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PubMed2005

Caffeine promotes hyperthermia and serotonergic loss following co-administration of the substituted amphetamines, MDMA ("Ecstasy") and MDA ("Love").

The present study determined the effect of caffeine co-administration on the core body temperature response and long-term serotonin (5-HT) loss induced by methylenedioxymethamphetamine (MDMA; "Ecstasy") and its metabolite methylenedioxyamphetamine (MDA; "Love") to rats. In group-housed animals, caffeine (10 mg/kg) enhanced the acute toxicity of MDMA (15 mg/kg) and MDA (7.5 mg/kg), resulting in an exaggerated hyperthermic response (+2 degrees C for 5 h following MDMA and +1.5 degrees C for 3 h following MDA) when compared to MDMA (+1 degree C for 3 h) and MDA (+1 degree C for 1 h) alone. Co-administration of caffeine with MDMA or MDA was also associated with increased lethality. To reduce the risk of lethality, doses of MDMA and MDA were reduced in further experiments and the animals were housed individually. To examine the effects of repeated administration, animals received MDMA (10 mg/kg) or MDA (5 mg/kg) with or without caffeine (10 mg/kg) twice daily for 4 consecutive days. MDMA and MDA alone induced hypothermia (fall of 1 to 2 degrees C) over the 4 treatment days. Co-administration of caffeine with MDMA or MDA resulted in hyperthermia (increase of up to 2.5 degrees C) following acute administration compared to animals treated with caffeine or MDMA/MDA alone. This hyperthermic response to caffeine and MDMA was not observed with repeated administration, unlike caffeine + MDA, where hyperthermia was obtained over the 4 day treatment period. In addition, 4 weeks after the last treatment, co-administration of caffeine with MDA (but not MDMA) induced a reduction in 5-HT and 5-hydroxyindole acetic acid (5-HIAA) concentrations in frontal cortex (to 61% and 58% of control, respectively), hippocampus (48% and 60%), striatum (79% and 64%) and amygdala (63% and 37%). However, when caffeine (10 mg/kg) and MDMA (2.5 mg/kg) were co-administered four times daily for 2 days to group-housed animals, both hyperthermia and hippocampal 5-HT loss were observed (reduced to 68% of control). Neither MDMA nor MDA alone induced a significant reduction in regional 5-HT or 5-HIAA concentrations following repeated administration. In conclusion, caffeine promotes the acute and long-term toxicity associated with MDMA and MDA. This is a serious drug interaction, which could have important acute and long-term health consequences for recreational drug users.

3,4-Methylenedioxyamphetamine↗
PubMed2005

"Coffee, tea and me": moderate doses of caffeine affect sexual behavior in female rats.

The present study evaluated the effects of acute caffeine administration on paced mating behavior and partner preference in ovariectomized rats primed with estrogen and progesterone. In Experiment 1, female rats were tested for paced mating behavior following acute administration of caffeine (15 mg/kg). Caffeine shortened the latency to return to a male following an ejaculation. Although this dose of caffeine did not alter the likelihood of leaving a male after receiving sexual stimulation, locomotor activity did increase significantly. Experiment 2 evaluated the dose response characteristics of caffeine (7.5, 15, 30 mg/kg) administration on paced mating behavior. Replicating Experiment 1, caffeine at the lower doses shortened the latency to return to a male following an ejaculation. Finally, to determine whether the effects of caffeine (15 mg/kg) on contact-return latency reflect a change in sexual motivation or merely an inability to inhibit locomotion, rats were tested for partner preference (intact male vs. estrous female) following caffeine administration (Experiment 3). Although caffeine did not disrupt preference for a sexual partner, caffeine selectively increased visits to the male when physical contact was possible. Collectively, these results suggest that the effects of caffeine on female mating behavior may reflect an increase in both sexual motivation and locomotor activity.

Animals↗
PubMed2005

Effect of chronic caffeine intake on choice reaction time, mood, and visual vigilance.

The stimulatory effects of acute caffeine intake on choice reaction time, mood state, and visual vigilance are well established. Little research exists, however, on the effects of chronic caffeine ingestion on psychomotor tasks. Therefore, the purpose of this study was to evaluate the effects of 5 days of controlled caffeine intake on cognitive and psychomotor performance. Three groups of 20 healthy males (age=22+/-3 years, mass=75.4+/-7.9 kg, body fat percentage=11.2+/-5.1%) twice completed a battery of cognitive and psychomotor tasks: after 6 days of 3 mg.kg(-1) day(-1) caffeine equilibration (Day 6), and after 5 days of experimental (0 [G0], 3 [G3], or 6 [G6] mg.kg(-1) day(-1)) caffeine intake (Day 11). Groups were randomized and stratified for age, mass, and body composition; all procedures were double-blind. Cognitive analyses involved a visual four-choice reaction time test, a mood state questionnaire, and a visual vigilance task. Experimental chronic caffeine intake did not significantly alter the number of correct responses or the mean latency of response for either the four-choice reaction time or the visual vigilance tasks. The Vigor-Activity subset of the mood state questionnaire was significantly greater in G3 than G0 or G6 on Day 11. All other mood constructs were unaffected by caffeine intake. In conclusion, few cognitive and psychomotor differences existed after 5 days of controlled caffeine ingestion between subjects consuming 0, 3, or 6 mg.kg(-1) day(-1) of caffeine, suggesting that chronic caffeine intake (1) has few perceptible effects on cognitive and psychomotor well-being and (2) may lead to a tolerance to some aspects of caffeine's acute effects.

Adult↗
PubMed2000

Lack of synergism between caffeine and SKF 38393 on rotational behavior in 6-hydroxydopamine-denervated rats.

We have recently shown a synergistic effect between caffeine and the dopamine D(2) receptor agonist, bromocriptine, on contralateral rotational behavior in unilaterally 6-hydroxydopamine-denervated rats. In addition, we found that bromocriptine prevented caffeine-induced tolerance to this behavior following repeated treatment. In the present study, we investigated whether or not the dopamine D(1) receptor agonist, (+/-)-phenyl-2,3,4, 5-tetrahydro-(1H)-3-benzazepine-7,8-diol (SKF 38393), presented similar characteristics. Different groups of rats received simultaneous injections of either vehicle plus vehicle, caffeine (40 mg/kg) plus vehicle, SKF 38393 (0.5, 1, 2, and 4 mg/kg) plus vehicle, or caffeine plus SKF 38393 (0.5, 1, 2, and 4 mg/kg) for 5 consecutive days, and both ipsilateral and contralateral rotational behavior was measured. Results showed that, on the first day of treatment, caffeine produced significantly more rotational behavior than did a low dose of SKF 38393 (0.5 mg/kg), and significantly less turning than at higher doses (2 and 4 mg/kg). Combined treatment with caffeine and a high dose of SKF 38393 (4 mg/kg) produced significantly more rotational behavior than did caffeine plus vehicle. With repeated administration, caffeine produced sustained tolerance to its effects on rotational behavior, whereas SKF 38393 did not. In the groups treated with low doses of SKF 38393 (0.5, and 1 mg/kg) plus caffeine, tolerance was observed while in the groups that received high doses of SKF 38393 (2 and 4 mg/kg) plus caffeine, no tolerance was observed to rotational behavior. These results suggest that maximal stimulation of dopamine D(1) receptors may be needed to prevent the tolerance effects of caffeine in this animal model. This finding may have clinical relevance to the therapeutic treatment of Parkinson's disease.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed2003

Caffeine and muscarinic antagonists act in synergy to inhibit haloperidol-induced catalepsy.

The possible synergism between caffeine and muscarinic antagonists to inhibit haloperidol-induced catalepsy was investigated with the bar test in rats. Pretreatment with low doses of caffeine (1-3 mg/kg), a non-selective adenosine antagonist, dose dependently reduced the intensity and increased the onset latency of catalepsy induced by haloperidol (0.5-2 mg/kg). Similar effects were produced by the muscarinic antagonists atropine (4.1 mg/kg), and trihexyphenidyl (THP, 0.01-3 mg/kg). THP inhibited catalepsy intensity with an ED(50) of 0.38 mg/kg, and increased its onset latency with an ED(50) of 0.52 mg/kg. The anticataleptic effect of anticholinergics was potentiated when a low dose of caffeine (1 mg/kg) was applied simultaneously. In the presence of caffeine, THP inhibited catalepsy intensity with an ED(50) of 0.19 mg/kg, and prolonged the latency with an ED(50) of 0.30 mg/kg. The synergism was more evident when THP was administered at subthreshold doses that were unable to modify haloperidol-induced catalepsy when applied alone, but produced a clear inhibition of catalepsy when injected with caffeine. To assess whether repeated administration of caffeine could induce tolerance to the synergism with THP, a group of rats was pretreated with three daily doses of caffeine (1 mg/kg) for seven days, and the catalepsy test was performed on the eighth day. In these animals, caffeine was still able to enhance the anticataleptic actions of THP, suggesting that repeated administration of 1 mg/kg caffeine does not induce tolerance to the synergism with anticholinergics. These results indicate that low doses of caffeine enhance the anticataleptic actions of muscarinic antagonists, and leave open the possibility of using caffeine as adjunctive therapy to reduce the doses and the adverse effects of anticholinergics in Parkinson's disease.

Animals↗
PubMed2000

Combination of low dose ethanol and caffeine protects brain from damage produced by focal ischemia in rats.

Caffeine and ethanol are two commonly overused psychoactive dietary components. The purpose of this study was to assess the effects of acute, chronic, oral (p.o.) and intravenous (i.v.) caffeine, ethanol and their combination on infarct volume following focal ischemia in rats. Rats received treatment either p.o. 3 h and 1 h before, or by i.v. infusion for 2.5 h beginning 30-180 min after, ischemia. There were six acute treatment groups. (1) oral dH2O (control); (2) oral caffeine (10 mg/kg); (3) oral ethanol (0.65 g/kg total); (4) oral ethanol plus caffeine; (5) intravenous saline; and (6) intravenous ethanol (0.65 g/kg) plus caffeine (10 mg/kg) in saline. A 7th group received oral ethanol plus caffeine for three weeks prior to ischemia. After 3 h of left MCA/CCA occlusion and 24 h reperfusion, infarct volume was determined. Control animal infarct volume was 102.4+/-42.0 mm3. Oral caffeine alone had no effect (122.4+/-30.2 mm3). Oral ethanol alone exacerbated infarct volume (177.2+/-27.8 mm3). Oral caffeine plus ethanol almost entirely eliminated the damage (17.89+/-10.41 mm3). When i.v. treatment with ethanol plus caffeine was initiated at 30, 60, 90 and 120 minutes post-ischemia the infarct volume was reduced by 71.7%, 49.8%, 64.8% and 47.1%, respectively. Chronic daily oral ethanol plus caffeine prior to ischemia eliminated the neuroprotection seen with acute treatment. These studies indicate that ethanol, which by itself aggravates cerebral ischemia, and caffeine, when combined together immediately before or for 2 h after focal stroke, reduces ischemic damage.

Animals↗
PubMed1992

Stimulus functions of caffeine in humans: relation to dependence potential.

The interoceptive stimulus functions common to drugs of dependence include positive subjective effects, discriminative functions, and reinforcing functions. Data from studies measuring these stimulus functions constitute the objective assessment of a drug's dependence potential. This paper reviews the subjective effects, discriminative stimulus, and reinforcing stimulus functions of caffeine in humans to assess the dependence potential of caffeine. The stimulus effects of caffeine are compared with those of d-amphetamine, a prototypic CNS stimulant that has been studied under similar conditions, to evaluate the relative dependence potential of caffeine. Finally, caffeine's effects are evaluated in terms of generally accepted criteria for defining drug dependence. It is concluded that caffeine partially meets the primary criteria of drug dependence: 1) the majority of caffeine use is highly controlled, but not compulsive; 2) caffeine is psychoactive; and 3) caffeine functions as a reinforcer under certain conditions in humans, but not in animals. Caffeine thus has limited dependence potential. Additionally, although caffeine shares stimulus functions with d-amphetamine, it does so under limited conditions and should be considered to have a relatively lower dependence potential.

Caffeine↗
PubMed2000

Caffeine promotes ethanol drinking in rats. Examination using a limited-access free choice paradigm.

There is growing evidence that caffeine may alter the pattern of intake of a variety of drugs. The present study was designed to assess the effect of caffeine pretreatment on voluntary ethanol consumption. The first experiment examined the effect of caffeine on the acquisition of ethanol intake in a limited-access-choice procedure in which water and ethanol were presented concurrently. Male Wistar rats, exposed to food and water ad lib, were presented with a daily 1-h choice session between water and progressively increasing concentrations of ethanol (2-10%). Each ethanol concentration was made available for 4-6 days for a total of 20 days of access to ethanol. Intraperitoneal injections of caffeine (5 or 10 mg/kg) or saline were administered to the rats 30 min prior to each choice session. Caffeine produced a dose-related facilitation in ethanol drinking whereby the lower caffeine dose produced enhancement in ethanol drinking. The second experiment examined the effect of caffeine on the maintenance of established ethanol consumption. Male Wistar rats, initially acclimatized to increasing concentrations of ethanol (2%-10), were presented with an additional 18 ethanol (10%) presentations, comprised of a 6-day baseline period followed by 6 days of treatment where animals were given one of three doses of caffeine (2.5, 5 or 10 mg/kg) or saline prior to ethanol presentation. A final 6-day post-treatment period followed treatment. These results revealed an inverted-U effect of caffeine dose on ethanol ingestion where the low and high caffeine doses produced no effect but the moderate dose of 5 mg/kg enhanced ethanol drinking that persisted throughout the post-treatment period. A third experiment revealed that caffeine did not alter levels of blood ethanol within the time period used for the ethanol drinking session.

Alcohol Drinking↗
PubMed2006

Caffeine intake, toxicity and dependence and lifetime risk for psychiatric and substance use disorders: an epidemiologic and co-twin control analysis.

BACKGROUND: Although caffeine is the most commonly used psychoactive substance and often produces symptoms of toxicity and dependence, little is known, especially in community samples, about the association between caffeine use, toxicity and dependence and risk for common psychiatric and substance use disorders. METHOD: Assessments of lifetime maximal caffeine use and symptoms of caffeine toxicity and dependence were available on over 3600 adult twins ascertained from the population-based Virginia Twin Registry. Lifetime histories of major depression (MD), generalized anxiety disorder (GAD) and panic disorder, alcohol dependence, adult antisocial behavior and cannabis and cocaine abuse/dependence were obtained at personal interview. Logistic regression analyses in the entire sample and within monozygotic (MZ) twin pairs were conducted in SAS. RESULTS: In the entire sample, measures of maximal caffeine use, heavy caffeine use, and caffeine-related toxicity and dependence were significantly and positively associated with all seven psychiatric and substance use disorders. However, within MZ twin pairs, controlling for genetic and family environmental factors, these associations, while positive, were all non-significant. These results were similar when excluding twins who denied regular caffeine use. CONCLUSIONS: Maximal lifetime caffeine intake and caffeine-associated toxicity and dependence are moderately associated with risk for a wide range of psychiatric and substance use disorders. Analyses of these relationships within MZ twin pairs suggest that most of the observed associations are not causal. Rather, familial factors, which are probably in part genetic, predispose to both caffeine intake, toxicity and dependence and the risk for a broad array of internalizing and externalizing disorders.

Adult↗
PubMed1999

Coffee, caffeine and blood pressure: a critical review.

OBJECTIVE: We review the published data relating to intake of coffee and caffeine on blood pressure in man. We also refer to studies on the possible mechanisms of actions of these effects of caffeine. DESIGN: The MEDLINE and Current Contents databases were searched from 1966 to April 1999 using the text words 'coffee or caffeine' and 'blood pressure or hypertension'. Controlled clinical and epidemiologic studies on the blood pressure effects of coffee or caffeine are reviewed. We also refer to studies on the possible mechanisms of action of these effects of caffeine. RESULTS: Acute intake of coffee and caffeine increases blood pressure. Caffeine is probably the main active component in coffee. The pressor response is strongest in hypertensive subjects. Some studies with repeated administration of caffeine showed a persistent pressor effect, whereas in others chronic caffeine ingestion did not increase blood pressure. Epidemiologic studies have produced contradictory findings regarding the association between blood pressure and coffee consumption. During regular use tolerance to the cardiovascular responses develops in some people, and therefore no systematic elevation of blood pressure in long-term and in population studies can be shown. CONCLUSIONS: We conclude that regular coffee may be harmful to some hypertension-prone subjects. The hemodynamic effects of chronic coffee and caffeine consumption have not been sufficiently studied. The possible mechanisms of the cardiovascular effects of caffeine include the blocking of adenosine receptors and the inhibition of phosphodiesterases.

Adolescent↗
PubMed2002

Caffeine reversal of ethanol effects on the multiple sleep latency test, memory, and psychomotor performance.

Caffeine has been shown to reverse some of the performance-impairing effects of ethanol. However, it is not known whether this antagonistic effect of caffeine is mediated by a reduction in sleepiness. The present study assessed physiological alertness/sleepiness, memory, and psychomotor performance following the administration of placebo, ethanol, and caffeine+ethanol combinations. A total of 13 healthy individuals (21-35 years old) underwent four conditions presented in a Latin Square Design: placebo-placebo, ethanol (0.5 g/kg)-placebo, ethanol (0.5 g/kg)-caffeine 150 mg, and ethanol (0.5 g/kg)-caffeine 300-mg. The Multiple Sleep Latency Test (MSLT), psychomotor performance battery, memory test, and mood/sleepiness questionnaires were administered following each condition. The peak breadth ethanol concentration (BrEC) was 0.043+/-0.0197% and did not differ among the three caffeine treatments. As expected, ethanol reduced mean latency on the MSLT. The lowest caffeine dose reversed this effect and the highest dose increased mean latency (greater alertness) significantly beyond placebo levels. Ethanol also impaired psychomotor performance and memory. The 300-mg caffeine dose restored performance and memory measures to placebo levels. Although visual analog ratings of dizziness were increased by ethanol, they were not diminished by either caffeine dose. In conclusion, Low-dose caffeine prevented the sleepiness and performance impairment associated with a moderate dose of ethanol. Thus, caffeine, similar to other stimulants, can reverse the physiologically sedating effects of ethanol, although other negative effects remain.

Adult↗
PubMed2001

Caffeine-induced depolarization in amphibian skeletal muscle fibres: role of Na+/Ca2+ exchange and K+ release.

Caffeine (4 mM) produces a depolarization of about 10 mV in frog muscle fibres (Leptodactylus ocellatus). The aim of this work was to study the mechanisms of this effect. An approximately threefold rise in membrane resistance [Cl--free (SO(4)2-) medium] substantially increased, and both Na+-free medium and Ni2+ (5 mM) reduced, the caffeine-induced depolarization. In voltage-clamped (-60 mV) short fibres from lumbricalis muscle of the toad (Buffo arenarum), caffeine generated an inward current of 4.13 +/- 0.48 microA cm(-2). This caffeine-induced current was reduced by 60% in Na+-free medium, 44% in the presence of 5 mM amiloride and 48% by 5 mM Ni2+, suggesting that the activation of the Na+-Ca2+ exchanger in its forward mode may play a role in the observed electrical effects of the drug. Caffeine also produced a marked release of K+. Net K+ efflux increased from 3.5 +/- 0.2 (control) to 22.1 +/- 2.3 pmol s(-1) cm(-2) (caffeine). It is shown that in the presence of the drug, [K+] in the lumen of the T tubules may well increase to levels which could produce, in part, both the observed depolarization and the caffeine-induced current under voltage clamp conditions. The caffeine-induced K+ efflux was not reduced by 5 mM Ni2+. At a holding potential of 30 mV the caffeine-induced current was reversed (outward) and roughly halved by 5 mM Ni2+. The Ni2+-sensitive fraction of the caffeine-induced current, assumed to represent the Na+-Ca2+ exchanger current, had an estimated reversal potential close to 12 mV ([Na+]o = 115 mM; [Ca2+]o = 1 mM). In conclusion, the depolarizing effect of caffeine described here would be produced by two mechanisms: (a) an inward current generated by the activation of the Na+-Ca2+ exchanger in its forward mode, and (b) the rise of the external [K+] in restricted spaces like the T tubules.

Amiloride↗
PubMed1999

Dietary caffeine as a probe agent for assessment of cytochrome P4501A2 activity in random urine samples.

AIMS: To validate the use of randomly collected urine samples for assessment of cytochrome P4501A2 (CYP1A2) activity based on dietary caffeine (caffeine metabolic ratio, MRcaff ), and to relate the MRcaff to caffeine intake and smoking habits in a larger group of individuals. METHODS: Nineteen healthy volunteers were included in the validation study. Caffeine (100 mg) was ingested and a urine sample was collected after 6 h. Within the following week a random urine sample was collected in the individuals without a preceding test dose of caffeine. Urine samples were analysed for caffeine and its metabolites by h.p.l.c. and the (AFMU+1U+1X)/1,7U metabolic ratio was used to reflect CYP1A2 activity. In an extended investigation of 522 healthy pregnant women the MRcaff was related to intake of caffeine from various sources, and to smoking. RESULTS: The results from the random and standardised sampling methods correlate with each other (correlation coefficient of MRcaff was 0. 91). The MRcaff as assessed by the random sampling method in a larger population was not affected by source or amount of caffeine ingested. Significantly higher MRcaff was found in smokers compared to non-smokers. In the large group of individuals the random sampling method was possible to use in 80% of the cases. In the residual 20% one or several of the metabolite concentrations were too low or unmeasurable. CONCLUSIONS: Our study demonstrates that the random urine caffeine phenotyping method is possible to use in as many as 80% of the individuals when based on dietary caffeine. Our approach should prove applicable in most countries with widely spread caffeine consumption. The method is useful in larger studies of drug metabolising enzyme activities and minimises the time consumption and costs.

Caffeine↗
PubMed2003

Reduced effect of caffeine on twitch contraction of oesophageal striated muscle from stroke-prone spontaneously hypertensive rats.

1. There are known differences in the sensitivity to caffeine between skeletal muscle (soleus) of normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The present study was performed in order to examine differences in the effects of caffeine on twitch contraction between visceral striated muscle using the outer layer of the oesophagus from WKY rats and stroke-prone SHR (SHRSP). 2. Caffeine, at concentrations ranging from 0.3 to 10 mmol/L, exhibited potentiating effects on twitch contraction in preparations from both WKY rats and SHRSP. The potentiating effect of caffeine was markedly less prominent in preparations from SHRSP compared with preparations from WKY rats. 3. The rate of contraction and relaxation, the time to peak tension and 80% relaxation time were not significantly altered by caffeine at concentrations lower than 3 mmol/L in preparations from either strain. 4. With 10 mmol/L caffeine, the rate of relaxation was markedly reduced and the 80% relaxation time was prolonged, with no significant changes in the rate of contraction, in preparations from WKY rats. These changes were significantly smaller in preparations from SHRSP. 5. The duration of the action potential was greater in preparations from SHRSP than in preparations from WKY rats, although the membrane potential and the amplitude of the action potential were not significantly different between preparations from WKY rats and SHRSP. 6. Caffeine, at 10 mmol/L, prolonged the duration of the action potential in preparations from both strains. The effect of caffeine was not different between preparations from WKY rats and SHRSP. 7. The results of the present study suggest that caffeine augments release of Ca2+ from the sarcoplasmic reticulum (SR) at low concentrations and attenuates Ca2+ re-uptake at 10 mmol/L. Decreased reactivity of SR to caffeine may be a cause of the lesser potentiation of twitch contraction by caffeine in preparations from SHRSP.

Animals↗
PubMed2000

The effect of sex and age on caffeine pharmacokinetics in cattle.

The aim of this study was to determine the effect of sex on the pharmacokinetics of caffeine in cattle at different ages. Ten female and 10 male Holstein cattle were subject to a caffeine test when they were aged 1, 2, 4, 6, 8, 12 and 18 months. Caffeine, 5 mg kg(-1)body weight, was given intravenously as a sterile isotonic solution. An automated, enzyme-multiplied, immunoassay technique (EMIT) was used to determine plasma caffeine concentration. The volume of distribution of caffeine (V(SS)) decreased significantly between 1 and 18 months of life. Mean V(SS)values observed in males and females were not statistically different. The experimental period was characterised by a steady decrease (statistically significant) in caffeine mean residence time (MRT). These values did not differ significantly between males and females under 8 months of age. In 8-, 12- and 18-month-old animals, the caffeine MRT in the females was significantly shorter than in the males. The total plasma clearance (Cl(tot)) of caffeine increased significantly between 1 and 18 months of age. No significant differences were observed between total plasma clearance of caffeine in males and females under 8 months of age. In 8-, 12- and 18-month-old animals, the Cl(tot)of caffeine was significantly higher in females than in males. In conclusion, we report a sex-linked difference in pharmacokinetics of caffeine in cattle over 8 months of age, the females being the more active metabolisers. The results of the present study support the hypothesis that the metabolism of xenobiotics is sexually different in ruminants.

Age Factors↗
PubMed1995

The effect of different dosages of caffeine on endurance performance time.

The effect of different dosages of caffeine (0-5-9-13 mg.kg body weight-1) on endurance performance was examined. Nine well-trained cyclists participated in this study (VO2max 65.1 +/- 2.6 ml.kg-1.min-1). Caffeine capsules were administered in random order and double-blind. One hour after capsule ingestion, subjects cycled until exhaustion at 80% Wmax on an electromagnetically braked cycle ergometer. Blood samples were taken before, during and after the exercise test. Before and after the test a urine sample was obtained. A significant increase in endurance performance was found for all caffeine tests compared to placebo (endurance time 47 +/- 13, 58 +/- 11, 59 +/- 12 and 58 +/- 12 min for 0, 5, 9 and 13 mg.kg-1 body weight, respectively). No differences were found in endurance performance between the three caffeine dosages which indicates that no dose-response relation of caffeine and endurance performance was found. An increased free fatty acid and glycerol concentration was found after caffeine consumption compared with placebo. The mean urinary caffeine concentrations after exercise were 4.8 +/- 1.8, 8.9 +/- 5.2 and 14.9 +/- 6.9 micrograms.ml-1 urine for 5, 9 and 13 mg of caffeine.kg-1 body weight. Only the lowest dose of caffeine resulted in urine caffeine concentrations below the doping limit of the International Olympic Committee of 12 micrograms.ml-1 urine in all individuals. It is concluded that caffeine is an ergogenic aid that stimulates endurance performance. A dose-response relation between caffeine and endurance time was not found for the dose-range investigated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Effects of caffeine on gastrointestinal myoelectric activity and colonic spike activity in dogs.

BACKGROUND: Caffeine is known to produce various effects on the gastrointestinal tract. Few studies have, however, investigated the effects of caffeine on gastrointestinal myoelectric activity under physiologic conditions. The aims of this study were to investigate the effects of caffeine on colonic motility (spike activity) and gastric and jejunal slow waves in conscious dogs. METHODS: The study was performed in eight healthy female hound dogs (15-20 kg) in which one pair of electrodes was implanted on the serosa of the stomach, one pair on the proximal jejunum, and another pair on the ascending colon. The protocol consisted of a 60-min recording as base line and a 90-min recording after intravenous injection of saline, a low dose of caffeine (125 mg), or a high dose of caffeine (250 mg). RESULTS: In the colon there was a significant increase in the number of spike bursts per minute after the injection of both the low (6.69+/-1.27 versus 8.22+/-1.31, P < 0.05) and the high dose (4.38+/-1.23 versus 6.92+/-0.98, P < 0.05) of caffeine. The increase in the total energy of spikes per minute after the injection of the high dose of caffeine was significantly higher than that after the low dose of caffeine (41.2+/-14.6 versus 133.4+/-39.2, P < 0.05). The characteristics of the gastric and jejunal slow waves were, however, not affected by caffeine. CONCLUSION: Caffeine increases spike activity in the colon, and its effect may be dose-dependent. Gastric and jejunal slow waves are not affected by caffeine.

Animals↗
PubMedDate not supplied

Specificity of co-promoting effects of caffeine on thyroid carcinogenesis in rats pretreated with N-bis(2-hydroxypropyl)nitrosamine.

The specificity of copromotion effects of caffeine with known goitrogenic factors on thyroid carcinogenesis was examined in rats pretreated with N-bis(2-hydroxypropyl)nitrosamine (DHPN). Male F344 rats were divided into 8 groups, each consisting of 10 animals, and received a single sc injection of 2,800 mg/kg DHPN. From one week after the DHPN initiation, they were given basal diet, iodine deficiency (ID) diet, 500 ppm phenobarbital (PB) solution or 1,000 ppm sulfadimethoxine (SDM) solution with or without 1,500 ppm caffeine feeding for 12 weeks. The caffeine, PB, SDM, and ID treatments significantly (p < 0.05 or 0.01) increased the relative thyroid weights, and the increases with PB or ID were further (p < 0.05 or 0.01) enhanced in combination with caffeine. SDM drastically promoted thyroid carcinogenesis in association with increased serum TSH levels regardless of the caffeine treatment. Thyroid follicular carcinomas and adenomas were more frequently observed in the additional caffeine groups than in the ID alone groups. The incidence and multiplicity of focal thyroid follicular hyperplasias in the ID-treated groups were significantly (p < 0.05 and 0.01) elevated in the case of combination with caffeine. Increases in serum TSH levels with PB or ID were also further enhanced in combination with caffeine. Serum thyroid hormone levels were significantly (p < 0.01) decreased by SDM but significantly (p < 0.05 or 0.01) increased by caffeine, PB or ID. Our results clearly indicate that dietary caffeine at a high dose of 1,500 ppm interacts with ID, but neither SDM nor PB, to promote rat thyroid carcinogenesis although the combined caffeine + PB treatment somewhat affected thyroid weights as well as thyroid hormone levels.

Animals↗