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PubMed2004

Caffeine improves physical performance during 24 h of active wakefulness.

BACKGROUND: Reductions in both cognitive and physical performance occur during periods of sleep loss with sustained operations. It was the purpose of this study to examine the effects of caffeine on activities chosen to simulate the physical challenges that might occur during a military scenario involving a period of sleep loss. METHODS: There were 16 subjects (26.7 +/- 7.8 yr, 83.8 +/- 11.0 kg) who completed a double-blind caffeine and placebo trial involving a control day and sleep period followed by 28 h of sleep deprivation. A 400-mg dose of caffeine was administered at 21:30 followed by subsequent 100-mg doses at 03:00 and 05:00. At 22:00, subjects began a 2-h forced march followed by a sandbag piling task. A treadmill run to exhaustion at 85% of maximal aerobic power was performed at 07:00 of the second day of sleep deprivation. RESULTS: Caffeine had no effect on the heart rate or oxygen consumption, but rating of perceived exertion (RPE) was reduced with caffeine during the forced march. Time to complete the sandbag piling task during set 1 was significantly reduced with caffeine (12.9 +/- 1.0 min) compared with placebo (13.8 +/- 1.0 min) but there was no difference during set 2 and RPE was increased. Time to exhaustion was significantly increased 25% during the run with caffeine (17.0 +/- 4.4 min) compared with placebo (13.5 +/- 3.3 min), and caffeine maintained performance at control levels (16.9 +/- 4.6 min). CONCLUSIONS: It was concluded that caffeine is an effective strategy to maintain physical performance during an overnight period of sleep loss at levels comparable to the rested state.

Adult↗
PubMed2004

Caffeine and psychiatric symptoms: a review.

Caffeine is a widely used psychoactive substance that has the potential to contribute to many psychiatric symptoms. This review article aims to address the specific research studies and case reports that relate caffeine to psychiatric symptoms. Caffeine can cause anxiety symptoms in normal individuals, especially in vulnerable patients, like those with pre-existing anxiety disorders. Caffeine use is also associated with symptoms of depression due to either a self-medication theory, or a theory that caffeine itself causes changes in mood. Psychosis can be induced in normal individuals ingesting caffeine at toxic doses, and psychotic symptoms can also be worsened in schizophrenic patients using caffeine. Sleep and symptoms of ADHD may be altered by caffeine as well. Prevention of caffeine-induced psychiatric symptoms is possible by recognizing, educating, and treating patients using a tapering approach.

Anxiety↗
PubMed1992

Caffeine-induced behavioral stimulation is dose-dependent and associated with A1 adenosine receptor occupancy.

Caffeine's psychomotor stimulant effects may relate to its blockade of central adenosine receptors. We examined acute caffeine effects on motor activity, adenosine receptor occupancy in vivo, and receptor affinity and density ex vivo. Acute doses of caffeine-sodium benzoate (0, 20, 40, and 60 mg/kg, intraperitoneally [0, 0.10, 0.21, 0.31 mu mol/kg]) were given to CD-1 mice and their activity was measured in an animal activity monitor over a 1-hour period. Adenosine receptor occupancy in vivo was quantified in mice 1 hour postdosage, using the high-affinity, A1 receptor selective adenosine antagonist [3H]-8-cyclopentyl-1,3-dipropylxanthine. Adenosine receptor binding affinities and densities were determined from analyses of binding studies in cortical, hippocampal, and brainstem membranes from treated mice (0 and 40 mg/kg caffeine). Caffeine doses of 20 and 40 mg/kg, corresponding to mean brain concentrations of 5 and 17 micrograms/g, increased all horizontal and vertical motor activity measures and stereotypy counts, as compared to doses of 0 and 60 mg/kg. Additionally, all acute caffeine doses significantly altered specific A1 binding in vivo (decreasing binding between 55% and 73% versus vehicle), presumably as it occupied A1 receptors. Therefore, at doses of 20 and 40 mg/kg, caffeine stimulated motor activity as it occupied A1 receptors; at a dose of 60 mg/kg (mean brain concentration of 26 micrograms/g) caffeine had no stimulant effect even though it appeared to occupy A1 receptors. Acute caffeine dosage did not alter ex vivo adenosine receptor binding affinity or density in any brain regions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Caffeine, theophylline, theobromine, and developmental growth of the mouse mammary gland.

The purpose of this study was to determine the comparative activities of three methylxanthines, i.e., 1,3,7-trimethylxanthine (caffeine), 1,3-dimethylxanthine (theophylline), and 3,7-dimethylxanthine (theobromine) on developmental growth of the mammary gland in ovarian-hormone treated, mature nulliparous female Balb/c mice. When caffeine or theophylline was administered daily (via drinking water, 500 mg/L) for 30 days to 17 beta-estradiol/progesterone-treated intact or ovariectomized mice, a significant (p less than 0.05) enhancement of hormone-induced mammary gland lobulo-alveolar differentiation was observed. Caffeine or theophylline thus accelerated and/or intensified mammae lobulo-alveolar differentiation induced by the ovarian steroids. In contrast, theobromine (500 mg/L drinking water) did not significantly modify this developmental process. The stimulatory effect of caffeine and theophylline on mammae development was comparable quantitatively. In an effort to determine whether or not the stimulatory effect of caffeine or theophylline was directly on the mammary gland, small slow-release Elvax-40P pellets containing these methylxanthines were implanted directly into the mammary gland of mice concurrently treated with estrogen and progesterone. No significant stimulatory effect of caffeine or theophylline (or theobromine) was observed. Furthermore, the addition of methylxanthines (caffeine, 100 microM) to the culture media of whole mouse mammary glands (organ cultures) did not enhance lobulo-alveolar differentiation induced by mammotrophic hormones. Thus, while a consistent significant stimulatory effect of caffeine and theophylline on mammary lobulo/alveolar differentiation was observed when the methylxanthines were consumed orally (drinking water), no direct effect of these methylxanthines, when placed directly into the mammary gland or in culture media, on mammae development was observed. These data demonstrate that certain methylxanthines (e.g., caffeine and theophylline) but not others (e.g., theobromine) can significantly enhance mammotrophic hormone-induced mammary lobulo-alveolar differentiation in female Balb/c mice, an effect that appears not to be manifested via a direct action of the methylxanthines on the mammary gland.

Administration, Oral↗
PubMed2005

[Effect of caffeine on camptothecin-induced apoptosis of Molt-4 cells].

BACKGROUND & OBJECTIVE: Caffeine could act on cell cycle checkpoints and affect the progression of cell cycle, but its impact on apoptosis of tumor cells is in debate. This study was carried out to investigate the effects of caffeine on camptothecin-induced apoptosis and cell cycle checkpoints of leukemia cell line Molt-4. METHODS: The cell apoptosis was induced by camptothecin, and caffeine was used to interfere with cell cycle checkpoints. The apoptosis rate and cell cycle during apoptosis were analyzed using sub-G1 method and Annexin V-propidium iodide (Annexin V/PI) staining. RESULTS: Caffeine (2.0-20.0 mmon/L) had no effect on proliferation of Molt-4 cells in exponentially growth phase. Camptothecin selectively induced apoptosis of Molt-4 cells in S phase; when induced with camptothecin (0.15 micromol/L) for 4 or 6 h, the apoptosis rates were (23.69+/-2.26)% and (36.99+/-1.42)%. This cell cycle-specific apoptosis were inhibited obviously by caffeine with the apoptosis rates of (4.79+/-0.64)% and (2.69+/-0.56)%. When caffeine was removed, the apoptosis rates increased obviously to (46.23+/-0.21)% and (55.81+/-0.41)%, and still mainly happened in S phase. CONCLUSIONS: Caffeine could inhibit camptothecin-induced apoptosis of Molt-4 cells. As a drug acting on cell cycle checkpoints, caffeine could transiently shield the surveillance of checkpoints to damaged cells and inhibit cell apoptosis. The effect may be reversed when caffeine is removed away.

Antineoplastic Agents, Phytogenic↗
PubMed1991

Caffeine, neuromuscular function and high-intensity exercise performance.

Caffeine is one of the most widely consumed drugs in the world. There is a strong belief that caffeine is an ergogenic aid to sports performance. Although much evidence suggests that caffeine may improve endurance exercise performance, questions still remain with regard to its effects on neuromuscular function and brief, high-intensity exercise performance. At the cellular level, caffeine stimulates the central nervous system (CNS), enhances neuromuscular transmission and improves skeletal muscle contractility. The former two effects seem to have facilitative effects on activities which require quick reactions and rapid movements. This is evident in that simple and choice reaction and movement times are reduced following ingestion of small quantities of caffeine. It appears, however, that the caffeine-induced increases in muscle contractility seen in vitro do not translate into improved strength, in vivo. Acute caffeine ingestion does not seem to increase maximal voluntary contractions or maximal power output nor delay fatigue. Thus use of caffeine to improve performance in activities requiring strength and short-term endurance seems unwarrented. Further research is needed before clear conclusions can be draw regarding caffeine's effects on neuromuscular function and high-intensity exercise performance.

Caffeine↗
PubMed1991

9-methyl-7-bromoeudistomin D, a powerful radio-labelable Ca++ releaser having caffeine-like properties, acts on Ca(++)-induced Ca++ release channels of sarcoplasmic reticulum.

9-Methyl-7-bromoeudistomin D (MBED), a derivative of eudistomin D isolated from a marine tunicate, induced Ca++ release from the heavy fraction of fragmented sarcoplasmic reticulum (HSR) in the same way as that of caffeine, followed by spontaneous Ca++ reuptake in the Ca++ electrode experiment. The rate of 45Ca++ efflux from HSR vesicles was accelerated markedly by MBED or caffeine in a concentration-dependent manner. The 50% effective concentrations of MBED and caffeine were approximately 1 microM and 1 mM, respectively, indicating that MBED is 1000 times more potent than caffeine in HSR. Procaine, ruthenium red or Mg++ caused concentration-dependent inhibition of MBED-triggered Ca++ release from HSR. The bell-shaped profile of Ca++ dependence for MBED is very similar to that of caffeine. The caffeine-produced maximum response of 45Ca++ efflux was increased further by adenosine-5'-(beta, gamma-methyl-ene)triphosphate, whereas that was not changed by MBED. MBED also caused Ca++ release from sarcoplasmic reticulum (SR) of chemically skinned fibers. These stimulatory effects of MBED on the Ca++ release from skeletal muscle SR were almost indistinguishable from those of caffeine except the difference in potencies. The [3H]ryanodine binding to junctional terminal cisternae membranes was not inhibited by MBED or caffeine. MBED did not cause Ca++ release from the light fraction of fragmented SR and turbidity change of mitochondrial suspension. These observations suggest a most likely idea that MBED binds to the caffeine-binding site in the Ca channel protein and thus produces the potentiation of Ca(++)-induced Ca++ release from SR.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Qualitative differences in the discriminative stimulus effects of low and high doses of caffeine in the rat.

Caffeine engenders qualitatively different subjective effects in humans at low and high doses. Low doses of caffeine are mildly reinforcing and produce psychomotor stimulation. High doses of caffeine can produce subjective feelings of anxiety, dysphoria and depression. The present study was designed to model these different subjective states in rats using a discrete trial shock avoidance/escape drug discrimination paradigm. Rats were trained to discriminate between i.p. injections of saline and either 10 or 56 mg/kg of caffeine. Rats trained at 10 mg/kg of caffeine acquired the discrimination in an average of 93 sessions and generalized completely to a variety of xanthine and nonxanthine behavioral stimulants including: d-amphetamine, apomorphine, 7-(beta-chloroethyl)theophylline, 9-chloro-2-(2-furanyl)-5,6-dihydro-1, 2,4-triazolo[1,5-c]quinazolin-5-imine (CGS 15943), cocaine, 1,7-dimethylxanthine, diethylpropion, beta-hydroxyethyltheophylline, methylphenidate, phenidimetrazine and theophylline. Rats trained at 56 mg/kg of caffeine acquired the discrimination in an average of 43 sessions and generalized completely only to theophylline. A variety of drugs representing diverse pharmacologic classifications including: benzodiazepine inverse agonists, pentylenetetrazol, yohimbine, ethylketocyclazocine and phencyclidine, were not generalized from either training dose, demonstrating the pharmacologic specificity of the discrimination. The discriminative effects of 10 mg/kg of caffeine appear to derive from a state of behavioral arousal, possibly mediated by catecholamines, and parallel the subjective effects produced by low doses of caffeine in humans. The discriminative effects of 56 mg/kg of caffeine are qualitatively different from those of 10 mg/kg but cannot be defined further at this time.

Adenosine↗
PubMed1991

Effect of caffeine ingestion on alveolar ventilation during moderate exercise.

The purpose of this study was to examine the effect of caffeine ingestion on alveolar ventilation and physiological dead space ventilation during exercise in high and low caffeine users. Eleven males (mean age 26.4 +/- 5.4 years), classified as either high caffeine users (greater than 350 mg/d, n = 6) or low caffeine users (less than 50 mg/d, n = 5) performed two treadmill exercise conditions at a constant work rate (50% VO2max) 45 min after ingestion of 3.3 mg of caffeine/kg body weight or placebo using a double-blind protocol. Open circuit spirometry was used to determine ventilatory and gas exchange variables every 10 min during the 50 min of walking exercise. Analysis of variance showed that caffeine produced significant differences in alveolar ventilation (VA) and the physiological dead space ventilation/tidal volume ratio (VD/VT) with VA increased from 1.36 to 1.54 L/breath and VD/VT decreased from 22.3 to 20.5% between the placebo and caffeine treatments, respectively. Additionally, caffeine ingestion produced a significant increase in tidal volume (VT) and a significant decrease in frequency of breathing (fb). We conclude that caffeine consumed prior to exercise enhances ventilatory dynamics during exercise without regard to prior habitual caffeine consumption.

Adult↗
PubMed1990

Caffeine consumption and anxiety and depressive symptomatology among medical students.

Caffeine is one of the most widely consumed psychoactive substances in the world and is ingested in a variety of favorites, such as coffee, tea, cola and so on. Although it has been suggested that high dose caffeine users have more anxiety and depressive symptoms than low users, this relationship is not clear in Japan, where caffeine consumption is considered to be less than in Western countries. A questionnaire survey was conducted among medical students and 291 out of 423 initial subjects completed it. Among males, caffeine consumption was significantly and positively correlated with anxiety symptoms, when alcohol use and smoking habit were adjusted. However, there was no relationship between caffeine consumption and depressive symptoms. Among females, although there was no association between caffeine consumption and anxiety symptoms, high dose caffeine users showed less depressive symptoms than moderate and low users, when alcohol use was adjusted. It is suggested that caffeine use is one of the important factors, in researching psychological health among the general population. We need further epidemiological studies to determine whether there is a causal relationship between caffeine and psychological ill health or not.

Adult↗
PubMed1990

Cardiac sarcolemma as a possible site of action of caffeine in rat heart.

Caffeine (0.1-10 mM) produced a biphasic effect on Na(+)-K+ ATPase activity in the rat heart sarcolemmal preparations. The Na(+)-K+ ATPase activity was stimulated by about 25% at low concentrations (0.1-1 mM), whereas the enzyme was inhibited by about 25% at higher concentrations (10 mM) of caffeine. The stimulatory effect of 1 mM caffeine was associated with about 30% increase in the Vmax value for Na(+)-K+ ATPase, whereas the depressant action of 10 mM caffeine was associated with an increase of the Km value from 1.4 to 2.1 mM ATP. The Na(+)-induced Ca++ release from the sarcolemmal vesicles was stimulated with caffeine in a concentration-dependent manner; about 80% increase in the activity was observed at 0.1 mM caffeine. The apparent Ka (millimolar Na+) values for the Na(+)-induced Ca++ release were about 17 and 6 in the absence and presence of 1 mM caffeine, respectively. However, the sarcolemmal Na(+)-dependent Ca++ uptake and ATP-independent Ca++ binding were not affected, whereas the ATP-dependent Ca++ accumulation and Ca+(+)-stimulated ATPase activities were depressed by 1 to 10 mM caffeine. This agent at concentrations of 0.1 to 10 mM produced a biphasic effect on the contractile activity of the isolated perfused rat heart. The initial transient positive inotropic (30-60%) effect was followed by a sustained negative inotropic (50-80%) response of the drug; the delayed decrease in contractile force was associated with a significant increase (35-50%) in the resting tension. The initial positive inotropic effect of caffeine was dependent on the concentration of Ca++ (0.2-3 mM) in the perfusion medium; however, this response was attenuated either by lowering the concentration of Na+ from 140 to 35 mM or by different concentrations (0.5-1 mM) of amiloride in the medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1990

Low-dose caffeine discrimination in humans.

A novel drug discrimination procedure was used to study the discriminability and subjective effects of caffeine in seven human volunteers who abstained from dietary sources of caffeine. Daily sessions involved p.o. ingestion of two capsules sequentially, one of which contained caffeine and the other placebo, under double-blind conditions. Each day subjects attempted to identify and were later informed which capsule contained caffeine and which contained placebo. All subjects acquired rapidly the initial discrimination (100 or 178 mg vs. placebo). Examination of progressively lower caffeine doses showed that accuracy and ratings of confidence in accuracy were increasing functions of dose. There were individual differences in the lowest discriminable dose: three subjects discriminated 56 mg, three discriminated 18 mg and one discriminated 10 mg. Discrimination accuracy was usually higher after the second capsule than after the first capsule. All subjects indicated that they believed that they made the discrimination predominantly on the basis of central effects of caffeine vs. placebo, such as changes in mood and socializing. Compared to placebo, 100 mg of caffeine increased ratings of alertness, well-being, social disposition, motivation for work, concentration, energy and self-confidence and decreased ratings of headache and sleepiness. This dose of caffeine also produced a large increase in a measure of "euphoria." The present study documents biological activity of caffeine at lower doses than heretofore recognized. The general approach to investigating the effects of low drug doses may have broad application in human psychopharmacology research for characterizing other subtle psychotropic effects.

Adult↗
PubMedDate not supplied

Studies on contractures induced in mouse diaphragm by caffeine and cupric and selenite ions.

Mouse diaphragm contractures induced by Cu2+, caffeine and selenite were studied comparatively. Both Cu2+- and caffeine-contractures were produced rapidly and relaxed spontaneously; the selenite-contracture occurred after a latent period of about 45 min and lasted for more than 3 hr. All contractures were myogenic, since neither d-tubocurarine nor tetrodotoxin prevented them. The susceptibility of these contractures to the depletion and replenishment of Ca2+ differed: the Cu2+-contracture increased proportionally with rising extracellular Ca2+ concentrations ranging from 2.5 to 12.5 mM and were abolished by 5 mM EGTA. Caffeine- and selenite-contractures were not affected by changes in extracellular Ca2+ concentration. The caffeine-contracture was abolished by EGTA in high concentration (30 mM) and the selenite-contracture was inhibited by 50 mM EGTA. After removal of Ca2+ with 5 mM EGTA, followed by replacement with 2.5 mM Ca2+ for 1 min, the Cu2(+)-contracture was fully restored. Caffeine- and selenite-contractures were restored only after a longer period (10-20 min) of re-exposure to Ca2+. These findings suggest that the Cu2(+)-contracture is dependent on external Ca2+ and probably caused by an increasing Ca2+ entry through sarcolemma. Caffeine- and selenite-contractures apparently result from internal Ca2+ release by sarcoplasmic reticulum. Substitution of either Sr2+ or Co2+ for Ca2+ fully supports the Cu2(+)-contracture. 45Ca2+ uptake and calcium content of the diaphragm were markedly increased by Cu2+ but not by selenite. Furthermore, the Cu2(+)-contracture was inhibited by exposing the outer membrane to trypsin, phospholipase C or saponin. The selenite-contracture was inhibited only by trypsin. The caffeine-contracture was unaffected by these treatments. These results support the notion that the Cu2(+)-contracture is induced by an increased entry of Ca2+ through the outer membrane. Cu2(+)-, caffeine- and selenite-contractures were respectively abolished, potentiated and unaffected by chronic denervation of the diaphragm. This and the other findings provide evidence that Cu2(+)-, caffeine- and selenite-contractures are induced in mouse diaphragm muscle via different sites of action.

Animals↗
PubMed1989

Massive caffeine ingestion resulting in death.

Caffeine has long been recognized as an addictive substance with numerous toxic effects. Death due to caffeine overdose is rare, due in part to its marked gastric irritation resulting in spontaneous emesis. Caffeine can be found in food, beverages, analgesics, and over-the-counter weight loss products. We report a fatality resulting from the ingestion of mail order diet pills containing caffeine as their only active ingredient. A 22-year-old female arrived in the emergency department in cardiac arrest after ingesting these diet pills. Resuscitation efforts were unsuccessful. A serum toxicology screen revealed the presence of caffeine with a level of 1,560 micrograms/ml (lethal greater than 100 micrograms/ml). To our knowledge this is the highest reported fatal caffeine level. No other drugs were identified on the screen. Based on the absence of pathology on autopsy and the high caffeine level, death was attributed to acute caffeine toxicity. This case illustrates that deaths resulting from caffeine, although rare, continue to occur.

Adult↗
PubMed1989

Interaction between caffeine and methamphetamine by means of ambulatory activity in mice.

Effects of repeated administration of caffeine as well as interaction between caffeine and methamphetamine were investigated by means of ambulatory activity in mice. The single administration of caffeine increased the ambulatory activity at 10 and 30 mg/kg, sc, but scarcely increased at 3 mg/kg and at 100 mg/kg which is a subconvulsive dose. Methamphetamine 2 mg/kg, sc also increased the ambulatory activity. The combined administration of caffeine (1-100 mg/kg) and methamphetamine (2 mg/kg) showed a synergistic action as compared with the effects of the individual drugs. The repeated 5-times administration of caffeine (10, 30, and 100 mg/kg) at intervals of 3-4 days produced neither tolerance nor reverse tolerance to caffeine. The caffeine-experienced mice showed no marked change in the sensitivity to the ambulation-increasing effect of methamphetamine 2 mg/kg. In contrast, the repeated administration of methamphetamine 2 mg/kg induced not only reverse tolerance to methamphetamine itself but also cross reverse tolerance to caffeine (30 mg/kg). Furthermore, the methamphetamine-experienced mice also showed an increased activity after challenge administration of saline. The present results suggest that, although caffeine showed central stimulant effect, the characteristics are different from those of methamphetamine.

Animals↗
PubMed1988

The role of caffeine-sensitive calcium stores in the regulation of the intracellular free calcium concentration in rat sympathetic neurons in vitro.

Intracellular Ca2+ stores were studied in sympathetic neurons grown in primary culture from the superior cervical ganglion of the rat. The [Ca2+]i was measured in single cells using the fluorescent Ca2+ indicator fura-2 and a sensitive microfluorimeter. Superfusion of the cells with 10 mM caffeine elicited a rapid and transient increase in [Ca2+]i in the absence of extracellular Ca2+, indicating the presence of a caffeine-sensitive intracellular Ca2+ storage site. After depletion of the store by mobilization of Ca2+ with caffeine, it could be refilled by elevating [Ca2+]i, allowing multiple caffeine-induced [Ca2+]i transients to be elicited from a single neuron. Ryanodine (1 microM), an alkaloid that promotes Ca2+ release from the sarcoplasmic reticulum, was an effective inhibitor of the caffeine-induced [Ca2+]i transients in sympathetic neurons. Exposure to ryanodine in the presence of caffeine was required to produce a subsequent inhibition of the caffeine-induced response, suggesting a "use-dependent" inhibition that may result from depletion of the Ca2+ stores. In contrast, dantrolene Na (10 microM), an agent known to interfere with Ca2+ release from the sarcoplasmic reticulum, also blocked the caffeine-induced [Ca2+]i transients, but in a time-dependent rather than a use-dependent manner. Electrophysiological measurements using the whole cell version of the patch-clamp technique were made simultaneously with [Ca2+]i microfluorimetric recordings. The magnitude of the [Ca2+]i transients elicited by step depolarizations closely paralleled the magnitude of Ca2+ influx via voltage-sensitive Ca2+ channels, regardless of whether the magnitude of the Ca2+ current was modified by varying the test pulse duration or potential. The relationship between the magnitude of Ca2+ influx and the resulting increase in [Ca2+]i saturated at large Ca2+ influxes resulting from long depolarizations, consistent with the activation of a large capacity, low affinity [Ca2+]i buffering mechanism. Caffeine (10 mM) and ryanodine (10 microM), applied singly or together, produced a small and variable decrease in the [Ca2+]i transient resulting from cell depolarization using the whole-cell patch-clamp technique. We conclude that mammalian sympathetic neurons possess intracellular Ca2+ stores with pharmacological characteristics that closely resemble those found in muscle but that these are relatively small and produce little amplification of [Ca2+]i transients resulting from Ca2+ influx through voltage-sensitive Ca2+ channels.

Animals↗
PubMed1987

A high carbohydrate diet negates the metabolic effects of caffeine during exercise.

We tested the hypothesis that unrecognized nutritional factors might influence the serum free fatty acid response to caffeine. The time course and extent of the serum free fatty acid response to a fatty meal alone, to caffeine ingestion after a high carbohydrate meal, or to caffeine in combination with either a fatty meal or a high carbohydrate meal (the latter following 3 d of a high carbohydrate diet) were studied in six trained runners. The metabolic response to 120 min of exercise at 75% of maximum oxygen consumption after caffeine ingestion was also studied in runners after a high carbohydrate diet and ingestion of a high carbohydrate meal. Serum free fatty acid levels were highest 3 h after caffeine ingestion alone and were lower following a fatty meal with or without caffeine ingestion (P less than 0.05). The high carbohydrate diet combined with the ingestion of a high carbohydrate meal prevented the expected rise in serum free fatty acid levels following caffeine ingestion. The metabolic response to prolonged submaximal exercise was also not influenced by the ingestion of caffeine by subjects who had eaten a high carbohydrate diet. Nutritional factors, in particular the state of the body carbohydrate stores and the simultaneous ingestion of carbohydrate, influence the response of serum free fatty acid levels to caffeine ingestion.

Adult↗
PubMed1987

Effect of caffeine on cytotoxicity and sister chromatid exchange induction in sensitive and resistant rat brain tumor cells treated with 1,3-bis(2-chloroethyl)-1-nitrosourea.

Treatment of 9L and 9L-2 cells, which are, respectively, sensitive and resistant to 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU), with various concentrations of BCNU followed by treatment with 1 mM caffeine potentiated BCNU cytotoxicity by 10-fold with dose modification factors of 1.5 to 1.7. The synergistic effect of caffeine on cellular toxicity diminished when caffeine was added 6 to 24 h after treatment of BCNU. The number of sister chromatid exchanges (SCEs) induced by treatment with BCNU in both cell lines showed a good correlation with cytotoxicity; the number of SCEs induced in 9L cells is 6-fold higher than the number induced in 9L-2 cells. Caffeine potentiated BCNU induction of SCEs in both 9L or 9L-2 cells by the same amount. Caffeine potentiation of BCNU-induced SCEs was also time dependent and was eliminated by a delay of 6 h between BCNU treatment and addition of caffeine. Caffeine had no effect on the formation and removal of DNA cross-links in either 9L or 9L-2 cells after BCNU treatment as determined with the alkaline elution assay. Eighteen to 24 h after BCNU treatment there was an accumulation of 9L cells in late-S-G2-M phase of the cell cycle which diminished with time. Caffeine treatment potentiated the BCNU-induced accumulation of cells in late-S-G2-M phase of the cell cycle. Our results suggest that caffeine potentiates BCNU cytotoxicity and induction of SCEs by a mechanism that is independent of repair of alkylation products, but that may depend on alterations of cellular replication in BCNU-treated cells.

Animals↗