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The ergogenic effect of L-arginine on an endurance-trained population is not well studied. The few studies that have investigated L-arginine on this population have not been conducted in a laboratory setting or measured aerobic variables. The purpose of the current study is to determine if 28 days of L-arginine supplementation in trained male cyclists affects VO2max and ventilatory threshold (VT). Eighteen (18) endurance-trained male cyclists (mean ± SD, age: 36.3 ± 7.9 years; height: 182.4 ± 4.6 cm; and body mass: 79.5 ± 4.7 kg) performed a graded exercise test (GXT; 50 W + 25 W·min) before and after 28 days of supplementation with L-arginine (ARG; 2 × 6 g·d) or placebo (PLA; cornstarch). The GXT was conducted on the subject's own bicycle using the RacerMate CompuTrainer (Seattle, WA, USA). VO2 was continuously recorded using the ParvoMedics TrueOne 2400 metabolic cart (Salt Lake City, UT, USA) and VT was established by plotting the ventilatory equivalent for O2 (VE/VO2) and the ventilatory equivalent for CO2 (VE/VCO2) and identifying the point at which VE/VO2 increases with no substantial changes in VE/VCO2. L-arginine supplementation had no effect from initial VO2max (PL, 58.7 ± 7.1 ml·kg·min; ARG, 63.5 ± 7.3 ml·kg·min) to postsupplement VO2max (PL, 58.9 ± 6.0 ml·kg·min; ARG, 63.2 ± 7.2 ml·kg·min). Also, no effect was seen from initial VT (PL, 75.7 ± 4.6% VO2max; ARG, 76.0 ± 5.3% VO2max) to postsupplement VT (PL, 74.3 ± 8.1% VO2max; ARG, 74.2 ± 6.4% VO2max). These results indicate that L-arginine does not impact VO2max or VT in trained male cyclists.

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Postactivation potentiation (PAP) has been hypothesized previously to occur during voluntary, concentric actions. We tested the hypothesis that one of at least three different intensities of conditioning exercises would evoke potentiation of power during the concentric, bench press throw (BPT). Twelve men (age = 22.9 ± 2.7 years, bench press 1 repetition maximum (1RM) = 1.20 ± 0.12 kg·kg-1 body weight) completed five isotonic conditioning presses at ~55, 70, and 86% 1RM, in counterbalanced order, and on separate days. Average and peak power of the BPT using a load of 55% 1RM along with surface electromyography (EMG) of the triceps brachii were collected prior to and 4-minutes following each conditioning bout. Both average and peak power and EMG values (mean ± SD), respectively, were evaluated using two-way analyses of variance with repeated measures. Significant main effect decreases (p < 0.05) in average (-18.6 ± 4.9 W) and peak power (-37.4 ± 9.9 W) occurred across the three different intensities evaluated. No main effects or interactions were observed with the EMG data. Contrary to the previously reported hypothesis, we were unable to demonstrate that conditioning exercise, with three different intensities, can evoke potentiation of power using a load equating to that which is optimum for power production.

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The A1 adenosine receptor (A1AR) has been suggested to participate in insulin- and contraction-stimulated glucose transport in skeletal muscle, but the qualitative and quantitative nature of the effect are controversial. We sought to determine if A1AR is expressed in rat soleus muscle and then characterize its role in glucose transport in this muscle. A1AR mRNA and protein expression were determined by RT-PCR and Western blotting, respectively. To examine the role of adenosine in 3-O-methylglucose transport, isolated muscles were exposed to adenosine deaminase and alpha,beta-methylene adenosine diphosphate to remove endogenous adenosine and were left unstimulated (basal) or stimulated with insulin. To assess the functional participation of A1AR in 3-O-methylglucose transport, muscles were incubated with A1-selective agonist and (or) antagonist in the absence of endogenous adenosine and with or without insulin. A1AR mRNA was expressed in soleus muscle and A1AR was present at the plasma membrane. Removal of endogenous adenosine reduced glucose transport in response to 100 microU/mL insulin (approximately 50%). The A1-selective agonist, N6-cyclopentyladenosine, increased submaximal (100 microU/mL) insulin-stimulated glucose transport in a dose-dependent manner (0.001-1.0 micromol/L). This stimulatory effect was inhibited by the A1-selective receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine in a concentration-dependent manner (0.001-1.0 micromol/L). However, neither activation nor inhibition of A1AR altered basal or maximal (10 mU/mL) insulin-stimulated glucose transport. Our results suggest that adenosine contributes approximately 50% to insulin-stimulated muscle glucose transport by activating the A1AR. This effect is limited to increasing insulin sensitivity, but not to either basal or maximal insulin-stimulated glucose uptake in rat soleus muscle.

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The ergogenic effect of caffeine and its mechanism of action on short-term, high-intensity exercise are controversial. One proposed mechanism is caffeine's stimulatory effect on the central nervous system and thus, motor-unit excitation. The latter is non-invasively determined from surface electromyographic signal (EMG) frequency measures. The purpose of this study was to determine if power output and surface EMG frequency variables during high-intensity cycling were altered following caffeine ingestion. Eighteen recreationally active college males (mean +/- SD age, 21.5 +/- 1.8 y; height, 181.8 +/- 0.5 cm; body mass, 84.7 +/- 11.4 kg) performed the Wingate test (WG) after ingestion of gelatin capsules containing either placebo (PL; dextrose) or caffeine (CAFF; 5 mg/kg body mass). The trials were separated by 1 week and subjects were asked to withdraw from all caffeine-containing products for 48 h before each trial. From the resulting power-time records, peak power (PP; highest power output in 5 s), minimum power (MP; lowest power output in 5 s), and the percent decline in power (Pd) were calculated. Surface EMG records of the right vastus lateralis (VL) and the gastrocnemius (GA) muscles corresponding to the PP and MP periods were collected and used to determine the integrated electromyogram (IEMG), the mean (MNPF), and the median (MDPF) of the signal's power spectrum. A 2-way repeated measures analysis of variance (ANOVA) (treatment x time) was conducted to determine the effect of caffeine on these variables across levels of time. Caffeine ingestion had no effect on PP (PL, 1049 +/- 192 W; CAFF, 1098 +/- 198 W), MP (PL, 762 +/- 104 W; CAFF, 802 +/- 124 W), or the Pd (PL, 47% +/- 8.9%; CAFF, 48.2% +/- 7.3%) compared with the placebo. For both muscles, MNPF and MDPF diminished significantly (p < 0.001) across time and to a similar degree in both the CAFF and PL trials. Regardless of muscle, CAFF had no effect on the percent change in IEMG from the first 5 s to the last 5 s. For both treatments, the GA displayed a significantly (p < 0.05) greater pre vs. post percent decline in the EMG signal amplitude compared with the VL. These results indicate that caffeine does not impact power output during a 30 s high-intensity cycling bout. Furthermore, these data suggest that caffeine does not impact the neuromuscular drive as indicated by the similar IEMG scores between treatments. Similarly, caffeine does not seem to impact the frequency content of the surface EMG signal and thus the nature of recruited motor units before and after the expression of fatigue. The lack of decline in the IEMG in the VL despite the decline in power output over the course of the WG suggests a peripheral as opposed to a neural mechanism of fatigue in this muscle. The significant difference in the pre vs. post percent decline in the GA IEMG score further supports this notion. The pre vs. post decline in the IEMG noted in the GA may suggest a fatigue-triggered change in pedaling mechanics that may promote dominance of knee extensors with less reliance on plantar flexors.

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BACKGROUND: Mass media may effect communitywide changes in health awareness, attitude, and behavior, but the approach remains unproven for physical activity. METHODS: Wheeling Walks promoted walking among sedentary 50- to 65-year-old adults in a West Virginia city of 31,420 people. This quasi-experimental communication intervention used theory of planned behavior and transtheoretical model constructs to change behavior by promoting 30 min of daily walking through paid media, public relations, and public health activities. Impact was determined by pre- and postintervention telephone surveys with 719 adults in the intervention community and 753 adults in the comparison community and observations of walkers at 10 community sites. RESULTS: Behavior observation showed a 23% increase in the number of walkers in the intervention community versus no change in the comparison community (OR = 1.31, 95% CI = 1.14-1.50). Thirty-two percent (32.2) of the baseline sedentary population in the intervention community reported meeting the CDC/ACSM/Surgeon General recommendation for moderate-intensity physical activity by walking at least 30 min at least five times per week versus 18.0% in the comparison community (OR = 2.12, 95% CI = 1.41-2.24). The intervention community also realized a pre to post increase in positive stage change (P < 0.001). CONCLUSIONS: This theory-based mass media campaign demonstrated increases in those meeting the recommended standard for moderate-intensity physical activity through walking and significant positive stage change.

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