Ibuprofen intake increases exercise time to exhaustion: A possible role for preventing exercise‐induced fatigue

Abstract

Although the intake of nonsteroidal anti-inflammatory drugs (NSAIDs) intake by athletes prevents soreness, little is known concerning their role in exercise performance. This study assessed the effects of ibuprofen intake on an exhaustive protocol test after 6 weeks of swimming training in rats. Animals were divided into sedentary and training groups. After training, animals were subdivided into two subsets: saline or ibuprofen. Afterwards, three repeated swimming bouts were performed by the groups. Ibuprofen (15 mg/kg) was administered once a day. Pain measurements were performed and inflammatory and oxidative stress parameters were assayed in cerebral cortex and gastrocnemius muscle. Training, ibuprofen administration, or both combined (P < 0.05; 211 ± 18s, 200 ± 31s, and 279 ± 23s) increased exercise time to exhaustion. Training decreased the acetylcholinesterase (AChE) activity (P < 0.05; 149 ± 11) in cerebral cortex. Ibuprofen intake decreased the AChE activity after exhaustive protocol test in trained and sedentary rats (P < 0.05; 270 ± 60; 171 ± 38; and 273 ± 29). It also prevented neuronal tumor necrosis factor-α (TNF-α) and interleukin (IL 1β) increase. Fatigue elicited by this exhaustive protocol may involve disturbances of the central nervous system. Additive anti-inflammatory effects of exercise and ibuprofen intake support the hypothesis that this combination may constitute a more effective approach. In addition, ergogenic aids may be a useful means to prevent exercise-induced fatigue.

Analgesic and anti‐inflammatory drugs in sports: Implications for exercise performance and training adaptations

“…These findings suggested that exercise performance was, at least in part, regulated by pain perception, and hence, paracetamol could improve exercise performance through increased pain tolerance and lower perceived exertion. This is also supported by animal data showing that ibuprofen improved swimming performance (time to exhaustion) in rats, plausibly through reduced susceptibility to exercise‐induced fatigue …”

“…This is also supported by animal data showing that ibuprofen improved swimming performance (time to exhaustion) in rats, plausibly through reduced susceptibility to exercise-induced fatigue. 20 In a follow-up study to the cycle time trial, the same group sought to determine whether paracetamol could also improve exercise capacity in the heat. 21 The background to this hypothesis comes from the fact that paracetamol has antipyretic effects for fever management, and perhaps also in afebrile patients.…”

Increased xanthine oxidase-related ROS production and TRPV1 synthesis preceding DOMS post-eccentric exercise in rats

“…Once those peripheral nociceptors are sensitized (hyperalgesia), innocuous tactile stimuli, such as allodynia, are felt in other distal parts of the body innervated by the same sensory neuron or branches of the main neuron [22,26]. Thus, considering that the nociceptive process radiates to other distal areas of the body, we decided to evaluate the nociception of animals using von Frey filaments, which is one of the most used tools for this determination in animal models [13,33,45,52]. Moreover, the present protocol also induced strength decreases at 3, 12, 48 and 72 h post-exercise.…”

Diclofenac attenuates inflammation through TLR4 pathway and improves exercise performance after exhaustive swimming

“…We have previously found a similar effect following ibuprofen administration. 23 As already reported, diclofenac treatment interferes in the synthesis of inflammatory markers in different organs, including the liver. 30 The production of these molecules is mediated by nuclear transcription factors, which, in turn, might be activated by these cytokines in a physiological feedforward.…”

“…Diclofenac was administered for nine days (10 mg/kg daily) and removed 24 hours before the last exhaustive bout because there is no evidence about side effect, and this period would not be enough to stop a possible therapeutic effect. 23 Interestingly, pre-treatment with diclofenac proved effective in increasing the time to exhaustion, which has not yet been demonstrated in humans. 15 This may occur due to differences in muscle glycogen that has a more central role in glucose homeostasis in humans (threefold to eightfold more muscle glycogen than liver glycogen when compared to mice).…”