratory tract infection immediately postexercise.

FIGURE 1. Experimental design

URI: upper respiratory tract infection; R: right nasal cavity; L: left nasal cavity; PBS: phosphate buffered saline.

FIGURE 2. Antimicrobial cholesteryl ester concentrations in nasal fluid aspirate collected Pre (open bars) and post (patterned bars) exercise bout

CL: cholesteryl linoleate; CA: cholesteryl arachidonate. * p = 0.036 in univariate ANOVA for post inactive versus post active. Shown are means ±SEM, n =10 for inactive and n = 12 for active subjects.

FIGURE 3. Change of nasal fluid aspirate volume collected pre (open bars) and post (patterned bars) exercise bout

* p = 0.001 in repeated measures analysis for pre versus post in both, inactive and active subjects. Shown are means ±SEM, n =10 for inactive and n = 12 for active subjects.

FIGURE 4. Antimicrobial cholesteryl esters in nasal fluid aspirate collected pre (open bars) and post (patterned bars) exercise bout after adjustment to albumin

CL: cholesteryl linoleate; CA: cholesteryl arachidonate. Shown are means ±SEM, n =10 for inactive and n = 12 for active subjects.