The Athlete Paradox: Why Do Elite Athletes Appear to Suffer More From COVID/Spike Protein Exposure?

High-intensity exercise may disturb the ROS/NO balance leading to diminished endothelial function.

Production of nitric oxide (NO) and reactive oxygen species (ROS) in response to different exercise intensities. During mild-intensity exercise, NO and ROS are constant, resulting in no change in endothelial function. Production of NO and that of ROS are greater during moderate-intensity exercise than during mild-intensity exercise. During moderate-intensity exercise, production of NO is greater than production of ROS, resulting in augmentation of endothelial function. Production of NO and that of ROS are greater during high-intensity exercise than during moderate-intensity exercise. During high-intensity exercise, production of ROS is greater than production of NO, resulting in diminished endothelial function. 

It has long puzzled many of us. What SHOULD be protecting us from COVID and the Spike Protein, a healthy lifestyle, diet and exercise, seems to fail those who are elite athletes. I decided to investigate this counterintuitive phenomenon and am now able to offer an explanation. In short, it is because of too much of a good thing. 

We have well established that COVID/Spike Protein Disease is, at its core, and endothelial disease. Indeed, I have called what the Spike Protein does to the endothelieum SPED (Spike Protein Endothelial Disease). There is much evidence for this. 

This essay explores the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease. Cytokines, protein pro-inflammatory mediators, serve as key danger signals that shift endothelial functions from the homeostatic into the defensive mode. The endgame of COVID-19 usually involves a cytokine storm, a phlogistic phenomenon fed by well-understood positive feedback loops that govern cytokine production and overwhelm counter-regulatory mechanisms. The concept of COVID-19 as an endothelial disease provides a unifying pathophysiological picture of this raging infection, and also provides a framework for a rational treatment strategy at a time when we possess an indeed modest evidence base to guide our therapeutic attempts to confront this novel pandemic. 

COVID-19 is, in the end, an endothelial disease 
https://academic.oup.com/eurheartj/article/41/32/3038/5901158 

Among the direct effects, the role of the spike protein on endothelial cell activation is emerging as a potent, noninfectious mechanism that underlies endotheliitis in COVID-19. An ever-increasing number of studies demonstrate that the spike protein of SARS-CoV-2 directly induces the activation of proinflammatory and prothrombogenic pathways in endothelial cells, leading to multiple instances of endothelial injury. 

SARS-CoV-2 and the spike protein in endotheliopathy 
https://www.cell.com/trends/microbiology/fulltext/S0966-842X(23)00189-0 

After much research, I have concluded that there is a concrete reason why elite athletes may suffer more from COVID and Spike Protein exposure than a physically average indivudual. The repetitive, high-intensity exercise that elite athletes partake in reduces their endothelial function. This allows the virus and its proteins a more vigorous, and somtimes deadly attack on multiple organs. The mechanism is as follows: 

We have shown that a 12-week period of exercise of high-intensity increases the indices of oxidative stress, including plasma concentration of 8-hydroxy-2′-deoxyguanosine and serum concentration of malondialdehyde-modified low-density lipoprotein, and decreased endothelium-dependent vasodilation in forearm circulation in healthy men.20 Davies et al.21 reported that the massive increase in oxygen uptake that occurs in skeletal muscle during exercise is associated with an increase in ROS. These findings suggest that high-intensity exercise increases oxidative stress in humans. Therefore, it is thought that increased oxidative stress induced by high-intensity exercise diminishes endothelium-dependent vasodilation in humans. 

Exercise is a double-edged sword for endothelial function 
https://www.nature.com/articles/hr2015127 

A similar finding was found in female athletes. 

We concluded that young female track and field athletes subjected to physical training developed impairment of endothelial function that was associated with anabolic-catabolic hormone balance disturbances. Given that training-induced impairment of endothelial function may have a detrimental effects on vascular health, endothelial status should be regularly monitored in the time-course of training process to minimalize vascular health-risk in athletes. 

Training-induced impairment of endothelial function in track and field female athletes 
https://www.nature.com/articles/s41598-023-30165-2 

So, we now have a satisfactory explanation as to why some elite athletes are experiencing severe effects from COVID and Spike Protein exposure. Exercise is a good thing and moderate amounts DO protect our endothelium. However, to combat this elite athlete exception, it may be that elite athletes should refrain from extreme (any?) physical activity if they are infected with COVID or have been exposed to the Spike Protein. I will continue to research therapeutics. 

Thank you, as always, for your readership, dialog and support.