The effects of acute dopamine reuptake inhibition on cognitive function during passive hyperthermia.

Dopamine activity can modulate physical performance in the heat, but less is known about its effects on cognition during thermal stress. Twelves males completed a randomized, double-blinded protocol consisting of oral ingestion of 20 mg of methylphenidate (MPH) or placebo (lactose pill) during passive heating using a water-perfused suit (water temperature ∼49 °C). To identify the impact of peripheral versus central thermal strain, a cognitive test battery was completed at 4 different thermal states: baseline (BASE; 37.2 ± 0.6 °C core, 32.9 ± 0.7 °C skin), neutral core-hot skin (NC-HS; 37.2 ± 0.3 °C, 37.4 ± 0.3 °C), hyperthermic core-hot skin (HC-HS; 38.7 ± 0.4 °C, 38.7 ± 0.2 °C), and hyperthermic core-cooled skin (HC-CS; 38.5 ± 0.4 °C, 35.1 ± 0.8 °C). The cognitive test battery consisted of the 2-back task (i.e., working memory), set-shifting (i.e., executive function), Groton Maze Learning Task (i.e., executive function) and detection task (i.e., psychomotor processing). MPH led to significantly higher heart rates (∼5-15 b·min-1) at BASE, NC-HS, and HC-HS (all p < 0.05). There were no significant differences in the number of errors made on each task (all p < 0.05). Participants were significantly faster (p < 0.05) on the set-shifting task in the HC-HS timepoint, irrespective of drug condition (p > 0.05). In summary, we demonstrated that 20 mg of MPH did not significantly alter cognitive function during either normothermia or moderate hyperthermia. Novelty: Twenty milligrams of MPH did not significantly alter cognitive function during passive heat stress. MPH led to significant higher heart rates (∼5-15 b·min-1) in thermoneutral and during passive heat stress. Future studies are needed to determine the mechanisms of why MPH improves physical but not cognitive performance during heat stress.

Acute versus chronic supplementation of sodium citrate on 200 m performance in adolescent swimmers.

BACKGROUND: A double-blinded, placebo-controlled, cross-over design was used to investigate whether two different sodium citrate dihydrate (Na-CIT) supplementation protocols improve 200 m swimming performance in adolescent swimmers. METHODS: Ten, male swimmers (14.9 ± 0.4 years of age; 63.5 ± 4 kg) performed four 200 m time trials with the following treatments: acute (ACU) supplementation (0.5 g kg(-1) administered 120 min pre-trial), acute placebo (PLC-A), chronic (CHR) supplementation (0.1 g∙kg(-1) for three days and 0.3 g kg(-1) on the forth day 120 min pre-trial), and chronic placebo (PLC-C). The order of the trials was randomized, with at least a six-day wash-out period between trials. Blood samples were collected by finger prick pre-ingestion, 100 min post-ingestion, and 3 min post-trial. Performance time, rate of perceived exertion, pH, base excess, bicarbonate and lactate concentration were measured. RESULTS: Post-ingestion bicarbonate and base excess were higher (P < 0.05) in both the ACU and CHR trials compared to placebo showing adequate pre-exercise alkalosis. However, performance time, rate of perceived exertion as well as post-trial pH and lactate concentration were not significantly different between trials. Further analysis revealed that five swimmers, identified as responders, improved their performance time by 1.03% (P < 0.05) and attained higher post-trial lactate concentrations in the ACU versus PLC-A trial (P < 0.05). They also had significantly higher post-trial lactate concentrations compared to the non-responders in the ACU and CHR trials. CONCLUSIONS: Acute supplementation of Na-CIT prior to 200 m swimming performance led to a modest time improvement and higher blood lactate concentrations in only half of the swimmers while the chronic Na-CIT supplementation did not provide any ergogenic effect in this group of adolescent swimmers. TRIAL REGISTRATION: Clinicaltrials.gov NCT01835912.