Abstract
AIM: Acetaminophen is a commonly used medicine for pain relief and emerging evidence suggests that it may improve endurance exercise performance. This study investigated some of the physiological mechanisms by which acute acetaminophen ingestion might blunt muscle fatigue development. METHODS: Thirteen active males completed 60 × 3 s maximum voluntary contractions (MVC) of the knee extensors with each contraction separated by a 2 s passive recovery period. This protocol was completed 60 min after ingesting 1 g of maltodextrin (placebo) or 1 g of acetaminophen on two separate visits. Peripheral nerve stimulation was administered every 6th contraction for assessment of neuromuscular fatigue development, with the critical torque (CT), which reflects the maximal sustainable rate of oxidative metabolism, taken as the mean torque over the last 12 contractions. Surface electromyography was recorded continuously as a measure of muscle activation. RESULTS: Mean torque (61 ± 11 vs. 58 ± 14% pre-exercise MVC) and CT (44 ± 13 vs. 40 ± 15% pre-exercise MVC) were greater in the acetaminophen trial compared to placebo (both P < 0.05). Voluntary activation and potentiated twitch declined at a similar rate in both conditions (P > 0.05). However, the decline in electromyography amplitude was attenuated in the acetaminophen trial, with electromyography amplitude being greater compared to placebo from 210 s onwards (P < 0.05). CONCLUSION: These findings indicate that acute acetaminophen ingestion might be ergogenic by increasing CT and preserving muscle activation during high-intensity exercise.