Potential Impact of Nutrition on Immune System Recovery from Heavy Exertion: A Metabolomics Perspective

Abstract

This review describes effective and ineffective immunonutrition support strategies for the athlete, with a focus on the benefits of carbohydrates and polyphenols as determined from metabolomics-based procedures. Athletes experience regular cycles of physiological stress accompanied by transient inflammation, oxidative stress, and immune perturbations, and there are increasing data indicating that these are sensitive to nutritional influences. The most effective nutritional countermeasures, especially when considered from a metabolomics perspective, include acute and chronic increases in dietary carbohydrate and polyphenols. Carbohydrate supplementation reduces post-exercise stress hormone levels, inflammation, and fatty acid mobilization and oxidation. Ingestion of fruits high in carbohydrates, polyphenols, and metabolites effectively supports performance, with added benefits including enhancement of oxidative and anti-viral capacity through fruit metabolites, and increased plasma levels of gut-derived phenolics. Metabolomics and lipidomics data indicate that intensive and prolonged exercise is associated with extensive lipid mobilization and oxidation, including many components of the linoleic acid conversion pathway and related oxidized derivatives called oxylipins. Many of the oxylipins are elevated with increased adiposity, and although low in resting athletes, rise to high levels during recovery. Future targeted lipidomics-based studies will help discover whether n-3-polyunsaturated fatty acid (n-3-PUFA) supplementation enhances inflammation resolution in athletes post-exercise.

Keywords: immune function; immunometabolism; immunonutrition; metabolomics; sports nutrition.

Figure 1

Depiction of the path towards overreaching and the overtraining syndrome compared to performance enhancement.

Figure 2

Comparison of the immune responses to a marathon race and a walking bout. (DTH = delayed-type hypersensitivity; NK = natural killer; OB = oxidative burst activity; Ne/Ly = ratio of neutrophil to lymphocyte cell counts, a marker of exercise-induced inflammation).

Figure 3

Model linking carbohydrate ingestion with attenuated inflammation and enhanced recovery from metabolic perturbation.

Figure 4

Plasma gut-derived phenolics measured using metabolomics in flavonoid versus placebo groups before and after 14-days supplementation, and immediately and 14-h following a three-day period of intensified exercise. * p < 0.05 flavonoid and placebo group contrasts at time point. Data from Reference [17].

Figure 5

Comparison of banana flesh (dopamine sulfate, ferulic acid 4-sulfate) and lipid metabolites during recovery from 75-km cycling in athletes ingesting water only or water with bananas. (* Data from Reference [18]).

Figure 6

Metabolites increasing ≥5-fold in 24 runners following a treadmill run to exhaustion at 70% VO_2max. Data from Reference [21].

Figure 7

Effect of 75-km cycling on components of the linoleic acid conversion pathway and oxidized linoleic acid derivatives 9+13-HODE, 9,10 DiHOME, and 12,13 DiHOME. Data from Reference [23].

Figure 8

COX, CYP, LOX, and nonenzymatic pathways for biosynthesis of lipid mediators from arachidonic acid. COX = cyclooxygenases; LOX = lipoxygenases; HETEs = hydroxyeicosatetraenoic acids; EETs = epoxyeicosatrienoic acids; CYP = cytochrome P450; CYP4A = cytochrome P450 4A; ROS = reactive oxygen species; HODEs = hydroxyoctadecadienoic acids; DiHOMEs = dihydroxyoctadecenoic acids.

Figure 9

CYP, LOX, and nonenzymatic pathways for biosynthesis of lipid mediators from EPA and DHA.

Figure 10

Comparison of selected arachidonic acid lipid mediators in obese subjects and cyclists in the resting state, and acute responses to 75-km cycling.

Figure 11

Comparison of selected EPA lipid mediators in obese subjects and cyclists in the resting state, and acute responses to 75-km cycling.

Figure 12

Comparison of selected DHA lipid mediators in obese subjects and cyclists in the resting state, and acute responses to 75-km cycling.