Antibiotic Therapy and Athletes: Is the Mitochondrial Dysfunction the Real Achilles' Heel?

Abstract

It is widely recognized that athletes consume oral antibiotics almost twice as often as observed in the non-sports population in order to reduce as much as possible the period of inactivity due to bacterial diseases. However, increasing evidences have demonstrated the ability of some classes of antibiotics to induce muscle weakness, pain, and a feeling of fatigue upon resuming physical activity conditions that considerably limit the athletic performance of athletes, ascribable to alterations in the biochemical mechanisms underlying normal musculoskeletal activity, such as mitochondrial respiration. For this reason, tailoring a treatment plan for effective antibiotics that limit an athlete's risk is paramount to their safety and ability to maintain adequate athletic performance. The present review illustrates and critically analyzes the evidence on the use of antibiotics in sports, deepening the molecular mechanisms underlying the onset and development of muscle-tendon alterations in athletes as well as delineating the pharmacological strategies aimed at counteracting such adverse events.

Keywords: antibiotics; mitochondria; reactive oxygen species; skeletal muscle; tendon.

Figure 1

Schematic representation regarding the main steps in mitochondrial activity. In particular, mitochondrial respiration is the set of metabolic reactions and processes requiring oxygen that takes place in mitochondria to convert the energy stored in macronutrients to adenosine triphosphate (ATP). In this context, several antibiotics exert detrimental effects on mitochondrial activity, which can be counteracted by the concomitant administration of several food supplements aimed at restoring mitochondrial homeostasis. Abbreviations: FAD: flavin adenine dinucleotide; FMN: flavin mononucleotide; NADH: nicotinamide adenine dinucleotide.

Figure 2

Schematic representation of the main detrimental mechanisms underlying tendon injury induced by fluoroquinolones. Abbreviations: CX43: connexin 43; MMP: metalloproteinase; VEGF: vascular endothelial growth factor.