No additive effect of creatine, caffeine, and sodium bicarbonate on intense exercise performance in endurance-trained individuals.

BACKGROUND: Athletes commonly use creatine, caffeine, and sodium bicarbonate for performance enhancement. While their isolated effects are well-described, less is known about their potential additive effects. METHODS: Following a baseline trial, we randomized 12 endurance-trained males (age: 25 ± 5 years, VO2max: 56.7 ± 4.6 mL kg-1 min-1; mean ± SD) and 11 females (age: 25 ± 3 years, VO2max: 50.2 ± 3.4 mL kg-1 min-1) to 5 days of creatine monohydrate (0.3 g kg-1 per day) or placebo loading, followed by a daily maintenance dose (0.04 g kg-1) throughout the study. After the loading period, subjects completed four trials in randomized order where they ingested caffeine (3 mg kg-1), sodium bicarbonate (0.3 g kg-1), placebo, or both caffeine and sodium bicarbonate before a maximal voluntary contraction (MVC), 15-s sprint, and 6-min time trial. RESULTS: Compared to placebo, mean power output during 15-s sprint was higher following loading with creatine than placebo (+34 W, 95% CI: 10 to 58, p = 0.008), but with no additional effect of caffeine (+10 W, 95% CI: -7 to 24, p = 0.156) or sodium bicarbonate (+5 W, 95% CI: -4 to 13, p = 0.397). Mean power output during 6-min time trial was higher with caffeine (+12 W, 95% CI: 5 to 18, p = 0.001) and caffeine + sodium bicarbonate (+8 W, 95% CI: 0 to 15, p = 0.038), whereas sodium bicarbonate (-1 W, 95% CI: -7 to 6, p = 0.851) and creatine (-6 W, 95% CI: -15 to 4, p = 0.250) had no effects. CONCLUSION: While creatine and caffeine can enhance sprint- and time trial performance, respectively, these effects do not seem additive. Therefore, supplementing with either creatine or caffeine appears sufficient to enhance sprint or short intense exercise performance.

No additive effect of acetaminophen when co-ingested with caffeine on cycling performance in well-trained young men.

We investigated the effect of caffeine and acetaminophen on power output during a 6-min performance test, peripheral fatigue, and muscle protein kinase A (PKA) substrate phosphorylation. Fourteen men [age (means ± SD): 26 ± 6 yr; V̇o2max: 63.9 ± 5.0 mL·min-1·kg-1] completed four randomized trials with acetaminophen (1,500 mg), caffeine (5 mg·kg body wt-1), combined caffeine and acetaminophen (caffeine + acetaminophen), or placebo. Mean power output during the 6-min performance test (placebo mean: 312 ± 41 W) was higher with caffeine (+5 W; 95% CI: 1 to 9; P = 0.017) and caffeine + acetaminophen (+6 W; 95% CI: 0 to 12; P = 0.049) than placebo, but not with acetaminophen (+1 W; 95% CI: -4 to 7; P = 0.529). Decline in quadriceps maximal isometric voluntary torque immediately after the performance test was lower (treatment × time; P = 0.035) with acetaminophen (-40 N·m; 95% CI: -53 to -30; P < 0.001) and caffeine + acetaminophen (-44 N·m; 95% CI: -58 to -30; P < 0.001) than placebo (-53 N·m; 95% CI: -71 to -39; P < 0.001) but was similar with caffeine (-54 N·m; 95% CI: -69 to -38; P < 0.001). Muscle phosphocreatine content decreased more during the performance test (treatment × time; P = 0.036) with caffeine + acetaminophen (-55 mmol·kg dry wt-1; 95% CI: -65 to -46; P < 0.001) than placebo (-40 mmol·kg dry wt-1; 95% CI: -52 to -24; P < 0.001). Muscle net lactate accumulation was not different from placebo (+85 mmol·kg dry wt-1; 95% CI: 60 to 110; P < 0.001) for any treatment (treatment × time; P = 0.066), being +75 mmol·kg dry wt-1 (95% CI: 51 to 99; P < 0.001) with caffeine, +76 mmol·kg dry wt-1 (95% CI: 58 to 96; P < 0.001) with acetaminophen, and +103 mmol·kg dry wt-1 (95% CI: 89 to 115; P < 0.001) with caffeine + acetaminophen. Decline in muscle ATP and glycogen content and increase in PKA substrate phosphorylation was not different between treatments (treatment × time; P > 0.1). Thus, acetaminophen provides no additive performance enhancing effect to caffeine during 6-min maximal cycling. In addition, change in PKA activity is likely not a major mechanism of performance improvement with caffeine.NEW & NOTEWORTHY Here, we show that acetaminophen does not provide additive performance improvement to caffeine during a 6-min cycling ergometer performance test, and that acetaminophen does not improve performance on its own. Neither substance affects peripheral fatigue, muscle glycolytic energy production, or phosphorylation of muscle proteins of importance for ion handling. In contrast to previous suggestions, increased epinephrine action on muscle cells does not appear to be a major contributor to the performance enhancement with caffeine.

Effect of tapering after a period of high-volume sprint interval training on running performance and muscular adaptations in moderately trained runners.

The effect of tapering following a period of high-volume sprint interval training (SIT) and a basic volume of aerobic training on performance and muscle adaptations in moderately trained runners was examined. Eleven (8 men, 3 women) runners [maximum oxygen uptake (V̇o2max): 56.8 ± 2.9 ml·min-1·kg-1; mean ± SD] conducted high-volume SIT (HV; 20 SIT sessions; 8-12 × 30 s all-out) for 40 days followed by 18 days of tapering (TAP; 4 SIT sessions; 4 × 30 s all-out). Before and after HV as well as midway through and at the end of TAP, the subjects completed a 10-km running test and a repeated running test at 90% of vV̇o2max to exhaustion (RRT). In addition, a biopsy from the vastus lateralis muscle was obtained at rest. Performance during RRT was better ( P < 0.01) at the end of TAP than before HV (6.8 ± 0.5 vs. 5.6 ± 0.5 min; means ± SE), and 10-km performance was 2.7% better ( P < 0.05) midway through (40.7 ± 0.7 min) and at the end of (40.7 ± 0.6 min) TAP than after HV (41.8 ± 0.9 min). The expression of muscle Na+-K+-ATPase (NKA)α1, NKAß1, phospholemman (FXYD1), and sarcoplasmic reticulum calcium transport ATPase (SERCA1) increased ( P < 0.05) during HV and remained higher during TAP. In addition, oxygen uptake at 60% of vV̇o2max was lower ( P < 0.05) at the end of TAP than before and after HV. Thus short-duration exercise capacity and running economy were better than before the HV period together with higher expression of muscle proteins related to Na+/K+ transport and Ca2+ reuptake, while 10-km performance was not significantly improved by the combination of HV and tapering. NEW & NOTEWORTHY Short-duration performance became better after 18 days of tapering from ~6 wk of high-volume sprint interval training (SIT), whereas 10-km performance was not significantly affected by the combination of high-volume SIT and tapering. Higher expression of muscle NKAα1, NKAß1, FXYD1, and SERCA1 may reflect faster Na+/K+ transport and Ca2+ reuptake that could explain the better short-duration performance. These results suggest that the type of competition should determine the duration of tapering to optimize performance.

Serotonin-induced down-regulation of cell surface serotonin transporter.

The serotonin transporter (SERT) terminates serotonergic signaling and enables refilling of synaptic vesicles by mediating reuptake of serotonin (5-HT) released into the synaptic cleft. The molecular and cellular mechanisms controlling SERT activity and surface expression are not fully understood. Here we demonstrate that the substrate 5-HT itself causes acute down-regulation of SERT cell surface expression. To assess surface SERT expression by ELISA, we used a SERT variant (TacSERT) where the N-terminus of SERT was fused to the intracellular tail of the extracellularly FLAG-tagged single-membrane spanning protein Tac. In stably transfected HEK293 cells, 5-HT caused a dose-dependent reduction in TacSERT surface signal with an EC50 value equivalent to the Km value observed for 5-HT uptake. The 5-HT-induced reduction in surface signal reached maximum within 40-60min and was blocked by the selective SERT inhibitor S-citalopram. 5-HT-induced reduction in SERT expression was further supported by surface biotinylation experiments showing 5-HT-induced reduction in wild type SERT plasma membrane levels. Moreover, preincubation with 5-HT lowered the Vmax for 5-HT uptake in cultured raphe serotonergic neurons, indicting that endogenous cell-surface resident SERT likewise is down-regulated in the presence of substrate.

Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function.

Six sessions of high-intensity interval training (HIT) are sufficient to improve exercise capacity. The mechanisms explaining such improvements are unclear. Accordingly, the aim of this study was to perform a comprehensive evaluation of physiologically relevant adaptations occurring after six sessions of HIT to determine the mechanisms explaining improvements in exercise performance. Sixteen untrained (43 ± 6 ml·kg(-1)·min(-1)) subjects completed six sessions of repeated (8-12) 60 s intervals of high-intensity cycling (100% peak power output elicited during incremental maximal exercise test) intermixed with 75 s of recovery cycling at a low intensity (30 W) over a 2-wk period. Potential training-induced alterations in skeletal muscle respiratory capacity, mitochondrial content, skeletal muscle oxygenation, cardiac capacity, blood volumes, and peripheral fatigue resistance were all assessed prior to and again following training. Maximal measures of oxygen uptake (Vo2peak; ∼8%; P = 0.026) and cycling time to complete a set amount of work (∼5%; P = 0.008) improved. Skeletal muscle respiratory capacities increased, most likely as a result of an expansion of skeletal muscle mitochondria (∼20%, P = 0.026), as assessed by cytochrome c oxidase activity. Skeletal muscle deoxygenation also increased while maximal cardiac output, total hemoglobin, plasma volume, total blood volume, and relative measures of peripheral fatigue resistance were all unaltered with training. These results suggest that increases in mitochondrial content following six HIT sessions may facilitate improvements in respiratory capacity and oxygen extraction, and ultimately are responsible for the improvements in maximal whole body exercise capacity and endurance performance in previously untrained individuals.

Effect of additional speed endurance training on performance and muscle adaptations.

PURPOSE: The present study examined the effect of additional speed endurance training (SET) during the season on muscle adaptations and performance of trained soccer players. METHODS: Eighteen subelite soccer players performed one session with six to nine 30-s intervals at an intensity of 90%-95% of maximal intensity (SET) a week for 5 wk (SET intervention). Before and after the SET intervention, the players carried out the Yo-Yo intermittent recovery level 2 (Yo-Yo IR2) test, a sprint test (10 and 30 m), and an agility test. In addition, seven of the players had a resting muscle biopsy specimen taken and they carried out a running protocol on a motorized treadmill before and after the SET intervention. RESULTS: After the SET intervention, the Yo-Yo IR2 test (n = 13) performance was 11% better (P < 0.05), whereas sprint (n = 15) and agility (n = 13) performances were unchanged. The expression of the monocarboxylate transporter 1 (n = 6) was 9% higher (P < 0.05). and the expression of the Na(+)/K(+) pump subunit ß(1) (n = 6) was 13% lower (P < 0.05) after the SET intervention. The Na(+)/K(+) pump subunits α(1), α(2), as well as the monocarboxylate transporter 4 and the Na(+)/H(+) exchanger 1 (n = 6) were unchanged. After the SET intervention, the relative number of Type IIx fibers and oxygen consumption at 10 km.h(-1) were lower (P < 0.05), whereas VO(2max) was unchanged. CONCLUSIONS: In conclusion, adding ∼30 min of SET once a week during the season for trained soccer players did lead to an improved ability to perform repeated high-intensity exercise, with a concomitant increase in the expression of monocarboxylate transporter 1 and an improved running economy.