Is Physical Activity an Efficient Strategy to Control the Adverse Effects of Persistent Organic Pollutants in the Context of Obesity? A Narrative Review

Abstract

Obesity affects nearly 660 million adults worldwide and is known for its many comorbidities. Although the phenomenon of obesity is not fully understood, science regularly reveals new determinants of this pathology. Among them, persistent organic pollutants (POPs) have been recently highlighted. Mainly lipophilic, POPs are normally stored in adipose tissue and can lead to adverse metabolic effects when released into the bloodstream. The main objective of this narrative review is to discuss the different pathways by which physical activity may counteract POPs' adverse effects. The research that we carried out seems to indicate that physical activity could positively influence several pathways negatively influenced by POPs, such as insulin resistance, inflammation, lipid accumulation, adipogenesis, and gut microbiota dysbiosis, that are associated with the development of obesity. This review also indicates how, through the controlled mobilization of POPs, physical activity could be a valuable approach to reduce the concentration of POPs in the bloodstream. These findings suggest that physical activity should be used to counteract the adverse effects of POPs. However, future studies should accurately assess its impact in specific situations such as bariatric surgery, where weight loss promotes POPs' blood release.

Keywords: adipogenesis; adipose tissue; bariatric surgery; endocrine disruptors; inflammation; insulin resistance; lipid; microbiota.

Figure 1

Potential interactions between POPs and PA on insulin sensitivity. Numerous mechanisms interact to ensure stable insulin sensitivity. However, POPs can disrupt these mechanisms (red arrows), and conversely, PA could limit their disruption (green arrows). However, these results are based on studies that did not directly compare exposure to POPs and the practice of PA. There is therefore a lack of knowledge about the level of protection that PA can provide following exposure to POPs (yellow question marks).

Figure 2

Potential mechanisms showing how physical activity (PA) may counteract the adverse effects of persistent organic pollutants (POPs) in the context of obesity. These different factors may interact with each other by direct or indirect mechanisms. With its positive impact on insulin function, lipid accumulation, adipogenesis, inflammation, and gut microbiota, PA can counteract a large variety of alterations caused by POPs. By increasing or improving physiological mechanisms such as sweat, urine, biotransformation, and biliary clearance, PA may reduce POP blood concentrations. The effects of POPs and PA can be modulated by the environment and inter-individual differences. The scheme is only an analytical summary of the isolated effects of POPs, and its validity needs to be confirmed in the case of POP cocktails or for different concentrations. Red box (global POPs’ potential negative influence), green box (global PA potential positive influence). Red arrows (potential adverse effects of POPs), green arrows (potential protective effects of PA). AhR (aryl hydrocarbon receptor), AI cytokines (anti-inflammatory cytokines), Akt (or Protein Kinase B (PKB)), AMPK (AMP-activated protein kinase), Ao-enzymes (antioxidant enzymes), C/EBPα (CCAAT enhancer-binding protein alpha), C/EBPβ (CCAAT enhancer-binding protein beta), C/EBPδ (CCAAT enhancer-binding protein delta), CRP (C-reactive protein), FABP (fatty acid-binding protein), FAS (fatty acid synthase), GLUT4 (glucose transporter type 4), IL-1β (interleukin 1 beta), IR (insulin receptor), IRS (insulin receptor substrate), JNK (Jun N-terminal kinase), lipid management (includes alterations of lipolysis, thermogenic function, triglyceride synthesis, β-oxidation, and lipid export), M respiration (mitochondrial respiration), NF-κB (nuclear factor-kappa B), PA (physical activity), PI3K (phosphoinositide 3-kinase), POPs (persistent organic pollutants), PPARγ (peroxisome proliferator-activated receptor gamma), PI cytokines (proinflammatory cytokines), PTEN (phosphatase and TENsin homolog), ROS (reactive oxygen species), SREBP-1 (sterol regulatory element-binding protein-1), TNFα (tumor necrosis factor), TYK-2/STAT-3 pathway (tyrosine kinase 2/signaling transducer and activator of transcription 3 pathway).

Figure 3

Potential effects of PA and POPs post-bariatric surgery. Green arrows (potential beneficial effects of PA post bariatric surgery), Red arrows (potential adverse effects of POPs post bariatric surgery).

Figure 4

The possible relationships between bariatric surgery, persistent organic pollutants (POPs), and physical activity (PA). Physical activity as well as bariatric surgery can promote POPs’ adipose tissue degradation, resulting in an increase in several determinants of POPs’ hazards. The balance between POPs’ release following adipose tissue degradation and POPs’ excretion/transformation may depend on the physical activity modality (aerobic vs. resistance training). Minus and plus signs in green (potential beneficial effects post bariatric surgery), Plus sign in red (potential adverse effects post bariatric surgery).

Figure 5

The hypothetical adverse consequences of using aerobic training shortly after bariatric surgery. Aerobic training used shortly after bariatric surgery may increase lipolysis and POPs’ release into the blood.

Figure 6

Hypothetical utilization of resistance training and aerobic exercise following bariatric surgery to protect the individual from POPs’ blood release.