1) mejora el sprint, en principio reduciendo la nocicepción
Eur J Appl Physiol. 2013 Oct 12. [Epub ahead of print]
The influence of acetaminophen on repeated sprint cycling performance.
Foster J, Taylor L, Chrismas BC, Watkins SL, Mauger AR.
The aim of this study was to investigate the effect of acetaminophen on repeated sprint cycling performance.
Nine recreationally active male participants completed a graded exercise test, a familiarisation set of Wingate Anaerobic Tests (WAnTs) and two experimental sets of WAnTs (8 × 30 s sprints, 2 min active rest intervals). In the experimental WAnTs, participants ingested either 1.5 g acetaminophen or a placebo in a double-blind, randomised, crossover design. During the WAnT trials, participants provided ratings of perceived pain 20 s into each sprint. Mean and peak power output and heart rate were recorded immediately following each sprint, and percentage decrement in mean power output was subsequently calculated.
Participants cycled at a significantly greater mean power output over the course of 8 WAnTs (p < 0.05) following the ingestion of acetaminophen (391 ± 74 vs. 372 ± 90 W), due to a significantly greater mean power output during sprints 6, 7 and 8 (p < 0.05). Percentage decrements in mean power output were also significantly reduced (p < 0.05) following acetaminophen ingestion (17 ± 14 vs. 24 ± 17 %). No significant differences in peak power output, perceived pain or heart rate were observed between conditions.
Acetaminophen may have improved performance through the reduction of pain for a given work rate, thereby enabling participants to exercise closer to a true physiological limit. These results suggest that exercise may be regulated by pain perception, and that an increased pain tolerance can improve exercise performance.
2) suaviza el impacto emocional en una situación de rechazo social
Acetaminophen Reduces Social Pain
Behavioral and Neural Evidence
Pain, whether caused by physical injury or social rejection, is an inevitable part of life. These two types of pain—physical and social—may rely on some of the same behavioral and neural mechanisms that register pain-related affect. To the extent that these pain processes overlap, acetaminophen, a physical pain suppressant that acts through central (rather than peripheral) neural mechanisms, may also reduce behavioral and neural responses to social rejection. In two experiments, participants took acetaminophen or placebo daily for 3 weeks. Doses of acetaminophen reduced reports of social pain on a daily basis (Experiment 1). We used functional magnetic resonance imaging to measure participants’ brain activity (Experiment 2), and found that acetaminophen reduced neural responses to social rejection in brain regions previously associated with distress caused by social pain and the affective component of physical pain (dorsal anterior cingulate cortex, anterior insula). Thus, acetaminophen reduces behavioral and neural responses associated with the pain of social rejection, demonstrating substantial overlap between social and physical pain.
Prog Neuropsychopharmacol Biol Psychiatry. 2009 Oct 1;33(7):1191-9. Epub 2009 Jul 4.
Endocannabinoids mediate anxiolytic-like effect of acetaminophen via CB1 receptors.
Acetaminophen (Paracetamol), a most commonly used antipyretic/analgesic agent, is metabolized to AM404 (N-arachidonoylphenolamine) that inhibits uptake and degradation of anandamide which is reported to mediate the analgesic action of acetaminophen via CB1 receptor. AM404 and anandamide are also reported to produce anxiolytic-like behavior. In view of the implication of endocannabinoids in the effect of acetaminophen, we contemplated that acetaminophen may have anxiolytic-like effect. Therefore, this possibility was tested by observing the effects of various doses of acetaminophen in mice on anxiety-related indices of Vogel conflict test and social interaction test. The results from both the tests indicated that acetaminophen (50, 100, or 200 mg/kg, i.p.) or anandamide (10 or 20 microg/mouse, i.c.v.) dose dependently elicited anxiolytic-like effect, that was comparable to diazepam (2 mg/kg, i.p.). Moreover, co-administration of sub-effective dose of acetaminophen (25 mg/kg, i.p.) and anandamide (5 microg/mouse, i.c.v) produced similar anxiolytic effect. Further, pre-treatment with AM251 (a CB1 receptor antagonist; 1 mg/kg, i.p.) antagonized the effects of acetaminophen and anandamide with no per se effect at 1 mg/kg dose, while anxiogenic effect was evident at a higher dose (5 mg/kg, i.p.). None of the treatment/s was found to induce any antinociceptive or locomotor impairment effects. In conclusion, the findings suggested that acetaminophen (50, 100, or 200 mg/kg, i.p.) exhibited dose dependent anxiolytic effect in mice and probably involved endocannabinoid-mediated mechanism in its effect.
4) Mejora la memoria y es neuroprotector en algunos modelos animales
Nootropic activity of acetaminophen against colchicine induced cognitive impairment in rats.
Alzheimer's disease is a devastating neurodegenerative disorder, the most common among the dementing illnesses. Acetaminophen has gaining importance in neurodegenerative diseases by attenuating the dopaminergic neurodegeneration in Caenorhabditis elegans model, decreasing the chemokines and the cytokines and increasing the anti apoptotic protein such as Bcl-2 in neuronal cell culture. The low concentration acetaminophen improved the facilitation to find the hidden platform in Morris Water Maze Test. Also some data suggest that acetaminophen could contribute in neurodegeneration. The present study was aimed to evaluate the effect of acetaminophen against colchicine induced cognitive impairment and oxidative stress in wistar rats. The cognitive learning and memory behaviour was assessed using step through passive avoidance paradigm and acetylcholine esterase activity. The parameters of oxidative stress were assessed by measuring the malondialdehyde, reduced glutathione and catalase levels in the whole brain homogenates. There was a significant memory improvement in the rats received acetaminophen treatment and it has also decreased the acetylcholine esterase enzyme level, confirming its nootropic activity. Acetaminophen neither increases nor decreases the reduced glutathione and catalase in the whole brain homogenates, showing that acetaminophen is devoid of any adverse effect on brain antioxidant defense system.
En otros modelos animales las dosis continuadas pueden producir daño cerebral.