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Citrus Aurantium and caffeine complex versus placebo on biomarkers of metabolism: a double blind crossover design

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  • Citrus Aurantium and caffeine complex versus placebo on biomarkers of metabolism: a double blind crossover design

    The primary purpose of this study was to examine the claim that CA + C supplementation can alter resting metabolic profile, with a secondary aim to evaluate post-exercise metabolic recovery following an exhaustive exercise protocol in habitual caffeine consumers. The major findings of the study indicate that CA + C consumption resulted in a maintenance of glucose levels following the ingestion period, while a significant drop occurred following the consumption of the PLA. No significant trial differences occurred in insulin, lactate or triglycerides throughout the ingestion period. The recovery period for both the CA + C and the PLA trials reveled no trial-based differences.

    The ingestion period of the study occurred over a 45-min time frame in a quiet, relaxed setting following the consumption of CA + C or PLA. Under normal fasted conditions it is not uncommon to observe a slight decrease in blood glucose with concurrent decreases in insulin concentration over a prolong period of rest [17, 18]. Blood glucose concentration following the PLA trial is reflective of this response, with a significant drop occurring at I2. Interestingly, the CA + C ingestion period did not follow this trend. No changes in glucose concentration occurred and was found to be significantly higher than that of the PLA trial at the I2 time point. The glucose response following the CA + C trial is closer to those found by Ratamess et al. [2], who observed a significant increase in concentration following the 45-min ingestion period of p-synephrine + caffeine. However, the Ratamess study observed equivalent changes in blood glucose following the 45-min ingestion periods in the placebo, p-synephrine, and p-synephrine + caffeine trials. This increase in blood glucose could be attributed to the 16 g of carbohydrate used in their supplement compound [2]. The medium by which the supplements were delivered in the current study were capsules absent of carbohydrate and would rationalize the difference in observations between the two studies.

    Similar to glucose, insulin has been shown to be maintained or decrease during resting and fasted conditions [19]. The findings in our study are supportive of the expected response, with insulin concentration being maintained in both PLA and CA + C throughout the ingestion period. This is in contrast to Graham et al. [20] who found that caffeine supplementation significantly elevated serum insulin levels when compared to placebo during an oral glucose tolerance test. However, the differences in observations can likely be attributed to the dosage of caffeine Graham et al. [20] used, which was almost five times greater than that of the current study. Though there were no apparent changes in the concentration of insulin following the CA + C trial, several studies have demonstrated that caffeine causes a decrease in insulin sensitivity [21]. This may be a possible mechanism explaining the glucose maintenance observed following the CA + C consumption.

    The caffeine components role in sympathetic nervous system (SNS) mediated glucose release [22] may be another likely contributor to the observed glucose response. Following the consumption of CA + C, both plasma E and NE significantly increased, while no changes occurred with the PLA trial. This is in agreement with Graham and Spriet [23], who observed a two-time increase in plasma E following the consumption of 9 mg/kg of caffeine. Additionally, Stuart et al. [24], demonstrated a significantly higher level of plasma E 70-min following the consumption of 6 mg/kg of caffeine when compared to the placebo group. The caffeine concentration given in this trial was a single dose of 100 mg (1.13–1.44 mg/kg), which is far less than the examined dosages of the aforementioned studies. This may in part explain the modest increase in E and NE observed at I2 in the CA + C trial and consequent glucose maintenance as opposed to more robust glucose responses observed in other studies [22]. The CA component of the complex is another mechanism by which the maintenance of blood glucose could have occurred. Specifically, the active ingredient p-synephrine acts on beta-3 receptors in order to increase lipolysis [1], thereby acting to spare blood glucose. However, the findings in our study do not suggest this due to triglycerides remaining unchanged following the consumption of PLA or CA + C. Overall, the present study suggests that the consumption of CA + C in the current dosage appears to promote glucose maintenance at resting conditions. Future research should examine varying concentrations in order to determine a dose effect.


    The exhaustive exercise trial selected for this study was a repeated Wingate protocol designed to induce a high metabolic stress and fatigue. Following the completion of the trials, no differences in glucose, insulin, triglycerides, or catecholamines were observed. Blood glucose nearly doubled for both CA + C and PLA compared to baseline values, which indicates a normal metabolic response to an acute high intensity protocol [25]. However, insulin did not statistically elevate immediately post-exercise but demonstrated a non-statistical increase at the end of the recovery period. Previous research has demonstrated insulin spikes immediately following prolonged high-intensity protocols [25]; however, the duration of those protocols was ultimately longer than the one used previous studies and may have led to the different insulin response. Though fat oxidation was not directly measured throughout this study, plasma triglycerides were obtained to determine changes in metabolic function. A primary function of the Citrus Aurantium is improved lipid peroxidation through p-synephrine and beta-3 activation, which may alter the release of triglycerides following exercise based on demand, and ultimately influence metabolic recovery. Post-exercise plasma triglycerides have been shown to account for half of the delayed component of excess post exercise oxygen consumption (EPOC) [26, 27], which is a beneficial response to high-intensity exercise. Interestingly, both trials showed spikes in plasma triglycerides at R1 when compared to I2, though no difference was observed between trials. Following the 45-min recovery, both trials demonstrate similar rates in recovery in triglycerides, suggesting that CA + C had no influence.

    Though this study was a novel attempt to evaluate the general metabolic responses to the consumption of the CA + C complex, it was not without its limitations. Currently there is no recommended dosage for the CA + C complex, and the current concentrations selected for this study was based on previous research [2]. The primary purpose of the study was to evaluate the CA + C complex; however, future research should examine the individual components to determine a causal relationship. Furthermore, various dosages of this complex should be evaluated in order to better determine a dose-response effect. The markers used to examine metabolism were glucose, insulin, and triglycerides; future research should examine a more extensive metabolic profile including substrate utilization and free fatty acids. Though a priori analysis based on a power of 0.8, alpha level of 0.05, and effect size of 0.3 determined the necessary n size to be 10 [28], a larger population sample should be used in order to better evaluate effects and trends.
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