Chronic Caffeine Intake Research Articles

Subclinical brain manifestations of repeated mild traumatic brain injury are changed by chronic exposure to sleep loss, caffeine, and sleep aids

IntroductionAfter mild traumatic brain injury (mTBI), the brain is labile for weeks and months and vulnerable to repeated concussions. During this time, patients are exposed to everyday circumstances that, in themselves, affect brain metabolism and blood flow and neural processing. How commonplace activities interact with the injured brain is unknown. The present study in an animal model investigated the extent to which three commonly experienced exposures—daily caffeine usage, chronic sleep loss, and chronic sleep aid medication—affect the injured brain in the chronic phase. MethodsSubclinical trauma by repeated mTBIs was produced by our head rotational acceleration injury model, which causes brain injury consistent with the mechanism of concussion in humans. Forty-eight hours after a third mTBI, chronic administrations of caffeine, sleep restriction, or zolpidem (sedative hypnotic) began and were continued for 70 days. On Days 30 and 60 post injury, resting state functional magnetic resonance imaging (fMRI) and diffusion tensor imaging (DTI) were performed. ResultsChronic caffeine, sleep restriction, and zolpidem each changed the subclinical brain characteristics of mTBI at both 30 and 60 days post injury, detected by different MRI modalities. Each treatment caused microstructural alterations in DTI metrics in the insular cortex and retrosplenial cortex compared with mTBI, but also uniquely affected other gray and white matter regions. Zolpidem administration affected the largest number of individual structures in mTBI at both 30 and 60 days, and not necessarily toward normalization (sham treatment). Chronic sleep restriction changed local functional connectivity at 30 days in diametrical opposition to chronic caffeine ingestion, and both treatment outcomes were different from sham, mTBI-only and zolpidem comparisons. The results indicate that commonly encountered exposures modify subclinical brain activity and structure long after healing is expected to be complete. ConclusionsChanges in activity and structure detected by fMRI are widely understood to reflect changes in the functions of the affected region which conceivably underlie mTBI neuropathology and symptomatology in the chronic phase after injury.

Dietary Caffeine and Brain Dopaminergic Function in Parkinson Disease.

This study was undertaken to investigate the effects of dietary caffeine intake on striatal dopamine function and clinical symptoms in Parkinson disease in a cross-sectional and longitudinal setting. One hundred sixty-three early Parkinson disease patients and 40 healthy controls were investigated with [123I]FP-CIT single photon emission computed tomography, and striatal dopamine transporter binding was evaluated in association with the level of daily coffee consumption and clinical measures. After a median interval of 6.1 years, 44 patients with various caffeine consumption levels underwent clinical and imaging reexamination including blood caffeine metabolite profiling. Unmedicated early Parkinson disease patients with high coffee consumption had 8.3 to 15.4% lower dopamine transporter binding in all studied striatal regions than low consumers, after accounting for age, sex, and motor symptom severity. Higher caffeine consumption was further associated with a progressive decline in striatal binding over time. No significant effects of caffeine on motor function were observed. Blood analyses demonstrated a positive correlation between caffeine metabolites after recent caffeine intake and dopamine transporter binding in the ipsilateral putamen. Chronic caffeine intake prompts compensatory and cumulative dopamine transporter downregulation, consistent with caffeine's reported risk reduction in Parkinson disease. However, this decline does not manifest in symptom changes. Transiently increased dopamine transporter binding after recent caffeine intake has implications for dopaminergic imaging guidelines. ANN NEUROL 2024;96:262-275.

Chronic caffeine intake alters collagen deposition in long bones: an experimental preliminary study

This study explores the impact of chronic caffeine intake on collagen deposition in long bones and correlates it with morphometric and metabolic alterations in Wistar rats. Animals had either regular drinking water (Control group) or caffeinated drinking water in a 300 mg/L dose (Caffeine group) for 12 wk. Using Picro-Sirius red collagen staining, cortical (78.07 ± 1.27 vs 82.12 ± 1.22) and trabecular (74.29 ± 1.09 vs 77.97 ± 1.03) collagen percentages in the caffeine group were markedly (p = 0.0448 and p = 0.0351; respectively) lower than the control group. Caffeine intake induced apparent alterations in the microstructure of cortical diaphysis and femoral head trabecular density as determined by micro-CT. In caffeinated animals, levels of bone-related metabolic biomarkers including BALP (1.41 ± 0.06 vs 1.12 ± 0.07), CTX (313.5 ± 20.78 vs 224.3 ± 27.19), DPD (11.61 ± 0.72 vs 9.26 ± 0.62), BGP (10.35 ± 0.43 vs 9.14 ± 0.34), and TRAP (4.34 ± 0.08 vs 4.01 ± 0.11) were increased (p = 0.0136, p = 0.0262, p = 0.0343, p = 0.0571, and p = 0.0461; respectively) as compared to control animals. Except for BALP (p = 0.0175) and DPD (p = 0.0423), the Pearson correlation between collagen bone deposition and microstructures and metabolic changes was not statistically significant. Collectively, chronic caffeine consumption restricts cortical and trabecular collagen deposition in long bones leading to microstructure and metabolic alterations.

Headache Prevalence and Its Associated Factors in Makkah, Saudi Arabia.

Primary headaches are more prevalent and associated with several risk factors, such as chronic diseases, unhealthy lifestyles, smoking, caffeine intake, work, and stress. However, these factors are not associated with specific headache disorders. We investigated the prevalence of primary headache disorders and the associated risk factors in Makkah. This cross-sectional study, conducted over a 6-month period, used an anonymous survey disseminated through online platforms. The questionnaire was a modified version of a validated questionnaire used to assess headaches in relation to modifiable and non-modifiable risk factors. In total, 1177 participants aged 18-65 (mean, 31.5 ± 12.6) years were included. Headaches were diagnosed among 44.2% of participants aged 20-59 years, with a high prevalence among young adults; additionally, 71.5% of participants with headaches reported experiencing headaches for <15 days per month. Chronic headaches were found in 28.5% of participants. Age, chronic diseases, work, caffeine consumption, and smoking were associated with having a significant effect on headache prevalence. The prevalence of headaches in Makkah has increased in comparison to that reported in previous studies. Certain modifiable and non-modifiable risk factors have been associated with headaches. Headaches impact all life aspects of individuals and communities. An educational program for professionals and patients can improve patient outcomes.

Maternal chronic caffeine intake impairs fertility, placental vascularization and fetal development in mice

Caffeine is commonly consumed by pregnant women to avoid fatigue or as a habit. However, it is not clearly determined its side effects to the conceptuses. This study evaluated placental morphofunctional alterations after maternal chronic caffeine intake and the effects on fetal growth. Female Swiss mice received, via gavage, caffeine doses (either 60, 120 or 240 mg/kg/day) seven days before mating until gestational days-(GD) 11.5 or 17.5. Fetal biometrical parameters were assessed, and placentae were either submitted to histomorphometrical or molecular evaluation of angiogenesis (placental growth factor-1[PlGF-1]), apoptosis (Caspase-3) and proliferation (Ki-67) markers (evaluated in Swiss dams) and to intravital microscopy (evaluated in C57BL/6 dams). Caffeine exposed fetuses exhibited intrauterine growth restriction in a sex-dependent manner, with greater commitment of female fetuses (P < 0.05). In addition, placentae from dams that received 120 mg/kg/day showed less irrigation by maternal blood and greater development of fetal vasculature, characterized by higher number of larger vessels (P < 0.05). Although no effects on apoptosis (Caspase-3) and angiogenesis (PlGF-1) were observed, dams treated with 60 mg/kg/day showed greater placental cell proliferation (Ki-67 staining) at GD 11.5 (P < 0.05). The group treated with 240 mg/kg/day exhibited only one pregnant dam for each gestational age, suggesting that this high caffeine consumption may compromise fertility. Taken together, even in the doses currently ingested by many pregnant women, caffeine has detrimental effects on placental vasculature and fetal development in mice. Therefore, our results strongly suggest that caffeine consumption in human pregnancies greater than the recommended doses should be avoided.

Combined Exposure to Chronic Sleep Deprivation and Caffeine Potentiates Behavioural Deficits by Altering Neurochemical Profile and Synaptophysin Expression in Long-Evans Rats.

Using the Unpredictable Chronic Sleep Deprivation (UCSD) paradigm we developed, the combined effects of chronic sleep deprivation and high caffeine intake on prefrontal cortical synaptophysin expression, neurochemical profiles, and behavioural outcomes in Long-Evans rats were evaluated. The combination of chronic sleep deprivation and high-dose caffeine treatment produced varying degrees of behavioural impairments, depletion of antioxidants, serotonin, and an upregulation of acetylcholinesterase (AChE) activity in the prefrontal cortex. An immunohistochemical assessment revealed a reduction in synaptophysin protein expression in the prefrontal cortex following exposure to high-dose caffeine and chronic sleep deprivation. Overall, our findings support the advocacy for adequate sleep for optimal mental performance as a high intake of caffeine to attenuate the effects of sleep deprivation that may alter the neurochemical profile and synaptic plasticity in the prefrontal cortex, significantly increasing the risk of neuropsychiatric/degenerative disorders.

Effects of chronic caffeine intake and withdrawal on neural activity assessed via resting-state functional magnetic resonance imaging in mice

Caffeine is a psychoactive substance that not only improves wakefulness, but also slows the cognitive decline caused by aging. However, at present, there are no reports about the effects of caffeine withdrawal, including headaches and changes in brain functional networks (nerve activity). Headache may occur approximately 24 h after discontinuing caffeine intake in chronic caffeine drinkers.The current study aimed to examine the brain functional activity via resting-state functional magnetic resonance imaging in chronically caffeinated and decaffeinated groups to investigate changes in brain activity caused by caffeine.C57BL/6J mice were included in the analysis, and they underwent 9.4-T ultrahigh-field magnetic resonance imaging. The mice were classified into the control, chronic caffeinated, and caffeine withdrawal grsoups. Mice were divided into three groups: 1) not exposed to caffeine (control); 2) treated with caffeine at a concentration of 0.3 mg/mL for 4 weeks (chronic caffeinated); and 3) treated as before with caffeine and withdrawn from caffeine for 24 h. After the three groups were examined, functional connectivity matrices were calculated using brain imaging analysis tools, and independent component analysis was performed.The results showed that caffeine administration activated neural activity areas in the stress response system. Furthermore, 24h after caffeine withdrawal, the results showed an increase in pain-related neural activity. In addition, caffeine administration was shown to activate the dentate gyrus, one of the hippocampal regions, and to decrease the neural activity in the olfactory bulb and anterior cingulate cortex.In the current research, the neural activity of specific brain regions changed after chronic caffeine administration and withdrawal.

Effect of caffeine on mitochondrial biogenesis in the skeletal muscle - A narrative review.

Caffeine is one of the most widely used substances as recreational drug for performance-enhancement in sport, underpinned by a strong evidence base. Although the effects of caffeine are widely investigated within the scope of performance physiology, the molecular effects of caffeine within skeletal muscle remain unclear. Evidence from invitro and invivo models suggest that caffeine regulates the glucose metabolism in the skeletal muscle. Moreover, caffeine seems to stimulate CaMKII, PPARδ/β, AMPK and PGC1α, classical markers of exercise-adaptations, including mitochondrial biogenesis and mitochondrial content. This review summarizes evidence to suggest caffeine-effects within skeletal muscle fibers, focusing on the putative role of caffeine on mitochondrial biogenesis to explore whether caffeine supplementation might be a strategy to enhance mitochondrial biogenesis.

Chronic caffeine ingestion improves memory and learning and increases neuronal population and dendritic length in the hippocampus of adult mice

Caffeine is the most widely consumed psychoactive drug in the world, ingested as natural components of chocolate, coffee and tea and as added components to soda and energy drinks. Here we assessed behavioural changes caused by chronic caffeine administration as well as morphological changes within specific regions of the adult mice brain: the hippocampus and amygdala. Twenty-four adult male albino mice were randomly divided into three groups. Caffeine was administered daily by gavage for 8 weeks at a dosage of 20 mg/kg for low dose (LD) group and 60 mg/kg for high dose (HD) group while the third group served as control (CNT). After the period of administration, neurobehavioural tasks were carried out; Morris water maze for learning and memory open field test and elevated plus maze test for anxiety. The mice were sacrificed; their brain tissues were harvested and processed for H&amp;E, Cresyl violet and Golgi staining, and assessed qualitatively and quantitatively. Quantitative data from the neurobehavioural tests and neuronal cell counts were expressed as means ± standard errors of means and compared across the groups using analysis of variance (ANOVA). Significance was set at p&lt; 0.05. Mice in the high dose group learnt faster and had significantly increased number of platform crossings in the Morris water maze test. There was, however, a slightly increased level of anxiety in the caffeine-treated mice, compared to controls. Histo-morphometric analysis revealed significantly increased number of pyramidal neurons in the hippocampus in the low dose group, but a decreased neuronal count in the amydala of the low dose and high dose groups compared to controls. The pyramidal neurons in the hippocampus of the caffeine-treated mice had increased apical dendritic length compared to the controls. Our findings strengthen the available data suggesting that prolonged caffeine intake improves cognition, and this process could be mediated by promoting the growth of dendrites and increased number of neurons. However, this is coupled with an increased tendency to be anxiogenic.

Acute Effects of High Doses of Caffeine on Bar Velocity during the Bench Press Throw in Athletes Habituated to Caffeine: A Randomized, Double-Blind and Crossover Study.

Chronic intake of caffeine may produce a reduction in the potential performance benefits obtained with the acute intake of this substance. For this reason, athletes habituated to caffeine often use high doses of caffeine (≥9 mg/kg) to overcome tolerance to caffeine ergogenicity due to chronic intake. The main objective of the current investigation was to evaluate the effects of high caffeine doses on bar velocity during an explosive bench press throw in athletes habituated to caffeine. Twelve resistance-trained athletes, with a moderate-to-high chronic intake of caffeine (~5.3 mg/kg/day) participated in a randomized double-blind and randomized experimental design. Each participant performed three identical experimental sessions 60 min after the intake of a placebo (PLAC) or after the intake of 9 (CAF-9) or 12 mg/kg (CAF-12) of caffeine. In each experimental session, the athletes performed five sets of two repetitions of the bench press throw exercise with a load equivalent to 30% of their one-repetition maximum. In comparison to PLAC, the intake of caffeine increased peak and mean velocity (p < 0.01) during the five sets of the bench press throw exercise. There were no significant differences in peak and mean bar velocity between the two doses of caffeine (CAF-9 vs. CAF-12; p = 0.91, = 0.96, respectively). The ingestion of high doses of caffeine was effective in producing an increase in mean and peak bar velocity during the bench press throw in a group of habitual caffeine users. However, using CAF-12 did not offer additional benefits for performance with respect to CAF-9.

Chronic Caffeine Ingestion Down-Regulates Liver and Visceral Adipose Tissue Inflammatory Gene Expression in High-Fat Diet-Induced Obesity

Chronic Caffeine Ingestion Down-Regulates Liver and Visceral Adipose Tissue Inflammatory Gene Expression in High-Fat Diet-Induced Obesity

Feasibility and acceptability of a randomized controlled trial to investigate withdrawal symptoms in response to caffeinated sugary drink cessation among children

BackgroundSugary drinks (SDs) are key contributors to excess added sugar intake and the predominant source of caffeine among children. Chronic caffeine intake causes dependence, and evidence for sugar dependence is emerging. Development of withdrawal symptoms may pose an obstacle to SD cessation among children. We examined the feasibility and acceptability of a three-arm randomized controlled trial (RCT) designed to investigate withdrawal symptoms resulting from replacement of children's usual caffeinated SD intake with either caffeine-free alternatives or caffeine-free and sugar-free alternatives, compared with continued consumption of caffeinated SDs. MethodsTwenty-nine children 8–12 years old, who consumed ≥12 ounces caffeinated SDs daily, enrolled. The two-week RCT required three in-person meetings and daily completion of electronic questionnaires to assess withdrawal symptoms and intervention adherence. Children were randomized to replace their usual caffeinated SD consumption with 1) caffeine-free alternatives, 2) caffeine-free and sugar-free alternatives, or 3) caffeinated SDs (control), provided by the study team. Feasibility and acceptability were assessed quantitatively and qualitatively. ResultsTwenty-eight participants (97%) completed the study. Adherence was high, with 73% reporting compliance with beverage assignments, and 76% completing all questionnaires. In qualitative interviews at follow-up, children described feelings of importance and commitment, and parents did not find the procedures to be overly burdensome. While challenges to adherence were reported (e.g., child wanting other SDs, time commitment), participants described innovative strategies (e.g., designating a place for study drinks in the refrigerator) to maintain adherence. ConclusionResults indicated high levels of RCT feasibility and acceptability. The reported barriers and strategies for adherence will inform modifications required to design a larger and longer-term trial investigating withdrawal symptoms after SD cessation in children.

Pre-exercise Caffeine Intake Enhances Bench Press Strength Training Adaptations.

Previous research has identified acute caffeine intake as an effective ergogenic aid to enhance velocity and power during bench press exercise. However, no previous investigation has analyzed the effects of chronic intake of caffeine on training adaptations induced by bench press strength training. Thus, the aim of this investigation was to determine the effects of pre-exercise caffeine intake on training adaptations induced by a bench press training protocol. Using a double-blind, randomized experimental design, 16 healthy participants underwent a bench press training protocol for 4 weeks (12 sessions). Seven participants ingested a placebo and nine participants ingested 3 mg/kg/BM of caffeine before each training session. Three days before, and 3 days after the completion of the training protocol, participants performed a one-repetition maximum (1RM) bench press and force-velocity test (from 10 to 100% 1RM). From comparable pre-training values, the strength training similarly increased 1RM in the caffeine and placebo groups (+13.5 ± 7.8% vs. +11.3 ± 5.3%, respectively; p = 0.53). In the caffeine group, the strength training induced a higher mean velocity at 40%, (0.81 ± 0.08 vs. 0.90 ± 0.14 m/s), 60% (0.60 ± 0.06 vs. 0.65 ± 0.06 m/s), 70% (0.47 ± 0.05 vs. 0.55 ± 0.06 m/s), 80% (0.37 ± 0.06 vs. 0.45 ± 0.05 m/s), 90% (0.26 ± 0.07 vs. 0.34 ± 0.06 m/s), and 100% 1RM (0.14 ± 0.04 vs. 0.25 ± 0.05 m/s; p < 0.05) while the increases in the placebo group were evident only at 30 (0.95 ± 0.06 vs. 1.03 ± 0.07 m/s), 70% (0.51 ± 0.03 vs. 0.57 ± 0.05 m/s) and 80% 1RM (0.37 ± 0.06 vs. 0.45 ± 0.05 m/s) (p < 0.05). The placebo group only increased peak velocity at 60 and 70% 1RM (p < 0.05) while peak velocity increased at 10%, and from 30 to 100% 1RM in the caffeine group (p < 0.05). The use of 3 mg/kg/BM of caffeine before exercise did not modify improvements in 1RM obtained during a 4 week bench press strength training program but induced more muscle performance adaptations over a wider range of load.

Chronic Caffeine Ingestion Improves Motor Function and Increases Dendritic Length and Arborization in the Motor Cortex, Striatum, and Cerebellum

Introduction: We assessed motor function after chronic caffeine ingestion and examined brain regions controlling them: the sensorimotor cortex, striatum, and cerebellar cortex. Materials and Method...

Children's Sugar-Sweetened Beverage Consumption: Striking Parallels With Substance Use Disorder Symptoms.

Sugar-sweetened beverage (SSB) intake contributes to obesity and cardiometabolic disease (1). Children's SSB consumption considerably exceeds public health recommendations (2), and efforts to reduce intake have had limited success (3). In addition to high sugar content, many SSBs also contain caffeine, and caffeinated SSBs are the predominant source of caffeine intakes among youth (4). Sugar activates central reward pathways, and similar to drugs of abuse, stimulates dopamine release (5), and meets several criteria for addiction (6). Chronic caffeine intake causes tolerance and withdrawal in children (7), which are core behavioral indicators of substance use disorders (SUDs) (6). Compelling evidence for addictive-like responses to excess sugar intake is emerging, with accumulating support in rodent models (5). Synergistic biopsychological effects of caffeine and sugar may reinforce unfavorable beverage consumption patterns (7). SSBs are a novel stimulus from an evolutionarily standpoint, yet products containing sugar and caffeine (e.g., energy drinks) are increasingly available (8) and heavily advertised to children (7). Children have developing brains and less inhibitory control compared to adults, and thus, are particularly vulnerable to addictive substances (9). Added caffeine in already highly palatable SSBs increases their hedonic and reinforcing properties (10) and may further promote excess added sugar intakes (11). Emerging evidence indicates that children's consumption of highly processed foods, typically high in added sugar and/or saturated fat, can lead to an addictive process reflected by core behavioral indicators of SUDs (12). These include craving, loss of control, tolerance, and withdrawal (12). Children who demonstrate more signs of addiction in their highly processed food consumption are more likely to have higher reward drive for food and higher body mass index (12). Signs of addiction have also been reported among children in response to frequent SSB consumption (13, 14). In our qualitative study (14), parents of children 8–17 years old reported that children experienced physical and affective withdrawal symptoms when caffeinated SSB intake was restricted. Similarly, Falbe et al. (13) reported that adolescents, who reported habitual SSB consumption, regardless of whether SSBs were caffeinated or caffeine-free indicated increased SSB cravings and headaches, and decreased motivation, contentment, concentration, and well-being during 72 h of SSB cessation. It is likely that other aspects of addiction (e.g., tolerance, craving, repeated unsuccessful efforts to reduce) represent important and overlooked obstacles to sustained SSB reduction. Herein, we propose that children's SSB consumption may reflect SUD symptomology and focus specifically on caffeinated SSBs, which are manufactured to contain a highly rewarding mixture of added sugar and caffeine, two ingredients that do not naturally occur in combination.

A 2 Adenosine Receptors Mediate Whole-Body Insulin Sensitivity in a Prediabetes Animal Model: Primary Effects on Skeletal Muscle.

Epidemiological studies showed that chronic caffeine intake decreased the risk of type 2 diabetes. Previously, we described that chronic caffeine intake prevents and reverses insulin resistance induced by hypercaloric diets and aging, in rats. Caffeine has several cellular mechanisms of action, being the antagonism of adenosine receptors the only attained with human coffee consumption. Here, we investigated the subtypes of adenosine receptors involved on the effects of chronic caffeine intake on insulin sensitivity and the mechanisms and sex differences behind this effect. Experiments were performed in male and female Wistar rats fed either a chow or high-sucrose (HSu) diet (35% of sucrose in drinking water) during 28 days, to induce insulin resistance. In the last 15 days of diet the animals were submitted to DPCPX (A1 antagonist, 0.4 mg/kg), SCH58261 (A2A antagonist, 0.5 mg/kg), or MRS1754 (A2B antagonist, 9.5 μg/kg) administration. Insulin sensitivity, fasting glycaemia, blood pressure, catecholamines, and fat depots were assessed. Expression of A1, A2A, A2B adenosine receptors and protein involved in insulin signaling pathways were evaluated in the liver, skeletal muscle, and visceral adipose tissue. UCP1 expression was measured in adipose tissue. Paradoxically, SCH58261 and MRS1754 decreased insulin sensitivity in control animals, whereas they both improved insulin response in HSu diet animals. DPCPX did not alter significantly insulin sensitivity in control or HSu animals, but reversed the increase in total and visceral fat induced by the HSu diet. In skeletal muscle, A1, A2A, and A2B adenosine receptor expression were increased in HSu group, an effect that was restored by SCH58261 and MRS1754. In the liver, A1, A2A expression was increased in HSu group, while A2B expression was decreased, being this last effect reversed by administration of MRS1754. In adipose tissue, A1 and A2A block upregulated the expression of these receptors. A2 adenosine antagonists restored impaired insulin signaling in the skeletal muscle of HSu rats, but did not affect liver or adipose insulin signaling. Our results show that adenosine receptors exert opposite effects on insulin sensitivity, in control and insulin resistant states and strongly suggest that A2 adenosine receptors in the skeletal muscle are the majors responsible for whole-body insulin sensitivity.

Chronic voluntary caffeine intake in male Wistar rats reveals individual differences in addiction-like behavior

Caffeine is the most widely consumed psychoactive substance in the world. However, there is controversy about whether becoming addicted to caffeine is possible and a lack of well-established animal models to examine caffeine consumption. The present study sought to establish a model of caffeine consumption in Wistar rats, identify different rat populations based on caffeine preference, and determine whether extended voluntary caffeine consumption produces compulsive-like caffeine intake and withdrawal symptoms.Male Wistar rats were used throughout the experiment. The optimal concentration of caffeine to maximize caffeine consumption and caffeine preference was determined. Rats were then given continuous access to caffeine, followed by intermittent access. Rats were tested for signs of withdrawal-like behavior by measuring mechanical nociception and irritability-like behavior. Rats were further examined for compulsive-like caffeine consumption using quinine adulteration.Dose-response testing indicated an optimal caffeine concentration of 0.3 mg/mL. During intermittent access to caffeine, the rats did not escalate their caffeine intake and instead exhibited a decrease in intake over sessions. Three groups of rats were identified based on caffeine preference (high, medium, and low) across continuous and intermittent access. These three groups of rats matched low (1 cup), medium (2 cups), and high (4 cups) levels of daily coffee consumption in humans. Caffeine-consuming rats did not exhibit differences in mechanical nociception or irritability-like behavior compared with controls. In high caffeine-preferring rats but not in medium or low caffeine-preferring rats, compulsive-like caffeine consumption was observed.The present study established a rodent model of caffeine consumption that resulted in large individual differences in caffeine intake, similar to humans. Compulsive-like caffeine consumption in high caffeine-preferring rats and differences in caffeine preference between groups suggest that caffeine may result in compulsive-like intake in a subpopulation of subjects. Further testing is necessary to determine the factors that contribute to differences in caffeine preference and compulsive-like intake.

The Effect of Low-Doses of Caffeine and Taurine on Convulsive Seizure Parameters in Rats.

Introduction: Caffeine, an adenosine-receptor blocker, is believed to have neuronal excitatory effects, while Taurine, a mammalian amino acid, was shown to have neuroinhibitory effects. Aim: The aim of this study was to investigate the effects of acute and chronic administration of low doses of Caffeine and Taurine on the seizure threshold in rats. Methods: Six-week-old Sprague-Dawley male rats (n = 280) were divided randomly into five groups (control, acute caffeine intake, acute taurine intake, chronic caffeine intake and chronic taurine intake), with five subgroups per group according to five different doses of Pentylenetetrazole (PTZ) injections. Each subgroup consisted of eight rats. Data was entered and analyzed using Microsoft EXCEL and AddinsoftTM XLSTAT (Version 2012.6.06; New York, NY, USA). p-value = 0.05 was regarded as statistically significant. Results: There was a significant decrease in the latency of PTZ-induced seizures with both acute (p-value < 0.05) and chronic (p-value < 0.01) Caffeine treatment groups. Chronic exposure to Caffeine exhibited an increase in the probability of seizures (p-value < 0.05). However, acute exposure to Caffeine did not show a significant impact on the probability of seizures. Neither acute nor chronic exposures to Taurine had an effect on the probability of seizures, nor on the latency of PTZ-induced seizures. Discussion: Our study found that acute as well as chronic exposure to low doses of Caffeine (50 and 80 mg/kg) reduces the threshold, and hence increases the likelihood for seizures since it favors a state of neuronal hyper excitability through blocking of all adenosine receptors. On the other hand, acute or chronic exposure to Taurine did not show a significant effect on the PTZ-induced seizures parameters.

Caffeine Supplementation for Powerlifting Competitions: An Evidence-Based Approach.

In this paper, we review the effects of caffeine on muscle strength and provide suggestions for caffeine supplementation in powerlifting competitions. The currently available studies indicate that caffeine ingestion may enhance strength in two powerlifting competition events, the squat and the bench press. For the deadlift, the same might be expected even though studies directly using this event are lacking. Optimal doses of caffeine are likely in the range from 2 to 6 mg·kg−1, and are highly individual. When using caffeine-containing capsules, 60 minutes pre-exercise seems to be a good timing of caffeine consumption. For other sources such as caffeinated chewing gum, a shorter period (5 to 10 min) from consumption to the start of the exercise seems to be effective. For shorter duration powerlifting competitions (e.g., 2 hours), one pre-competition dose of caffeine could be sufficient for acute performance-enhancing effects that might be maintained across all three events. For longer duration competitions (with longer rest periods between one repetition maximum attempts), there might be a benefit to repeated dosing with caffeine; for example, ingesting smaller doses of caffeine before each attempt or event. During training, powerlifters may consider ingesting caffeine only before the training sessions with the highest intensity. This approach might eliminate the attenuation of caffeine’s effects associated with chronic caffeine ingestion and would help in maximizing performance benefits from acute caffeine ingestion at the competition. Nonetheless, withdrawal from caffeine (e.g., no caffeine intake seven days before competition) does not seem necessary and may have some indirect negative effects.

Effects of chronic caffeine consumption on sleep and the sleep electroencephalogram in mice.

Background:Caffeine is one of the most widely consumed psychostimulants, and it impacts sleep and circadian physiology.Aim:Caffeine is generally used chronically on a daily basis. Therefore, in the current study, we investigated the chronic effect of caffeine on sleep in mice.Methods:We recorded the electroencephalogram and electromyogram on a control day, on the first day of caffeine consumption (acute), and following two weeks of continuous caffeine consumption (chronic). In the latter condition, a period of six-hour sleep deprivation was conducted during the light period. Control mice, which received normal drinking water, were also recorded and sleep deprived.Results:We found that caffeine induced differential effects following acute and chronic consumption. Over 24 h, waking increased following acute caffeine whereas no changes were found in the chronic condition. The daily amplitude of sleep–wake states increased in both acute and chronic conditions, with the highest amplitude in the chronic condition, showing an increase in sleep during the light and an increase in waking during the dark. Furthermore, electroencephalogram slow-wave-activity in non-rapid eye-movement sleep was increased, compared with both control conditions, during the first half of the light period in the chronic condition. It was particularly challenging to keep the animals awake during the sleep deprivation period under chronic caffeine.Conclusions:Together the data suggest an increased sleep pressure under chronic caffeine. In contrast to the traditional conception on the impact on sleep, chronic caffeine intake seems to increase the daily sleep–wake cycle amplitude and increase sleep pressure in mice.