**1. Background**

The term oxidative stress is defined as a disturbance in the homeostatic balance between pro-oxidants and antioxidants with a subsequent excessive generation of free radicals [1–3]. Free radicals are highly reactive compounds that contain one or more unpaired electrons in their outer atomic or molecular orbital [1,4], and thus readily react with various organic substrates in order to make themselves more stable [3]. Species derived from oxygen are generally referred to as reactive oxygen species (ROS) and are naturally occurring byproducts of the human metabolism. Thereby, redox reactions represent fundamental components of organic and biological chemistry [5]. While low to moderate ROS concentrations seem to be involved in cell signaling and muscle remodulation [5–7], prolonged exposure to high doses of ROS induces oxidative damage [3]. In case of an insufficient ROS scavenging by antioxidants, high ROS concentrations can lead to modification and damage of cellular molecules including deoxyribonucleic acid (DNA), proteins or lipids [2]. Previous studies have also shown that oxidative stress is involved in the pathophysiology of a wide range of chronic diseases including cancer [5,8], cardiovascular [3,9] and neurological diseases [10–13].

**Citation:** Zeng, Z.; Centner, C.; Gollhofer, A.; König, D. Effects of Dietary Strategies on Exercise-Induced Oxidative Stress: A Narrative Review of Human Studies. *Antioxidants* **2021**, *10*, 542. https:// doi.org/10.3390/antiox10040542

Academic Editor: Gareth Davison

Received: 16 March 2021 Accepted: 29 March 2021 Published: 31 March 2021

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**Copyright:** © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).

During exercise, the amount of generated ROS seems to be intensity-dependent, with higher exercise intensities leading to supraphysiological ROS formations [14,15]. Mitochondrial hormesis (mitohormesis) was proposed to describe that sublethal mitochondrial stress can trigger a favorable cellular response, resulting in an improved mitochondrial and nonmitochondrial adaptation, and thus maintain redox homeostasis [16] (Figure 1). As depicted in Figure 1, high-intensity exercise might induce mitochondrial stress, leading the mitochondria to emit ROS in order to facilitate adaptations and thus protect against subsequent cellular stress [17]. In case of excessive ROS production, this might lead to oxidative damage.

**Figure 1.** The mitohormesis-based model to explain the effects of dietary strategies on exerciseinduced oxidative stress. ROS = reactive oxygen species.

From another perspective, aerobic exercise has been suggested to be beneficial in ROS-associated diseases, including cardiovascular pathologies [18]. Previous studies have demonstrated that regular and moderate exercise can enhance endothelia function by increasing the bioavailability of NO and improving redox states in subjects with preexisting cardiovascular risk factors or diseases [19,20]. Nevertheless, a few studies also revealed conflicting results by showing that intense aerobic exercise could injure endothelia cells [21,22]. These results might be explained by the different exercise intensities and the resulting varying levels of oxidative damage.

As a potential countermeasure against excessive oxidative stress during exercise, antioxidative supplementations, which aim to protect against muscle damage and thus improve exercise performance, have been frequently discussed [4,22]. Nonetheless, many studies have indicated that large-dose antioxidant supplementation can interfere with intrinsic adaptive responses and may abolish the benefit of exercise [23,24]. These highly purified antioxidants can negatively affect ROS-mediated physiological processes through prooxidant mechanisms [22]. In a previously published meta-analysis, Stepanyan et al. [25] demonstrated that supplementation with vitamin E did not protect against exercise-induced lipid peroxidation or muscle damage. Instead of single antioxidative sources, it might be speculated that the intake of natural foods rich in antioxidants of phytochemicals (e.g., fruits and vegetables) might represent a more beneficial approach for enhancing the antioxidant status during exercise [26]. Along with their high antioxidant content, specific diets, including products such as oatmeal, dark chocolate, and mixed fruit beverages may also contain additional bioactive compounds which are not found in single-dose pharmacological antioxidant supplements but can act synergistically to reveal more beneficial effects than a single dose of antioxidant supplements [27,28]. Additionally, these compounds are more accessible than specific isolated antioxidants. Until now, few studies have investigated the clinical effects on exercise-induced oxidative stress by using a whole dietary strategy and consistent evidence from human study remains scarce.
