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PubMed1997

Influence of caffeine and caffeine withdrawal on headache and cerebral blood flow velocities.

Caffeine consumption may cause headache, particularly migraine. Its withdrawal also produces headaches and may be related to weekend migraine attacks. Transcranial Doppler sonography (TCD) has shown changes in cerebral blood flow velocities (BFV) during and between attacks of migraine. In order to examine whether headache and changes in BFV could develop from controlled caffeine alterations, 20 healthy volunteers without a headache history, underwent clinical evaluation, TCD and serum caffeine measurements on four occasions, comparing conditions of regular caffeine intake, caffeine withdrawal and "re-caffeination". After 24 h of complete caffeine abstinence, 10 suffered from moderate to severe headaches with complete recovery within 1 h after caffeine intake. The BFVs in both middle cerebral, both posterior cerebral and basilar arteries were higher following the withdrawal period, reaching statistical significance in the left middle cerebral basilar and both posterior cerebral arteries. BFVs decreased significantly within half an hour after caffeine intake in all subjects, and were similar to baseline values after 2 h. Our results emphasize the relationship between caffeine withdrawal, the development of headache and alterations in cerebral blood flow velocities. Also, these findings indicate that accurate interpretation of TCD measurements should account for the influence of caffeine on BFVs.

Adult↗

PubMed2005

Fluvoxamine impairs single-dose caffeine clearance without altering caffeine pharmacodynamics.

BACKGROUND: Coadministration of fluvoxamine impairs the clearance of caffeine and prolongs its elimination half-life, which is attributable to inhibition of CYP1A2 by fluvoxamine. The clinical importance of this interaction is not established. AIM: To evaluate the effects of fluvoxamine on the kinetics and dynamics of single doses of caffeine. METHODS: Seven healthy subjects received single 250 mg doses of caffeine (or matching placebo) together with fluvoxamine (four doses of 100 mg over 2 days) or with matching placebo in a double-blind, four-way crossover study. For 24 h after caffeine or placebo administration, plasma caffeine and fluvoxamine concentrations were determined. Psychomotor performance, sedation, and electroencephalographic (EEG) "beta" frequency activity were also assessed. RESULTS: Fluvoxamine significantly reduced apparent oral clearance of caffeine (105 vs. 9.1 mL min(-1), P < 0.01; mean difference: 95.7 mL min(-1), 95% CI: 54.9-135.6), and prolonged its elimination half-life (4.9 vs. 56 h, P < 0.01; mean difference: 51 h, 95% CI: 26-76). Caffeine produced CNS-stimulating effects compared with placebo. However, psychomotor performance, alertness, or EEG effects attributable to caffeine were not augmented by coadministration of fluvoxamine. CONCLUSIONS: Fluvoxamine greatly impaired caffeine clearance, but without detectable changes in caffeine pharmacodynamics. However, this study does not rule out possible adverse effects due to extensive accumulation of caffeine with daily ingestion in fluvoxamine-treated individuals.

Area Under Curve↗

PubMed1986

Chronic caffeine treatment reduces caffeine but not adenosine effects on cortical acetylcholine release.

The effects of both adenosine and caffeine on the release of acetylcholine (ACh) were investigated in slices of cerebral cortex taken from rats pretreated for 30 days with caffeine (100 mg kg-1 daily, dissolved in their drinking water) at rest and during electrical stimulation at frequencies of 0.2, 1 and 5 Hz. The effect of this treatment on adenosine binding sites was also investigated in cortical membranes using N-cyclohexyl-[3H]-adenosine ([3H]-CHA) as a ligand. The chronic caffeine treatment did not change animal growth patterns. Spontaneous exploratory activity appeared to be increased at the 3rd day but was unchanged at the 30th day when compared with controls. Caffeine-treatment increased the number of high affinity binding sites for [3H]-CHA by 64% over the control values. Low affinity binding site density and affinity constants were unaffected. Adenosine 30 microM added to the superfusion fluid decreased electrically stimulated ACh release both in rats drinking tap water and rats drinking caffeine. In rats drinking tap water, caffeine added to the superfusion fluid at a concentration of 50 microM enhanced ACh release, while at 0.5 mM it decreased ACh output from the slices. Both effects were abolished by pretreatment with caffeine in vivo. The results indicate that prolonged consumption of high doses of caffeine causes changes in the responsiveness of cholinergic neurones to caffeine. The change is not shared by adenosine, through whose recognition sites caffeine is believed to act. It is therefore possible that the adaptive changes following repeated caffeine administration involve either only the coupler-transducer mechanism activated by the antagonist, or effects unrelated to receptors.

Acetylcholine↗

PubMed1989

Caffeine treatment inhibits drug-induced calcium release from sarcoplasmic reticulum and caffeine contracture but not tetanus in frog skeletal muscle.

Effects of pretreatment with caffeine on Ca2+ release induced by caffeine, thymol, quercetin, or p-chloromercuriphenylsulfonic acid (pCMPS) from the heavy fraction of sarcoplasmic reticulum (SR) were studied and compared with those effects on caffeine contracture and tetanus tension in single fibers of frog skeletal muscle. Caffeine (1-5 mM) did induce transient Ca2+ release from SR vesicles, but subsequent further addition of caffeine (10 mM, final concentration) induced little Ca2+ release. Ca2+ release induced by thymol, quercetin, or pCMPS was also inhibited by pretreatment with caffeine. In single muscle fibers, pretreatment with caffeine (1-5 mM) partially reduced the contracture induced by 10 mM caffeine. However, tetanus tension was almost maximally induced by electrical stimulus in caffeine-treated fibers. These results indicate that SR, which becomes less sensitive to caffeine, thymol, quercetin, or pCMPS by pretreatment with caffeine, can still respond to a physiological signal transmitted from transverse tubules.

4-Chloromercuribenzenesulfonate↗

PubMed1992

Effect of caffeine on motor performance by caffeine-naive and -familiar subjects.

The purpose of this investigation was to assess the effect of caffeine on selected manipulation skills by caffeine-naive and caffeine-familiar subjects. The subjects were 20 caffeine-naive (less than 90 mg/d) and 20 caffeine-familiar (greater than 750 mg/d) college-age (21 +/- 1.7 yr.) women. Measurements included steadiness error time and frequency, duration of tracing, error time and frequency, and dexterity. Doses of 2.5, 5.0 mg.kg-1 body weight caffeine or a placebo (200 mg. methylcellulose) were administered randomly to all subjects on three separate occasions. A 2 x 3 repeated-measures analysis of variance yielded a significant group difference for steadiness error time between the 5 mg.kg-1 and 2.5 mg.kg-1 dose and between 5 mg.kg-1 and the placebo. For frequency of steadiness errors, the nonuser group posted significant gains for both 5.0 and 2.5 mg.kg-1 over the placebo control. On tracing error time and error frequency, 5.0 mg.kg-1 resulted in significant increases from both 2.5 mg.kg-1 and the placebo group. In the caffeine-naive group, both doses of caffeine led to significant increases in dexterity time from the placebo, and the 5.0 mg.kg-1 dose was significantly different from the 2.5 mg.kg-1 trial. It was concluded that caffeine had detrimental effects on selected performance skills of caffeine-naive women but not in caffeine-familiar women.

Adult↗

PubMed1975

[Caffeine as an inhibitor of the conjugation transfer of R-factors. A study of certain aspects of the mechanism of action of caffeine on the conjugation transfer of R-factors].

Some aspects of the inhibitory effect of caffeine on conjugation transfer of R-factors described by the authors earlier were studied. The effect of the above substance on the donor and recipient competence was tested in experiments with cultivation of the parent strains for 18 hours in the presence of caffeine. For this purpose the effect of caffeine on reduction of the donor and recipient cell competence after starvation in a physiological solution was investigated. It was shown that caffeine markedly decreased the donor competence of strain 15-3Mdrd of E. coli in the experiments of both types. Caffeine also inhibited reduction of the recipient competence of strain C600 of E. coli after starvation without its changing on 18-hour treatment. For the study of the caffeine effect on formation of the conjugation pairs experiments were carried out with dilution of the conjugation mixture after definite intervals which practically stopped formation of new conjugation pairs and eliminated further effect of caffeine on conjugation. Under such conditions transfer of R-factors may occur in the conjugation pairs after elimination of caffeine by dilution, if they were formed in the presence of caffeine before the mixture dilution. The experiments showed that caffeine inhibited not the formation of the conjugation pairs but the genetic transfer of R-factors. In addition, it was found that the substance insignificantly inhibited the process of phenotypic manifestation of the resistance markers. Inhibition of conjugation R-transfer by caffeine was associated with its eliminating effect, since the concentrations used did not induce elimination of the resistance markers in R+ strains.

Caffeine↗

PubMedDate not supplied

Pharmacokinetics of caffeine in breast milk and plasma after single oral administration of caffeine to lactating mothers.

Six healthy lactating women ranging in age from 28 to 35 years were selected to participate in the study. The women had been nursing their infants from 3 1/2 weeks up to 17 weeks. On the morning of the study each participant received 100 mg dose of caffeine. The oral dose of caffeine was taken with a glass of water on an empty stomach. Blood samples were collected from zero time to 24 h after caffeine administration. Each subject aseptically collected breast milk from the right and left breasts by manual expression or using a mechanical breast pump, from zero time to 24 h after caffeine administration. Caffeine in plasma and breast milk was determined by gas liquid chromatography using nitrogen phosphorous detection. Caffeine was rapidly absorbed producing plasma time to peaks ranging from 0.50 to 1.00 h, with values for peak concentrations between 3.60 and 6.15 micrograms ml-1 in plasma. In breast milk, time to peak ranged from 0.75 to 2.00 h and concentration values between 1.98 and 4.30 micrograms ml-1. No significant differences were found between attainment of the time of the peak in plasma and breast milk, p greater than 0.05. In addition, peak concentration for the right and left breast were not statistically different, p greater than 0.05. However, significant differences, p less than 0.05, between plasma and both breasts in regards to the peak concentrations were found. The overall breast milk/plasma ratio obtained from the respective area under the curves were 0.815 +/- 0.0521 and 0.809 +/- 0.202 for the right and left breast, respectively, and no statistical differences were observed between the right and left breasts, p greater than 0.05. In summary, caffeine is rapidly transferred to breast milk. Multiple dose studies are needed to provide more information about caffeine concentration in breast milk of women who receive multiple doses of caffeine or who chronically consume caffeine.

Administration, Oral↗

PubMed1995

24h withdrawal following repeated administration of caffeine attenuates brain serotonin but not tryptophan in rat brain: implications for caffeine-induced depression.

Caffeine injected at doses of 20, 40 and 80 mg/kg increased brain levels of tryptophan, 5-hydroxytryptamine (5-HT) and 5-hydroxyindole acetic acid (5-HIAA) in rat brain. In view of a possible role of 5-HT in caffeine-induced depression the effects of repeated administration of high doses of caffeine on brain 5-HT metabolism are investigated in rats. Caffeine was injected at doses of 80 mg/kg daily for five days. Control animals were injected with saline daily for five days. On the 6th day caffeine (80 mg/kg) injected to 5 day saline injected rats increased brain levels of tryptophan, 5-HT and 5-HIAA. Plasma total tryptophan levels were not affected and free tryptophan increased. Brain levels of 5-HT and 5-HIAA but not tryptophan decreased in 5 day caffeine injected rats injected with saline on the 6th day. Plasma total and free tryptophan were not altered in these rats. Caffeine-induced increases of brain tryptophan but not 5-HT and 5-HIAA were greater in 5 day caffeine than 5 day saline injected rats. The findings are discussed as repeated caffeine administration producing adaptive changes in the serotonergic neurons to decrease the conversion of tryptophan to 5-HT and this may precipitate depression particularly in conditions of caffeine withdrawal.

Analysis of Variance↗

PubMed1976

Replicative bypass repair of ultraviolet damage to DNA of mammalian cells: caffeine sensitive and caffeine resistant mechanisms.

Replicative bypass repair of UV damage to DNA was studied in a wide variety of human, mouse and hamster cells in culture. Survival curve analysis revealed that in established cell lines (mouse L, Chinese hamster V79, HeLa S3 and SV40-transformed xeroderma pigmentosum (XP)), post-UV caffeine treatment potentiated cell killing by reducing the extrapolation number and mean lethal UV fluence (Do). In the Do reduction as the result of random inactivation by caffeine of sensitive repair there were marked clonal differences among such cell lines, V79 being most sensitive to caffeine potentiation. However, other diploid cell lines (normal human, excision-defective XP and Syrian hamster) exhibited no obvious reduction in Do by caffeine. In parallel, alkaline sucrose sedimentation results showed that the conversion of initially smaller segments of DNA synthesized after irradiation with 10 J/m2 to high-molecular-weight DNA was inhibited by caffeine in transformed XP cells, but not in the diploid human cell lines. Exceptionally, diploid XP variants had a retarded ability of bypass repair which was drastically prevented by caffeine, so that caffeine enhanced the lethal effect of UV. Neutral CsC1 study on the bypass repair mechanism by use of bromodeoxyuridine for DNA synthesis on damaged template suggests that the pyrimidine dimerer acts as a block to replication and subsequently it is circumvented presumably by a new process involving replicative bypassing following strand displacement, rather than by gap-filling de novo. This mechanism worked similarly in normal and XP cells, whether or not caffeine was present, indicating that excision of dimer is not always necessary. However, replicative bypassing become defective in XP variant and transformed XP cells when caffeine was present. It appears, therefore, that the replicative bypass repair process is either caffeine resistant or sensitive, depending on the cell type used, but not necessarily on the excision repair capability.

Caffeine↗

PubMed1987

Autonomic nervous system effects of acute doses of caffeine in caffeine users and abstainers.

The effects of caffeine on autonomic nervous system (ANS) activity were tested in 20 adult males who were either high or low consumers of caffeine. Subjects received placebo, 3 mg/kg, and 10 mg/kg of caffeine in a counterbalanced order (double-blind) before 3 test sessions 48 h apart. Skin conductance (SC), heart rate, and skin temperature (ST) were recorded during a rest period, a series of non-signal tones, and a simple reaction time task. Caffeine increased resting electrodermal activity (EDA) and increased the SC orienting response to the first non-signal tone, but reduced the increase in tonic EDA due to task performance. ST was reduced by caffeine in both rest and task periods. Increases in nervous/jittery ratings occurred after caffeine ingestion, but task performance was not affected. Low consumers of caffeine showed significantly more ANS responsivity than high consumers under all conditions and did not differ in ANS, behavioral, or subjective effects of caffeine. The acute physiological changes are partly similar to those reported for patients with anxiety disorders, suggesting a possible role of ANS activity in mediating the anxiogenic effects of caffeine. Effects of user status may reflect a predisposing trait, but an effect of chronic caffeine use on ANS sensitivity cannot be ruled out.

Adolescent↗

PubMed2002

Caffeine's neuroprotection against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine toxicity shows no tolerance to chronic caffeine administration in mice.

We investigated the effect of chronic daily caffeine treatment on caffeine's neuroprotection against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic toxicity. Mice received either caffeine (20 mg/kg) or saline daily for 9 days. Caffeine-induced locomotion tolerance developed within 3 days of treatment and persisted for the duration of the experiment. On day 10, mice were treated with MPTP (20 mg/kg, x4). Caffeine (20 mg/kg) or saline was administered 10 min before each MPTP dose. Acute pretreatment with caffeine attenuated MPTP-induced loss of striatal dopamine and dopamine transporter binding sites, and this attenuation was identical in mice pretreated chronically with caffeine or with saline. Thus, in contrast to the locomotor stimulant effect of caffeine, its neuroprotectant effect did not show tolerance to prior caffeine exposure. These data raise the possibility that caffeine may induce neuroprotection and locomotion by distinct mechanisms.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2003

Subchronic caffeine exposure induces sensitization to caffeine and cross-sensitization to amphetamine ipsilateral turning behavior independent from dopamine release.

We have recently shown that repeated exposure to caffeine sensitizes rats to the motor activating effects of dopamine D(1) and D(2) receptor agonists. In order to study the role of dopamine in this effect, sensitization to caffeine and cross-sensitization between caffeine and amphetamine was evaluated by studying turning behavior and in vivo striatal dopamine release in unilaterally 6-hydroxydopamine-lesioned rats. Administration of caffeine (15 mg/kg) for 2 weeks, on alternate days, induced a significant increase in ipsilateral turning behavior during the course of treatment, indicating that sensitization to caffeine took place in the intact striatum. Caffeine modestly increased dopamine release in the intact dorsa-lateral striatum and no significant difference between the first (+38%) and the last (+51%) injection was observed. Amphetamine (2 mg/kg) induced a significantly higher ipsilateral turning behavior in caffeine-sensitized rats than in vehicle-pretreated rats, however, a similar increase in dopamine release (+900 and +800%) was observed in the two groups. The results are the first demonstration that caffeine pre-exposure sensitizes the motor-stimulant effects of caffeine itself and of amphetamine. Sensitized ipsilateral turning after caffeine and amphetamine are not correlated to modification in striatal dopamine release, rather, postsynaptic modifications in dopamine and adenosine receptor interaction might be involved in the sensitization phenomena observed.

Amphetamine↗

PubMed2000

Homologous recombination as a potential target for caffeine radiosensitization in mammalian cells: reduced caffeine radiosensitization in XRCC2 and XRCC3 mutants.

The radiosensitizing effect of caffeine has been associated with the disruption of multiple DNA damage-responsive cell cycle checkpoints, but several lines of evidence also implicate inhibition of DNA repair. The role of DNA repair inhibition in caffeine radiosensitization remains uncharacterized, and it is unknown which repair process, or lesion, is affected. We show that a radiosensitive cell line, mutant for the RAD51 homolog XRCC2 and defective in homologous recombination repair (HRR), displays significantly diminished caffeine radiosensitization that can be restored by expression of XRCC2. Despite the reduced radiosensitization, caffeine effectively abrogates checkpoints in S and G2 phases in XRCC2 mutant cells indicating that checkpoint abrogation is not sufficient for radiosensitization. Another radiosensitive line, mutant for XRCC3 and defective in HRR, similarly shows reduced caffeine radiosensitization. On the other hand, a radiosensitive mutant (irs-20) of DNA-PKcs with a defect in non-homologous end-joining (NHEJ) is radiosensitized by caffeine to an extent comparable to wild-type cells. In addition, rejoining of radiation-induced DNA DSBs, that mainly reflects NHEJ, remains unaffected by caffeine in XRCC2 and XRCC3 mutants, or their wild-type counterparts. These observations suggest that caffeine targets steps in HRR but not in NHEJ and that abrogation of checkpoint response is not sufficient to explain radiosensitization. Indeed, immortalized fibroblasts from AT patients show caffeine radiosensitization despite the checkpoint defects associated with ATM mutation. We propose that caffeine radiosensitization is mediated by inhibition of stages in DNA DSB repair requiring HRR and that checkpoint disruption contributes by allowing these DSBs to transit into irreparable states. Thus, checkpoints may contribute to genomic stability by promoting error-free HRR.

Animals↗

PubMed1983

Effects of caffeine on X-irradiated synchronous, asynchronous and plateau phase mouse ascites cells: the importance of progression through the cell cycle for caffeine enhancement of killing.

The effects of caffeine on X-irradiated synchronous, exponential and plateau phase cell populations was studied. Caffeine was found to potentiate the killing effect of X-rays on exponentially growing cells giving rise to exponential survival curves (D0 = (0 . 8 +/- 0 . 05)Gy) at 4mM and 14 hours treatment, presumably by expressing X-ray induced potentially lethal damage (PLD). Irradiated plateau phase cells were found to be less sensitive to caffeine. Exponentially growing cells also became less sensitive to the effects of caffeine when they were incubated in the conditioned medium of plateau phase cells (C-medium) in which cell growth was considerably inhibited. Low caffeine concentrations (2mM) also enhanced X-ray induced killing of cells irradiated in G1-, G1/S- or S-phase, but more effectively enhanced the killing of G2-phase cells. High caffeine concentrations (6mM) enhanced killing of cells in all phases of the cell cycle. Incubation of synchronized populations in C-medium during treatment with caffeine (both 2 mM and 6 mM) resulted in less potentiation than in cells treated in fresh medium. The expression of X-ray induced PLD caused by 6 mM caffeine in cells irradiated in various phases of the cell cycle resulted in an exponential survival curve with a mean lethal dose D0 = (0 . 8 +/- 0 . 05) Gy but the time of caffeine treatment necessary to reach this curve was different for cells irradiated in different phases of the cell cycle. The repair of PLD, measured as loss of sensitivity to 6 mM caffeine (4 hours treatment) was of 1-2 hours duration.

Animals↗

PubMed2005

Caffeinated coffee, decaffeinated coffee, and caffeine in relation to plasma C-peptide levels, a marker of insulin secretion, in U.S. women.

OBJECTIVE: Coffee consumption is associated with reduced risk of type 2 diabetes, but the mechanism is not clearly understood. Elevated C-peptide, as a marker of insulin secretion, has been linked to insulin-resistant type 2 diabetes. In this study, we examined consumption of caffeinated and decaffeinated coffee and total caffeine in relation to concentrations of plasma C-peptide. RESEARCH DESIGN AND METHODS: Plasma C-peptide concentrations were measured in a cross-sectional setting among 2,112 healthy women from the Nurses' Health Study I who provided blood samples in 1989-1990. Consumption of caffeinated and decaffeinated coffee and total caffeine was assessed using a semiquantitative food-frequency questionnaire in 1990. RESULTS: Intakes of caffeinated and decaffeinated coffee and caffeine in 1990 were each inversely associated with C-peptide concentration in age-adjusted, BMI-adjusted, and multivariable-adjusted analyses. In multivariable analysis, concentrations of C-peptide were 16% less in women who drank >4 cups/day of caffeinated or decaffeinated coffee compared with nondrinkers (P < 0.005 for each). Women in the highest quintile compared with the lowest quintile of caffeine intake had 10% lower C-peptide levels (P = 0.02). We did not find any association between tea and C-peptide. The inverse association between caffeinated coffee and C-peptide was considerably stronger in obese (27% reduction) and overweight women (20% reduction) than in normal weight women (11% reduction) (P = 0.005). CONCLUSIONS: Our findings suggest a potential reduction of insulin secretion by coffee in women. This reduction may be related to other components in coffee rather than caffeine.

Beverages↗

PubMed1991

Caffeine as an analgesic adjuvant. A double-blind study comparing aspirin with caffeine to aspirin and placebo in patients with sore throat.

Despite its frequent clinical use in analgesic agents, caffeine has not been accepted unequivocally as an analgesic adjuvant. To evaluate this activity of caffeine, we used new study methods in a randomized controlled trial on patients with acute sore throat due to tonsillopharyngitis. Patients were randomly assigned to receive a single dose of one of three treatments: 800 mg of aspirin with 64 mg of caffeine (n = 70), 800 mg of aspirin (n = 68), or placebo (n = 69). Under double-blind conditions, during a 2-hour evaluation period, patients used different rating scales to assess pain intensity, change in pain, relief, and two qualities of throat pain, how swollen the throat felt, and difficulty swallowing. Aspirin with caffeine and aspirin alone were significantly more effective than placebo for all efficacy measurements from 30 minutes through 2 hours and overall. The aspirin-caffeine combination also showed evidence of activity at 15 minutes on the relief scale. Aspirin with caffeine was more effective than aspirin alone after 30 minutes and over the entire study period. For patients with fever, both active treatments were equally effective antipyretic agents. We conclude, therefore, that 800 mg of aspirin, given alone or with 64 mg of caffeine, is an effective analgesic and antipyretic agent. Because the aspirin-caffeine combination is significantly more effective than aspirin alone as an analgesic, we also conclude that 64 mg of caffeine is an analgesic adjuvant.

Adult↗

PubMed2002

Caffeine enhances the calcium-dependent cardiac mitochondrial permeability transition: relevance for caffeine toxicity.

Caffeine (1,3,7-trimethylxanthine), a compound present in beverages such as tea and coffee, is known to be toxic at high concentrations. Some of the observed clinical conditions include cardiovascular disease and reproductive disorders, among others. The possible toxic effects of caffeine on heart mitochondria are still poorly understood. The influence of caffeine on the mitochondrial permeability transition has not been clarified so far. The objective of this study was to investigate whether caffeine, at toxic concentrations, had any stimulating effect on the permeability transition of heart mitochondria isolated from Wistar rats, as well as whether it influenced mitochondrial respiratory parameters. Our results show that caffeine reduced mitochondrial ability to accumulate calcium by increasing the susceptibility of heart mitochondria to the opening of the transition pore. Caffeine not only hindered mitochondrial capacity to recover membrane potential after calcium addition but also increased the rate of calcium-dependent mitochondrial swelling and calcium-induced calcium release. The increased swelling was also observed in nonenergized mitochondria. Caffeine also showed a complex array of effects on heart mitochondrial bioenergetics, as evaluated by respiratory parameter measurements. We observed an increase in state 4 respiration and a depression in state 3 respiration, although no effect was observed on succinate-sustained mitochondrial membrane potential in the absence of calcium. Our work may be relevant to cardiovascular problems linked to caffeine toxicity and also to in vitro experiences involving caffeine-induced calcium release from the sarcoplasmic reticulum and uptake by mitochondria.

Animals↗

PubMed1991

The effects of caffeine on graded exercise performance in caffeine naive versus habituated subjects.

The physiological effects of caffeine on subjects habituated to caffeine is relatively unstudied compared to those of caffeine naive subjects during graded exercise. Thus, the purpose of this investigation was to determine the effects of caffeine on maximal oxygen consumption (VO2max) and the anaerobic threshold in these two populations. Seventeen moderately trained males were classified according to caffeine usage: (1) caffeine consumption 25 mg.day-1 or less (CN) (n = 8) or (2) caffeine consumption above 300 mg.day-1 (CH) (n = 9). The subjects were tested post-absorptive on the same cycle ergometer on three occasions with 7 days separating the tests. One hour before each test the subject ingested either a gelatin capsule (C); 3 mg.kg-1 body weight of caffeine (C3); or 5 mg.kg-1 body weight of caffeine (C5). The subject then performed an incremental VO2max test beginning at 50 W and the work rate was increased 30 W every 2 min until the subject could not maintain the power output. Serial venous blood samples were drawn over 30 s at the end of each stage. The CN group significantly increased resting heart rate (fc) and expired ventilation volume (VE) after C3 and C5 and VO2 after C5. No significant differences were found for exercise VE, VO2, respiratory exchange ratio, fc or time to exhaustion. There were no significant differences (P less than 0.05) in the lactate threshold or the ventilatory threshold between treatment in either group. The CH subjects showed a significant increase (P less than 0.05) in resting plasma free fatty acid (FFA) concentration only during the C3 and C5 treatments.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗