However, caffeine ingestion had no affect upon any of the marksmanship measures, although it did alleviate cold stress and tiredness. That caffeine ingestion did not affect target detection and rifle marksmanship is a finding that differs from other studies, and is explained by a beneficial arousal caused by the mild level of cold stress experienced by the participants.

In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials.

Placebo administration in MH participants decreased alertness and increased headache. Caffeine did not increase alertness in NL participants. With frequent consumption, substantial tolerance develops to the anxiogenic effect of caffeine, even in genetically susceptible individuals, but no net benefit for alertness is gained, as caffeine abstinence reduces alertness and consumption merely returns it to baseline.

Caffeine and opening the eyes have additive effects on two measures of arousal, increasing SCL and reducing global EEG alpha. However, the independent variable effects are not equivalent, suggesting that one or both measures reflect additional non-arousal processes.

We confirm that acute doses of caffeine, at levels typically found in a cup of coffee, produce stimulant-like subjective effects and enhance performance in light, nondependent caffeine users. These findings support the idea that the drug has psychoactive effects even in the absence of withdrawal.

However, caffeine ingestion had no affect upon any of the marksmanship measures, although it did alleviate cold stress and tiredness. That caffeine ingestion did not affect target detection and rifle marksmanship is a finding that differs from other studies, and is explained by a beneficial arousal caused by the mild level of cold stress experienced by the participants.

In conclusion, caffeine ingestion caused not only increases in TYMP and mT(b) through thermogenesis, but also an increased sweating sensitivity via changes in sudomotor activity.

In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials.

A caffeine dose of at least 3 mg/kg in the form of an energy drink is necessary to significantly improve half-squat and bench-press maximal muscle power.

Although the effect of recovery duration on caffeine-induced responses to multiple sprint work requires further investigation, the results of the present study show that caffeine has ergogenic properties with the potential to benefit performance in both single and multiple sprint sports.

Caffeine has some potential to benefit training outcomes via the anabolic effects of the increase in testosterone concentration, but this benefit might be counteracted by the opposing catabolic effects of the increase in cortisol and resultant decline in the testosterone:cortisol ratio.

Caffeine improved RSA, including next day performance, but had little effect on RAT or sleep parameters.

Caffeine increased voluntary workload in professional athletes, even more so under conditions of self-reported limited sleep. Caffeine may prove worthwhile when athletes are tired, especially in those identified as responders.

Data suggest that a relatively high (5-mg·kg body weight) but not low (2-mg·kg body weight) caffeine dose is ergogenic for maximal knee extension/flexion exercise.

In conclusion, while a number of metabolic responses were increased during exercise after caffeine ingestion, perception of effort was reduced and this may be attributed to the direct stimulatory effect of caffeine on the central nervous system. However, this caffeine-induced reduction in effort perception did not improve exercise performance.

In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials.

It was concluded that caffeine dose of up to 15mg/kg seems not to have any ergogenic effect on maximum aerobic power of young black African male adults.

Rowers' performance in 2,000-m efforts can improve by ~2% with 6 mg/kg BM caffeine supplementation. When caffeine is combined with sodium bicarbonate, gastrointestinal symptoms may prevent performance enhancement, so further investigation of ingestion protocols that minimize side effects is required.

The results of this study show that caffeine supplementation has no effect on short-duration sprint cycling performance, irrespective of the dosage used.

These results indicate that caffeine ingestion reverses the morning neuromuscular declines in highly resistance-trained men, raising performance to the levels of the afternoon trial. Our electrical stimulation data, along with the NE values, suggest that caffeine increases neuromuscular performance having a direct effect in the muscle.

This study revealed that acute caffeine ingestion can significantly enhance performance of prolonged, intermittent-sprint ability in competitive, male, team-sport athletes.

A caffeine dose of 3 mg x kg(-1) body mass appears to improve cycling performance in well-trained and familiarised athletes. Doubling the dose to 6 mg x kg(-1) body mass does not confer any additional improvements in performance.

Across all treatments, pain perception was significantly increased (p < .05) during exercise, as well as from Bout 1 to 2, yet there was no effect (p > .05) of caffeine on pain perception or RPE. Various measures of muscle function were improved (p < .05) with a 5-mg/kg caffeine dose vs. the other treatments. In the 5-mg/kg trial, it is plausible that subjects were able to perform better with similar levels of pain perception and exertion.

CAF improved performance independent of environmental temperature. These findings suggest that caffeine at the dosage utilized (6 mg/kg body mass) is a, legal drug that provides an ergogenic benefit in 12 and 33°C.

Fatigue scores were greater postexercise (p = 0.001) compared to scores pre exercise across conditions. Caffeine ingestion enhances performance in short-term, resistance exercise to failure and may favorably change the mood state response to exercise compared to a placebo.

No significant difference was found in time to exhaustion between treatments. A significant main effect of treatment for reported pain (p < 0.001, Φ = 0.377) was observed. Thus, in a population of recreationally trained college-aged adults, low-dose caffeine may attenuate the individual's perception of pain during a grip to exhaustion task.

Perceived arousal was elevated during exercise but did not differ between trials. Overall, the results suggest that a moderate dose of CAF ingested 1h prior to exercise maintains a more positive subjective experience during prolonged cycling. This observation may partially explain caffeine's ergogenic effects.

Results suggest that individuals homozygous for the A allele of this polymorphism may have a larger ergogenic effect following caffeine ingestion.

Caffeine treatment increased epinephrine, fatty acids, lactate and norepinephrine at different times during test session and led to insulin-resistance. Hence, caffeine ingestion elicits a similar metabolic response in elderly participants at 70 years old to that seen in younger subjects.

The results suggest that lactate and triglyceride production and increased vascular smooth muscle tone may be responsible for the major part of the thermogenic effect of caffeine.

These data demonstrate the robustness of the lactate, ventilatory and heart rate variability thresholds when challenged by a physiological dose of caffeine.

These data demonstrate the robustness of the lactate, ventilatory and heart rate variability thresholds when challenged by a physiological dose of caffeine.

Caffeine has some potential to benefit training outcomes via the anabolic effects of the increase in testosterone concentration, but this benefit might be counteracted by the opposing catabolic effects of the increase in cortisol and resultant decline in the testosterone:cortisol ratio.

Caffeine increased voluntary workload in professional athletes, even more so under conditions of self-reported limited sleep. Caffeine may prove worthwhile when athletes are tired, especially in those identified as responders.

In conclusion, the usually consumed amount of caffeinated coffee does not have short-term effects on appetite, energy intake, glucose metabolism, and inflammatory markers, but it increases circulating cortisol concentrations in healthy men.

In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials.

Fatigue scores were greater postexercise (p = 0.001) compared to scores pre exercise across conditions. Caffeine ingestion enhances performance in short-term, resistance exercise to failure and may favorably change the mood state response to exercise compared to a placebo.

We confirm that acute doses of caffeine, at levels typically found in a cup of coffee, produce stimulant-like subjective effects and enhance performance in light, nondependent caffeine users. These findings support the idea that the drug has psychoactive effects even in the absence of withdrawal.

Placebo administration in MH participants decreased alertness and increased headache. Caffeine did not increase alertness in NL participants. With frequent consumption, substantial tolerance develops to the anxiogenic effect of caffeine, even in genetically susceptible individuals, but no net benefit for alertness is gained, as caffeine abstinence reduces alertness and consumption merely returns it to baseline.

A caffeine dose of 3 mg x kg(-1) body mass appears to improve cycling performance in well-trained and familiarised athletes. Doubling the dose to 6 mg x kg(-1) body mass does not confer any additional improvements in performance.

A caffeine dose of at least 3 mg/kg in the form of an energy drink is necessary to significantly improve half-squat and bench-press maximal muscle power.

Although the effect of recovery duration on caffeine-induced responses to multiple sprint work requires further investigation, the results of the present study show that caffeine has ergogenic properties with the potential to benefit performance in both single and multiple sprint sports.

Fatigue scores were greater postexercise (p = 0.001) compared to scores pre exercise across conditions. Caffeine ingestion enhances performance in short-term, resistance exercise to failure and may favorably change the mood state response to exercise compared to a placebo.

In conclusion, acute caffeine ingestion significantly improved endothelial function assessed by brachial artery FMD in subjects with and without CAD and was associated with lower plasma markers of inflammation.

These data demonstrate the robustness of the lactate, ventilatory and heart rate variability thresholds when challenged by a physiological dose of caffeine.

We report for the first time that acute ingestion of 1,3-dimethylamylamine alone and in combination with caffeine results in an increase in SBP, DBP, and RPP without an increase in HR. The largest increase is observed at 60 minutes post-ingestion of C + G 75 mg. These changes cannot be explained by circulating NE and EPI.

Although no changes in glycemia and/or insulin sensitivity were observed after 8 weeks of coffee consumption, improvements in adipocyte and liver function as indicated by changes in adiponectin and fetuin-A concentrations may contribute to beneficial metabolic effects of long-term coffee consumption.

The results suggest that lactate and triglyceride production and increased vascular smooth muscle tone may be responsible for the major part of the thermogenic effect of caffeine.

Variability in the acute BP response to coffee may be partly explained by genetic polymorphisms of the adenosine A2A receptors and α(2)-adrenergic receptors. This trial is registered at clinicaltrials.gov as NCT01330680.

We confirm that acute doses of caffeine, at levels typically found in a cup of coffee, produce stimulant-like subjective effects and enhance performance in light, nondependent caffeine users. These findings support the idea that the drug has psychoactive effects even in the absence of withdrawal.

Caffeine has some potential to benefit training outcomes via the anabolic effects of the increase in testosterone concentration, but this benefit might be counteracted by the opposing catabolic effects of the increase in cortisol and resultant decline in the testosterone:cortisol ratio.

Caffeine increased voluntary workload in professional athletes, even more so under conditions of self-reported limited sleep. Caffeine may prove worthwhile when athletes are tired, especially in those identified as responders.

However, caffeine ingestion had no affect upon any of the marksmanship measures, although it did alleviate cold stress and tiredness. That caffeine ingestion did not affect target detection and rifle marksmanship is a finding that differs from other studies, and is explained by a beneficial arousal caused by the mild level of cold stress experienced by the participants.

In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials.

A caffeine dose of at least 3 mg/kg in the form of an energy drink is necessary to significantly improve half-squat and bench-press maximal muscle power.

Caffeine can decrease insulin sensitivity in healthy humans, possibly as a result of elevated plasma epinephrine levels. Because dipyridamole did not affect glucose uptake, peripheral adenosine receptor antagonism does not appear to contribute to this effect.

Caffeine treatment increased epinephrine, fatty acids, lactate and norepinephrine at different times during test session and led to insulin-resistance. Hence, caffeine ingestion elicits a similar metabolic response in elderly participants at 70 years old to that seen in younger subjects.

Carbohydrate oxidation was depressed, while serum glucose and blood lactate were elevated in this trial compared to cold-placebo. Thus, caffeine increases plasma epinephrine; cold increases oxygen consumption and carbohydrate metabolism, while decreasing lipid metabolism; and the combination of caffeine and cold during exercise increases plasma epinephrine and lipid metabolism, but decreases carbohydrate metabolism.

The results suggest that lactate and triglyceride production and increased vascular smooth muscle tone may be responsible for the major part of the thermogenic effect of caffeine.

Although no changes in glycemia and/or insulin sensitivity were observed after 8 weeks of coffee consumption, improvements in adipocyte and liver function as indicated by changes in adiponectin and fetuin-A concentrations may contribute to beneficial metabolic effects of long-term coffee consumption.

Caffeine can decrease insulin sensitivity in healthy humans, possibly as a result of elevated plasma epinephrine levels. Because dipyridamole did not affect glucose uptake, peripheral adenosine receptor antagonism does not appear to contribute to this effect.

Caffeine ingestion also resulted in higher plasma epinephrine levels than placebo ingestion (P < 0.05). These data support our hypothesis that caffeine ingestion decreases glucose disposal and suggests that adenosine plays a role in regulating glucose disposal in resting humans.

Caffeine treatment increased epinephrine, fatty acids, lactate and norepinephrine at different times during test session and led to insulin-resistance. Hence, caffeine ingestion elicits a similar metabolic response in elderly participants at 70 years old to that seen in younger subjects.

The data suggest that caffeine intake induces a rise in blood glucose levels that is insulin independent.

Caffeine consumption led to significantly faster response times, but only for participants who typically consumed relatively little caffeine. We conclude that the TOVA can be administered to young adults outside the recommended time constraints without compromising the validity of test score interpretation but that the caffeine consumption of participants should be closely monitored.

Caffeine improved RSA, including next day performance, but had little effect on RAT or sleep parameters.

Caffeine ingestion may be beneficial to RA performance when athletes are fresh and fatigued.

The results indicate that the synergistic effects of caffeine and glucose can benefit sustained attention and verbal memory, even with adequate levels of activation of the subjects. However, further studies are required, controlling for different levels of cognitive effort and also considering measurements of neural activity.

We confirm that acute doses of caffeine, at levels typically found in a cup of coffee, produce stimulant-like subjective effects and enhance performance in light, nondependent caffeine users. These findings support the idea that the drug has psychoactive effects even in the absence of withdrawal.

A caffeine dose of at least 3 mg/kg in the form of an energy drink is necessary to significantly improve half-squat and bench-press maximal muscle power.

Although the effect of recovery duration on caffeine-induced responses to multiple sprint work requires further investigation, the results of the present study show that caffeine has ergogenic properties with the potential to benefit performance in both single and multiple sprint sports.

Caffeine has some potential to benefit training outcomes via the anabolic effects of the increase in testosterone concentration, but this benefit might be counteracted by the opposing catabolic effects of the increase in cortisol and resultant decline in the testosterone:cortisol ratio.

Caffeine improved RSA, including next day performance, but had little effect on RAT or sleep parameters.

Caffeine increased voluntary workload in professional athletes, even more so under conditions of self-reported limited sleep. Caffeine may prove worthwhile when athletes are tired, especially in those identified as responders.

Data suggest that a relatively high (5-mg·kg body weight) but not low (2-mg·kg body weight) caffeine dose is ergogenic for maximal knee extension/flexion exercise.

In conclusion, while a number of metabolic responses were increased during exercise after caffeine ingestion, perception of effort was reduced and this may be attributed to the direct stimulatory effect of caffeine on the central nervous system. However, this caffeine-induced reduction in effort perception did not improve exercise performance.

In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials.

It was concluded that caffeine dose of up to 15mg/kg seems not to have any ergogenic effect on maximum aerobic power of young black African male adults.

Rowers' performance in 2,000-m efforts can improve by ~2% with 6 mg/kg BM caffeine supplementation. When caffeine is combined with sodium bicarbonate, gastrointestinal symptoms may prevent performance enhancement, so further investigation of ingestion protocols that minimize side effects is required.

The results of this study show that caffeine supplementation has no effect on short-duration sprint cycling performance, irrespective of the dosage used.

These results indicate that caffeine ingestion reverses the morning neuromuscular declines in highly resistance-trained men, raising performance to the levels of the afternoon trial. Our electrical stimulation data, along with the NE values, suggest that caffeine increases neuromuscular performance having a direct effect in the muscle.

This study revealed that acute caffeine ingestion can significantly enhance performance of prolonged, intermittent-sprint ability in competitive, male, team-sport athletes.

A caffeine dose of 3 mg x kg(-1) body mass appears to improve cycling performance in well-trained and familiarised athletes. Doubling the dose to 6 mg x kg(-1) body mass does not confer any additional improvements in performance.

Across all treatments, pain perception was significantly increased (p < .05) during exercise, as well as from Bout 1 to 2, yet there was no effect (p > .05) of caffeine on pain perception or RPE. Various measures of muscle function were improved (p < .05) with a 5-mg/kg caffeine dose vs. the other treatments. In the 5-mg/kg trial, it is plausible that subjects were able to perform better with similar levels of pain perception and exertion.

CAF improved performance independent of environmental temperature. These findings suggest that caffeine at the dosage utilized (6 mg/kg body mass) is a, legal drug that provides an ergogenic benefit in 12 and 33°C.

Fatigue scores were greater postexercise (p = 0.001) compared to scores pre exercise across conditions. Caffeine ingestion enhances performance in short-term, resistance exercise to failure and may favorably change the mood state response to exercise compared to a placebo.

No significant difference was found in time to exhaustion between treatments. A significant main effect of treatment for reported pain (p < 0.001, Φ = 0.377) was observed. Thus, in a population of recreationally trained college-aged adults, low-dose caffeine may attenuate the individual's perception of pain during a grip to exhaustion task.

Perceived arousal was elevated during exercise but did not differ between trials. Overall, the results suggest that a moderate dose of CAF ingested 1h prior to exercise maintains a more positive subjective experience during prolonged cycling. This observation may partially explain caffeine's ergogenic effects.

Results suggest that individuals homozygous for the A allele of this polymorphism may have a larger ergogenic effect following caffeine ingestion.

These data demonstrate the robustness of the lactate, ventilatory and heart rate variability thresholds when challenged by a physiological dose of caffeine.

Caffeine treatment increased epinephrine, fatty acids, lactate and norepinephrine at different times during test session and led to insulin-resistance. Hence, caffeine ingestion elicits a similar metabolic response in elderly participants at 70 years old to that seen in younger subjects.

The results suggest that lactate and triglyceride production and increased vascular smooth muscle tone may be responsible for the major part of the thermogenic effect of caffeine.

Caffeine and opening the eyes have additive effects on two measures of arousal, increasing SCL and reducing global EEG alpha. However, the independent variable effects are not equivalent, suggesting that one or both measures reflect additional non-arousal processes.

We confirm that acute doses of caffeine, at levels typically found in a cup of coffee, produce stimulant-like subjective effects and enhance performance in light, nondependent caffeine users. These findings support the idea that the drug has psychoactive effects even in the absence of withdrawal.

Fatigue scores were greater postexercise (p = 0.001) compared to scores pre exercise across conditions. Caffeine ingestion enhances performance in short-term, resistance exercise to failure and may favorably change the mood state response to exercise compared to a placebo.

However, caffeine ingestion had no affect upon any of the marksmanship measures, although it did alleviate cold stress and tiredness. That caffeine ingestion did not affect target detection and rifle marksmanship is a finding that differs from other studies, and is explained by a beneficial arousal caused by the mild level of cold stress experienced by the participants.

In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials.

Caffeine consumption led to significantly faster response times, but only for participants who typically consumed relatively little caffeine. We conclude that the TOVA can be administered to young adults outside the recommended time constraints without compromising the validity of test score interpretation but that the caffeine consumption of participants should be closely monitored.

Caffeine improved RSA, including next day performance, but had little effect on RAT or sleep parameters.

Caffeine ingestion may be beneficial to RA performance when athletes are fresh and fatigued.

Placebo administration in MH participants decreased alertness and increased headache. Caffeine did not increase alertness in NL participants. With frequent consumption, substantial tolerance develops to the anxiogenic effect of caffeine, even in genetically susceptible individuals, but no net benefit for alertness is gained, as caffeine abstinence reduces alertness and consumption merely returns it to baseline.

The results indicate that the synergistic effects of caffeine and glucose can benefit sustained attention and verbal memory, even with adequate levels of activation of the subjects. However, further studies are required, controlling for different levels of cognitive effort and also considering measurements of neural activity.

Caffeine can decrease insulin sensitivity in healthy humans, possibly as a result of elevated plasma epinephrine levels. Because dipyridamole did not affect glucose uptake, peripheral adenosine receptor antagonism does not appear to contribute to this effect.

Caffeine has some potential to benefit training outcomes via the anabolic effects of the increase in testosterone concentration, but this benefit might be counteracted by the opposing catabolic effects of the increase in cortisol and resultant decline in the testosterone:cortisol ratio.

Caffeine increased voluntary workload in professional athletes, even more so under conditions of self-reported limited sleep. Caffeine may prove worthwhile when athletes are tired, especially in those identified as responders.

Caffeine treatment increased epinephrine, fatty acids, lactate and norepinephrine at different times during test session and led to insulin-resistance. Hence, caffeine ingestion elicits a similar metabolic response in elderly participants at 70 years old to that seen in younger subjects.

Carbohydrate oxidation was depressed, while serum glucose and blood lactate were elevated in this trial compared to cold-placebo. Thus, caffeine increases plasma epinephrine; cold increases oxygen consumption and carbohydrate metabolism, while decreasing lipid metabolism; and the combination of caffeine and cold during exercise increases plasma epinephrine and lipid metabolism, but decreases carbohydrate metabolism.

However, caffeine ingestion had no affect upon any of the marksmanship measures, although it did alleviate cold stress and tiredness. That caffeine ingestion did not affect target detection and rifle marksmanship is a finding that differs from other studies, and is explained by a beneficial arousal caused by the mild level of cold stress experienced by the participants.

In contrast, cortisol concentrations were not elevated until after the third exercise set; following the caffeine treatment cortisol was reduced by 21 ± 31% (ES -0.30; ± 0.34) relative to placebo. The acute ingestion of caffeine via chewing gum attenuated fatigue during repeated, high-intensity sprint exercise in competitive cyclists. Furthermore, the delayed fatigue was associated with substantially elevated testosterone concentrations and decreased cortisol in the caffeine trials.

Although no changes in glycemia and/or insulin sensitivity were observed after 8 weeks of coffee consumption, improvements in adipocyte and liver function as indicated by changes in adiponectin and fetuin-A concentrations may contribute to beneficial metabolic effects of long-term coffee consumption.

Caffeine ingestion also resulted in higher plasma epinephrine levels than placebo ingestion (P < 0.05). These data support our hypothesis that caffeine ingestion decreases glucose disposal and suggests that adenosine plays a role in regulating glucose disposal in resting humans.

In conclusion, the usually consumed amount of caffeinated coffee does not have short-term effects on appetite, energy intake, glucose metabolism, and inflammatory markers, but it increases circulating cortisol concentrations in healthy men.

The data suggest that caffeine intake induces a rise in blood glucose levels that is insulin independent.

A caffeine dose of 3 mg x kg(-1) body mass appears to improve cycling performance in well-trained and familiarised athletes. Doubling the dose to 6 mg x kg(-1) body mass does not confer any additional improvements in performance.

A caffeine dose of at least 3 mg/kg in the form of an energy drink is necessary to significantly improve half-squat and bench-press maximal muscle power.

Although the effect of recovery duration on caffeine-induced responses to multiple sprint work requires further investigation, the results of the present study show that caffeine has ergogenic properties with the potential to benefit performance in both single and multiple sprint sports.

Fatigue scores were greater postexercise (p = 0.001) compared to scores pre exercise across conditions. Caffeine ingestion enhances performance in short-term, resistance exercise to failure and may favorably change the mood state response to exercise compared to a placebo.

In conclusion, acute caffeine ingestion significantly improved endothelial function assessed by brachial artery FMD in subjects with and without CAD and was associated with lower plasma markers of inflammation.

These data demonstrate the robustness of the lactate, ventilatory and heart rate variability thresholds when challenged by a physiological dose of caffeine.

We report for the first time that acute ingestion of 1,3-dimethylamylamine alone and in combination with caffeine results in an increase in SBP, DBP, and RPP without an increase in HR. The largest increase is observed at 60 minutes post-ingestion of C + G 75 mg. These changes cannot be explained by circulating NE and EPI.

Although no changes in glycemia and/or insulin sensitivity were observed after 8 weeks of coffee consumption, improvements in adipocyte and liver function as indicated by changes in adiponectin and fetuin-A concentrations may contribute to beneficial metabolic effects of long-term coffee consumption.

The results suggest that lactate and triglyceride production and increased vascular smooth muscle tone may be responsible for the major part of the thermogenic effect of caffeine.

Variability in the acute BP response to coffee may be partly explained by genetic polymorphisms of the adenosine A2A receptors and α(2)-adrenergic receptors. This trial is registered at clinicaltrials.gov as NCT01330680.

We confirm that acute doses of caffeine, at levels typically found in a cup of coffee, produce stimulant-like subjective effects and enhance performance in light, nondependent caffeine users. These findings support the idea that the drug has psychoactive effects even in the absence of withdrawal.

A caffeine dose of at least 3 mg/kg in the form of an energy drink is necessary to significantly improve half-squat and bench-press maximal muscle power.

Caffeine can decrease insulin sensitivity in healthy humans, possibly as a result of elevated plasma epinephrine levels. Because dipyridamole did not affect glucose uptake, peripheral adenosine receptor antagonism does not appear to contribute to this effect.

Caffeine treatment increased epinephrine, fatty acids, lactate and norepinephrine at different times during test session and led to insulin-resistance. Hence, caffeine ingestion elicits a similar metabolic response in elderly participants at 70 years old to that seen in younger subjects.

In conclusion, caffeine ingestion caused not only increases in TYMP and mT(b) through thermogenesis, but also an increased sweating sensitivity via changes in sudomotor activity.

The results suggest that lactate and triglyceride production and increased vascular smooth muscle tone may be responsible for the major part of the thermogenic effect of caffeine.

Although no changes in glycemia and/or insulin sensitivity were observed after 8 weeks of coffee consumption, improvements in adipocyte and liver function as indicated by changes in adiponectin and fetuin-A concentrations may contribute to beneficial metabolic effects of long-term coffee consumption.

Caffeine ingestion also resulted in higher plasma epinephrine levels than placebo ingestion (P < 0.05). These data support our hypothesis that caffeine ingestion decreases glucose disposal and suggests that adenosine plays a role in regulating glucose disposal in resting humans.