Abstract

Amid intense exercise, the human body’s quick adaptability to stressful conditions is vital to cellular function, initiating what we recognize as an “adrenaline rush”. Despite findings on the in vitro interaction of adrenaline with the gut microbiome to regulate its virulence gene expression through AI-3 quorum sensing, studies conducted to examine the influence of the stress hormone adrenaline released through exercise on the function of the microbiome in our gut are yet insufficient. The human gut consists of a variety of microbes such as L. plantarum and E. hallii that hold vital roles in maintaining metabolic balance in the gut microbiome. Through our research, we envisioned investigating how adrenaline treatment at different time intervals or concentrations mirroring the various circumstances of exercise may affect bacterial growth, antibacterial substance production, and their antibacterial properties. While both bacteria were not affected in its growth for 48 hours, in L. plantarum, demonstrating decreased growth in the first 8 hours, its main functions — lactic acid production — were furthered with the hormone. In E. hallii, butyric acid production, with the hormone, significantly increased in its supernatant, and the intermediate treatment of adrenaline for 8 hours served to catalyze the rate at which the bacteria reached its stationary phase of growth. The study holds great promise for future investigations on how such a mechanism can be applied to therapies boosting our existing abilities of protein disposal directly correlated to the prevention of diseases. What remains is, nevertheless, the discussion regarding the true control center of these bacteria that interact with adrenaline to cause changes in the antibiotic properties, function, and growth. In other words, future studies can be oriented towards understanding the changes in the antibacterial properties of given bacteria not indirectly through chemicals with antibacterial traits but rather through the quantitative measurement of growth inhibition with other bacteria or organisms.

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