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PubMed2001

Effects of caffeine and high ambient temperature on haemodynamic and body temperature responses to dynamic exercise.

Caffeine can enhance mean arterial blood pressure (MAP) and attenuate forearm blood flow (FBF) and forearm vascular conductance (FVC) during exercise in thermal neutral conditions without altering body temperature. During exercise at higher ambient temperatures, where a greater transfer of heat from the body core to skin would be expected, caffeine-induced attenuation of FBF (i.e. cutaneous blood flow) could attenuate heat dissipation and increase body temperature (T(re)). We hypothesized that during exercise at an ambient temperature of 38 degrees C, caffeine increases MAP, and attenuates FBF and FVC such that T(re) is increased. Eleven caffeine-naive, active men, were studied at rest and during exercise after ingestion of a placebo or 6 mg kg(-1) of caffeine. MAP, heart rate (HR), FBF, FVC, T(re) skin temperature (T(sk)) and venous lactate concentrations (lactate) were assessed sequentially during rest at room temperature, after 45 min of exposure to an ambient temperature of 38 degrees C, and during 35 min of submaximal cycling. Heat exposure caused increases in MAP, FBF, FVC and T(sk) that were not altered by caffeine. HR, T(re), and lactate were unaffected. During exercise, only MAP (95 +/- 2 vs. 102 +/- 2 mmHg), HR (155 +/- 10 vs. 165 +/- 10 beats min(-1)), and lactate (2.0 +/- 0.4 vs. 2.3 +/- 0.4 mmol l(-1)) were increased by caffeine. These data indicate that increases in cutaneous blood flow during exercise in the heat are not reduced by caffeine. This may be because of activation of thermal reflexes that cause cutaneous vasodilation capable of offsetting caffeine-induced reductions in blood flow. Caffeine-induced increases in lactate, MAP and HR during exercise suggest that this drug and high ambient temperatures increase production of muscle metabolites that cause reflex cardiovascular responses.

Adult↗
PubMed1999

The confirmation and control of metabolic caffeine in standardbred horses after administration of theophylline.

The origin of caffeine detections in equine serum and urine after theophylline administrations was examined. Three different preparations containing theophylline were administered to standardbred mares. Both blood and urine samples were collected. Caffeine was detected and quantified in theophylline administration samples by high performance liquid chromatography (HPLC) and liquid chromatography-tandem mass spectrometry (LC-MS-MS). Further in vitro analysis showed that caffeine metabolites were not detected when caffeine, or caffeine-containing products, were added to urine. Data derived from HPLC-UV and LC-MS-MS analysis of dosages of theophylline and caffeine are used to propose the establishment of a threshold limit to control and discern between metabolic and administered caffeine concentrations. A serum caffeine concentration of 250 ng/mL and a urine caffeine concentration of 1000 ng/mL are suggested. Based on the data supplied, these threshold concentrations could effectively control orally administered caffeine in racehorses, up to the dosage used in this work, up to 72 h before sampling time.

Animals↗
PubMed2000

Differences in the effect of chronic and acute caffeine on self-administration of cocaine in mice.

We have compared the ability of an acute injection of caffeine (3 mg/kg, i.p.) and long-term peroral caffeine consumption for 10 days ( approximately 150 mg/kg/day in tap water) to affect cocaine self-administration in mice. The peak plasma and brain levels of caffeine and its metabolites were similar in the two experimental set-ups. Moreover, the levels reached are close to those obtained in humans upon coffee ingestion. Neither type of caffeine administration affected the reinforcing effect of cocaine, defined as a selective increase in nose-poke responses in mice self-administering cocaine compared to their yoked controls. However, caffeine injection increased the amount of cocaine self-administered whereas caffeine drinking reduced it. A low dose of cocaine, by itself essentially ineffective, produced an increase in c-fos and NGFI-A mRNA in the cerebral cortex in mice that had been drinking caffeine. An acute caffeine injection also enhanced the immediate early gene response to cocaine, but to a lesser degree. Cocaine and caffeine also synergistically increased NGFI-A expression in caudate-putamen. Thus, regular caffeine drinking decreased the cocaine intake without significantly affecting its reinforcing properties, perhaps because it enhanced the activation of the predominantly inhibitory frontal cortical areas produced by low doses of cocaine.

Animals↗
PubMed2001

The effect of short-term starvation or water deprivation on caffeine pharmacokinetics in calves.

The aim of this study was to determine the effect of short-term starvation or water deprivation on the pharmacokinetics of caffeine in calves. The experiment was carried out on 30 Holstein-Friesian calves (10 calves in a control group, 10 calves in a 'starved' group and 10 calves in a 'water-deprived' group) aged 24-25 days. Control group calves were given caffeine at 24-25 and 28-29 days of age. In the experimental groups caffeine studies were performed before and after 4 days of starvation or water deprivation. In the control group no significant differences between the pharmacokinetic parameters of caffeine in 24-25 and 28-29 day-old calves were observed. Starvation for 4 days was associated with an increase in the mean residence time (MRT) of caffeine in each subject. The increase was statistically significant (P < 0.01). After starvation the total plasma clearance of caffeine decreased (about 20 per cent). The decrease was statistically significant (P < 0.05). The volume of caffeine distribution (V(ss)) was slightly but not significantly increased. Similarly, water deprivation was associated with significant increase in the mean residence time of caffeine in each subject. The total plasma clearance of caffeine decreased (about 30 per cent). This decrease was statistically significant (P < 0.01). The volume of caffeine distribution was slightly but not significantly decreased. Results obtained in this study indicate that short-term (for 4 days) starvation or water deprivation leads to a general inhibition of hepatic P450 enzymatic system and may impair the elimination of drugs that undergo metabolism by these enzymes.

Animals↗
PubMed2001

Multiple effects of caffeine on Ca2+ release and influx in human B lymphocytes.

Caffeine has been used as a pharmacological tool to study the ryanodine receptor (RYR)-mediated Ca2+ release from caffeine-sensitive, inositol 1,4,5,-trisphosphate (IP3)-insensitive pools. In the present study, we demonstrate multiple effects of caffeine on Ca2+ homeostasis in human B lymphocytes. Although B cells express a functional RYR, which can be activated by 4-chloro-m-cresol following depletion of IP(3)-sensitive pools, caffeine does not activate RYR-mediated Ca2+ release. Instead, caffeine dose-dependently inhibited IP3 receptor (IP3R)-mediated Ca2+ release, RYR-mediated Ca2+ release and B cell receptor-initiated Ca2+ influx, while high concentrations of caffeine (> or = 25 mM) induced a Ca2+ influx. In contrast with its ability to suppress receptor-stimulated Ca2+ influx, caffeine had no significant effect on the store-operated Ca2+ (SOC) channel-dependent Ca2+ influx induced by thapsigargin. Thus, caffeine may act as an inhibitor on a single or multiple site(s) responsible for regulating the IP3R channel, RYR channel and presumably the receptor-mediated SOC channel. The present report may be the first demonstration of multiple effects of caffeine on Ca2+ mobilization in single cell type. Our results suggest the need for caution regarding use of caffeine simply as a RYR-activator to study Ca2+ homeostasis in eucaryotic cells.

B-Lymphocytes↗
PubMed1994

Acute maternal and fetal cardiovascular effects of caffeine ingestion.

Little data exist regarding the acute maternal and fetal cardiovascular effects of caffeine ingestion. The purpose of this study is assess the cardiovascular effects of caffeine ingestion in pregnant subjects and their fetuses. We examined seven caffeine-naive gravidas longitudinally at 25.7 (SE +/- 0.7) and 36.1 (+/- 0.7) weeks' gestation, before and after ingestion of a caffeine citrate solution (100 mg/m-2 body surface area). Maternal pulse, blood pressure, fetal heart rate, and fetal heart rate accelerations were determined before and after caffeine ingestion. Uterine artery, fetal aorta, and umbilical artery flow velocity waveforms were examined at similar intervals. Significant before and after caffeine differences, regardless of gestational age, were noted for maternal pulse (85.1 vs 74.2 beats/min), diastolic blood pressure (65.9 vs 73.8 torr), mean arterial blood pressure (81.5 vs 87.5 torr), uterine artery systolic-to-diastolic (S/D) ratio (1.9 vs 2.4), fetal heart rate (144.6 vs 135.4 beats/min), and fetal heart rate accelerations (1.6 vs 4.2 per 30 minutes). Differences for fetal aortic and umbilical artery S/D ratios were not significant with respect to caffeine administration. Fetal aortic peak velocities increased with caffeine (85.5 vs 130.2 cm/sec) and the increase was augmented with advancing gestational age. We conclude that maternal ingestion of modest amounts of caffeine citrate in caffeine-naive subjects significantly affects both the fetal and maternal cardiovascular systems.

Adult↗
PubMed1985

Influence of caffeine on blood lactate response during incremental exercise.

To test the hypothesis that caffeine ingestion prior to exercise would delay the onset of blood lactate accumulation, eight male subjects were studied during incremental exercise to maximal work rates on a cycle ergometer under two conditions: 1 h after ingestion of 200 ml of either decaffeinated, calorie-free cola (control trial) or the same cola drink with 5 mg caffeine/kg body weight added (caffeine trial). Maximal exercise values for oxygen consumption (VO2 max), ventilation, heart rate, respiratory exchange ratio (R), work rate, and blood lactate were not affected by caffeine. Submaximal exercise VO2, ventilation, and R also were unaffected by caffeine. During the caffeine trial, submaximal exercise blood lactate was significantly higher and heart rate significantly lower than during the control trial (P less than 0.05). The lower exercise heart rate at the same VO2 resulted in a significantly greater O2 pulse during all submaximal exercise intensities for the caffeine trial (P less than 0.05). Data on R indicated that caffeine had no effect on substrate utilization during exercise. Data on exercise blood lactate response suggested that caffeine does not delay and may accelerate the onset of blood lactate accumulation during incremental exercise. When defined as either a "breakpoint," delta l mM (above resting lactate), or fixed level of 4 mM, the lactate threshold (LT) did not differ between caffeine and control trials. However, in using a 2 mM lactate level as a criterion, the LT during the caffeine trial (2.13 +/- 0.22 l X min-1) was significantly (P less than 0.05) lower than during the control trial (2.71 +/- 0.17 l X min-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

The hypercholesterolaemic effect of caffeine in rats fed on diets with and without supplementary cholesterol.

1. The effect of caffeine (2.5 g/kg diet) on lipid metabolism was examined in rats fed on a stock (low-cholesterol) diet or on a cholesterol plus cholic acid-supplemented (high-cholesterol) semi-synthetic diet. 2. When caffeine was induced in the stock diet fed to rats for 7 d, there was a moderate but significant increase in the concentration of serum cholesterol compared to the levels observed in the control rats. This change can be accounted for by the increase that was observed in the rate of cholesterogenesis in the liver. 3. After 25 d of caffeine in the stock diet, hepatic cholesterogenesis was still increased but the concentration of serum cholesterol was now the same as in the control rats. During the experimental period there was a progressive increase in the faecal excretion of neutral sterols in the rats receiving caffeine. 4. When caffeine was added to a cholesterol plus cholic acid-supplemented diet, there was a marked increase in the concentration of serum cholesterol but hepatic cholesterogenesis was now reduced. 5. Caffeine in the high-cholesterol diet appeared to delay, but probably did not reduce, the absorption of an oral dose of radio-labelled cholesterol. This conclusion was confirmed using rats which had not previously received either caffeine or cholesterol in the diet. 6. When the effect of caffeine in the high-cholesterol diet was investigated during a 24 h period, an exacerbation of the hypercholesterolaemia was seen only at certain times. 7. After a 4-month period of feeding rats on the caffeine-supplemented high-cholesterol diet, histological examination did not detect any damage to the heart and aorta. 8. The metabolic regulations involved in the effects of caffeine in the two diets are discussed and the relevance of the present results to observations made with human subjects is considered.

Animals↗
PubMed2006

The effects of caffeine ingestion on performance time, speed and power during a laboratory-based 1 km cycling time-trial.

There is little published data in relation to the effects of caffeine upon cycling performance, speed and power in trained cyclists, especially during cycling of approximately 60 s duration. To address this, eight trained cyclists performed a 1 km time-trial on an electronically braked cycle ergometer under three conditions: after ingestion of 5 mg x kg-1 caffeine, after ingestion of a placebo, or a control condition. The three time-trials were performed in a randomized order and performance time, mean speed, mean power and peak power were determined. Caffeine ingestion resulted in improved performance time (caffeine vs. placebo vs. control: 71.1 +/- 2.0 vs. 73.4 +/- 2.3 vs. 73.3 +/- 2.7 s; P = 0.02; mean +/- s). This change represented a 3.1% (95% confidence interval: 0.7-5.6) improvement compared with the placebo condition. Mean speed was also higher in the caffeine than placebo and control conditions (caffeine vs. placebo vs. control: 50.7 +/- 1.4 vs. 49.1 +/- 1.5 vs. 49.2 +/- 1.7 km x h-1; P = 0.0005). Mean power increased after caffeine ingestion (caffeine vs. placebo vs. control: 523 +/- 43 vs. 505 +/- 46 vs. 504 +/- 38 W; P = 0.007). Peak power also increased from 864 +/- 107 W (placebo) and 830 +/- 87 W (control) to 940 +/- 83 W after caffeine ingestion (P = 0.027). These results provide support for previous research that found improved performance after caffeine ingestion during short-duration high-intensity exercise. The magnitude of the improvements observed in our study could be due to our use of sport-specific ergometry, a tablet form and trained participants.

Administration, Oral↗
PubMed2005

Survey of caffeine levels in retail beverages in Portugal.

The caffeine content of 85 retail beverage samples purchased from local supermarkets between 1995 and 2004 was determined. The potential intake of caffeine through the consumption of these beverages (but excluding coffee) was estimated for students of the University of Coimbra, Portugal. The caffeine content of the beverages ranged from 47.5 to 282.5 mg l(-1) for teas, from 20.1 to 47.2 mg l(-1) for tea extracts samples, and from 80.7 to 168.7 mg l(-1) for cola soft drinks. Caffeine was not completely absent from caffeine-free colas, and energy drinks had a far greater caffeine content than regular drinks, ranging from 21 to 2175 mg l(-1). Soft drinks were consumed by 72% of the individuals, although 14% of the survey participants did not drink any of the different types of the beverages studied. Contrary to expectations for this age group, no consumptions of energy drinks was reported. Daily caffeine intake was estimated to range from 4.7 to 200 mg day(-1), but with only 5% reporting a daily intake around 200 mg caffeine. Cola-type beverages were an important dietary source of caffeine for the population studied. Statistical differences in the caffeine intake between the male and female populations were found, with p = 0.014, being higher for the male population. Of the beverages studied, cola-type drinks showed statistical differences for the male population, p = 0.03, and tea showed statistical differences for female population p = 0.013, respectively.

Adult↗
PubMed1994

Effect of caffeine on circadian excretion of urinary calcium and magnesium.

OBJECTIVE: To determine if later renal conservation occurs in calcium (Ca) and magnesium (Mg) excretion after morning caffeine-induced increases in urinary Ca and Mg excretion. DESIGN: Before-after trial of caffeine abstinance and consumption was conducted on two consecutive days in a metabolic ward while subjects ate a controlled diet containing 11.3 mmol Ca and 12.7 mmol Mg. 17 healthy males and females, ages 17-41 yr volunteered. Two caffeine doses of 3 mg/kg lean body mass caffeine were consumed at 7 and 10 a.m. on second day. Salivary caffeine concentrations and urinary Ca, Mg, sodium and creatinine excretion were measured. RESULTS: Salivary caffeine peaked at 4.7 umol/mL at 11:30 a.m. and declined with a half-life of 7.3 hours. Urinary Ca and Mg were elevated significantly (p = 0.01 and p = 0.04) for six h after the second caffeine dose. Caffeine had no significant effect on urinary calcium or magnesium excretion between 4 p.m. and 1 a.m. Between 1 and 4 a.m., urinary Ca and Mg excretion was decreased after caffeine (p = 0.04 and p = 0.01). Creatinine excretion was not different at any time. CONCLUSIONS: Nighttime compensatory renal conservation was insufficient to offset morning caffeine-induced mineral losses, resulting in net 24-hour urinary increases of 0.32 mmol Ca and 0.16 mmol Mg.

Adolescent↗
PubMed1998

Dietary caffeine intake is not correlated with adolescent bone gain.

OBJECTIVE: This study was conducted to determine whether dietary caffeine consumed by American white females between ages 12 to 18 affects total body bone mineral gain during ages 12 to 18 or affects hip bone density measured at age 18. METHODS: The Penn State Young Women's Health Study is a longitudinal investigation of bone, endocrine and cardiovascular health in non-Hispanic, white, teenage women. Nutrient and food group intakes were obtained by averaging over 6 years of prospective diet records. The cohort, as of age 18, (n = 81) was separated into three subgroups according to mean daily caffeine intake averaged across ages 12 to 18. Group I (n = 37) consumed less than 25 mg caffeine per day; Group II (n = 33) consumed 25 to 50 mg caffeine per day; and Group III (n = 11) consumed greater than 50 mg caffeine per day. The group mean daily caffeine intakes (SD) were Group I = 14 (6) mg/day; Group II = 35 (7) mg/day; Group III = 77 (27) mg/day. Total body bone gain and hip bone density were determined by dual energy x-ray absorptiometry (DXA). RESULTS: There were no significant differences among the three caffeine intake groups for total body bone mineral gain during the ages 12 to 18 or of hip bone density at age 18. The low caffeine intake group consumed more milk (and therefore more calcium) and more fruit per day than did the other two groups. Group III, the highest caffeine intake group, consumed more sugar per day than did the other two groups. The observed differences in nutrient and food intakes among the three groups were not associated with any differences in anthropometric measurements or bone gain among the three groups. CONCLUSION: These findings indicate that dietary caffeine intake at levels presently consumed by American white, teenage women is not correlated with adolescent total bone mineral gain or hip bone density at age 18.

Absorptiometry, Photon↗
PubMed2001

Mechanism of protection against radiation-induced DNA damage in plasmid pBR322 by caffeine.

PURPOSE: Caffeine (1,3,7-trimethyl xanthine), a dietary component, has been shown to have widely varying effects on DNA damage induced by UV and ionizing radiation, depending upon pre- or post-irradiation administration and its concentration. Caffeine administered post-UV irradiation is known to inhibit enzymatic repair of DNA lesions, leading to potentiation of damage, whereas its presence before or during irradiation elicits protection in a wide range of test systems: bacteria, cultured human cells, plant seeds and mouse. The purpose of this study is to test whether caffeine present during gamma-irradiation of plasmid DNA, a system devoid of replication and repair, could elicit protection by scavenging free radicals. MATERIALS AND METHODS: Plasmid pBR322 DNA was exposed to gamma-radiation in the presence or absence of caffeine at a dose-rate of 1.20 Gy min(-1) and damage measured as single-strand breaks. To understand the mechanisms of the observed protection, especially under oxic conditions, reaction of caffeine with superoxide radical (O(2)(-)), hydrogen peroxide (H(2)O(2)) and the deoxyribose peroxyl radical (ROO(*)) were studied. RESULTS: Irradiation of pBR322 was observed to induce a dose-dependent increase in single-strand breaks. Caffeine itself did not induce strand breaks but reduced radiation-induced strand breaks at micromolar to millimolar concentrations. Caffeine has been shown to react with the radiation-derived oxidants. The reaction rate constants observed were 7.5x10(1) M(-1) s(-1) with O(2)(-) 1.05x10(8) M(-1) s(-1) with ROO(*) and 8.8x10(1) M(-1) s(-1) with H(2)O(2). CONCLUSIONS: Caffeine effectively protects DNA against ionizing radiation in a system devoid of repair and replication machinery. Thus, DNA protection shown by caffeine is possibly due to the scavenging of radiation-derived primary as well as secondary reactive oxygen species, and this physicochemical protective pathway possibly pre-empts any subsequent inhibitory effect of caffeine on the enzymatic repair of DNA.

Caffeine↗
PubMed1993

Effect of caffeine and reduced temperature (20 degrees C) on the organization of the pre-Golgi and the Golgi stack membranes.

In the present study we have dissected the transport pathways between the ER and the Golgi complex using a recently introduced (Kuismanen, E., J. Jäntti, V. Mäkiranta, and M. Sariola. 1992. J. Cell Sci. 102:505-513) inhibition of transport by caffeine at 20 degrees C. Recovery of the Golgi complex from brefeldin A (BFA) treatment was inhibited by caffeine at reduced temperature (20 degrees C) suggesting that caffeine inhibits the membrane traffic between the ER and the Golgi complex. Caffeine at 20 degrees C did not inhibit the BFA-induced retrograde movement of the Golgi membranes. Further, incubation of the cells in 10 mM caffeine at 20 degrees C had profound effects on the distribution and the organization of the pre-Golgi and the Golgi stack membranes. Caffeine treatment at 20 degrees C resulted in a selective and reversible translocation of the pre- and cis-Golgi marker protein (p58) to the periphery of the cell. This caffeine-induced effect on the Golgi complex was different from that induced by BFA, since mannosidase II, a Golgi stack marker, remained perinuclearly located and the Golgi stack coat protein, beta-COP, was not detached from Golgi membranes in the presence of 10 mM caffeine at 20 degrees C. Electron microscopic analysis showed that, in the presence of caffeine at 20 degrees C, the morphology of the Golgi stack was altered and accumulation of numerous small vesicles in the Golgi region was observed. The results in the present study suggest that caffeine at reduced temperature (20 degrees C) reveals a functional interface between the pre-Golgi and the Golgi stack.

Animals↗
PubMed1984

Calcium and magnesium contents and volume of the terminal cisternae in caffeine-treated skeletal muscle.

(a) The effects of caffeine on the composition and volume of the terminal cisternae (TC) of the sarcoplasmic reticulum (SR) in frog skeletal muscle were determined with rapid freezing, electron microscopy, and electron probe analysis. (b) Caffeine (5 mM) released approximately 65% of the Ca content of the TC in 1 min and 84% after 3 min. The release of Ca from the TC was associated with a highly significant increase in its Mg content. This increase in Mg was not reduced by valinomycin. There was also a small increase in the K content of the TC at 1 min, although not after 3 min of caffeine contracture. (c) On the basis of the increase in Mg content during caffeine contracture and during tetanus (Somlyo, A. V., H. Gonzalez-Serratos, H. Shuman, G. McClellan, and A. P. Somlyo, 1981, J. Cell Biol., 90:577-594), we suggest that both mechanisms of Ca release are associated with an increase in the Ca and Mg permeability of the SR membranes, the two ions possibly moving through a common channel. (d) There was a significant increase in the P content of the TC during caffeine contracture, while in tetanized muscle (see reference above) there was no increase in the P content of the TC. (e) Mitochondrial Ca content was significantly increased (at 1 and at 3 min) during caffeine contracture. Valinomycin (5 microM) blocked this mitochondrial Ca uptake. (f) The sustained Ca release caused by caffeine in situ contrasts with the transient Ca release observed in studies of fragmented SR preparations, and could be explained by mediation of the caffeine-induced Ca release by a second messenger produced more readily in intact muscle than in isolated SR. (g) The TC were not swollen in rapidly frozen, caffeine-treated muscles, in contrast to the swelling of the TC observed in conventionally fixed, caffeine-treated preparation, the latter finding being in agreement with previous studies. (h) The fractional volume of the TC in rapidly frozen control (resting) frog semitendinosus muscles (approximately 2.1%) was less than the volume (approximately 2.5%) after glutaraldehyde-osmium fixation.

Animals↗
PubMed1984

Excitation-contraction coupling in cardiac Purkinje fibers. Effects of caffeine on the intracellular [Ca2+] transient, membrane currents, and contraction.

The effects of caffeine on tension, membrane potential, membrane currents, and intracellular [Ca2+], measured as the light emitted by the Ca2+-activated photoprotein aequorin, were studied in canine cardiac Purkinje fibers. An initial, transient, positive inotropic effect of caffeine was accompanied by a transient increase in the second component of the aequorin signal (L2) but not the first (L1). In the steady state, 4 or 10 mM caffeine always decreased twitch tension and greatly reduced both L1 and L2. At a concentration of 2 mM, caffeine usually reduced but occasionally increased the steady state twitch tension. However, 2 mM caffeine always reduced both L1 and L2. Caffeine eliminated the diastolic oscillations of intracellular [Ca2+] induced by high extracellular [Ca2+]. In voltage-clamp experiments, 10 mM caffeine reduced the transient outward current and the peak tension elicited by step depolarization from a holding potential of -45 mV. In the presence of 20 mM Cs+, 10 mM caffeine reduced slow inward current. However, the time course of this reduction was far slower than that in tension and light observed in separate experiments. The simplest explanation of the results is that caffeine inhibits the sequestration of Ca2+ by the sarcoplasmic reticulum. The results also suggest that in Purkinje fibers caffeine increases the sensitivity of the myofilaments to Ca2+.

Action Potentials↗
PubMed2001

Caffeine intake increases the rate of bone loss in elderly women and interacts with vitamin D receptor genotypes.

BACKGROUND: The role of caffeine as a risk factor for bone loss is controversial. OBJECTIVE: Our goals were 1) to compare in both a cross-sectional study and a 3-y longitudinal study the bone mineral density (BMD) of postmenopausal women consuming high or low amounts of caffeine and 2) to study the interaction between caffeine intake, vitamin D receptor (VDR) polymorphism, and BMD in the longitudinal study. DESIGN: The results are derived from cross-sectional measurements of BMD in 489 elderly women (aged 65-77 y) and from longitudinal measurements made in 96 of these women who were treated with a placebo for 3 y. Changes in BMD were adjusted for confounding factors and were compared between groups with either low (< or =300 mg/d) or high (>300 mg/d) caffeine intakes and between the VDR genotype subgroups of the low- and high-caffeine groups. RESULTS: Women with high caffeine intakes had significantly higher rates of bone loss at the spine than did those with low intakes (-1.90 +/- 0.97% compared with 1.19 +/- 1.08%; P = 0.038). When the data were analyzed according to VDR genotype and caffeine intake, women with the tt genotype had significantly (P = 0.054) higher rates of bone loss at the spine (-8.14 +/- 2.62%) than did women with the TT genotype (-0.34 +/- 1.42%) when their caffeine intake was >300 mg/d. CONCLUSIONS: Intakes of caffeine in amounts >300 mg/d ( approximately 514 g, or 18 oz, brewed coffee) accelerate bone loss at the spine in elderly postmenopausal women. Furthermore, women with the tt genetic variant of VDR appear to be at a greater risk for this deleterious effect of caffeine on bone.

Absorptiometry, Photon↗
PubMed2005

Effect of administration of caffeine or green tea on the mutation profile in the p53 gene in early mutant p53-positive patches of epidermal cells induced by chronic UVB-irradiation of hairless SKH-1 mice.

Irradiation of SKH-1 mice with UVB light for 20 weeks resulted in a large number of patches of epidermal cells, which was visualized with an antibody that recognizes mutated p53 protein. Oral treatment of mice with caffeine (0.4 mg/ml) or green tea (6 mg tea solids/ml) as the drinking fluid during UVB irradiation decreased the number of patches by approximately 40%. Sequencing analysis of the p53 gene (exons 3 to 9) detected 88, 82 or 39 point mutations in 67, 70 or 29 patches from water, caffeine or tea treated mice, respectively. A major hotspot at codon 270 (Arg-->Cys) accounted for 47.7% (water), 70.7% (caffeine) or 46.2% (tea) of all mutations. Patches from caffeine treated mice had fewer types of mutations than patches from mice treated with water or tea. Administration of caffeine or tea during 20 weeks of UVB irradiation eliminated mutations at codons 149 (Pro-->Ser) and 210 (Arg-->Cys) but increased the frequency of mutations at codon 238 (Ser-->Phe). Topical applications of caffeine (1.2 mg in 100 microl acetone) once a day, five times a week for 6 weeks after stopping UVB decreased the number of patches by 63% when compared with mice treated with acetone. DNA sequencing analysis detected 63 and 68 mutations in 48 and 57 patches from acetone or caffeine treated mice, respectively. Although no differences in the frequency, position or types of mutations were observed, the caffeine group harbored less homozygous mutations (12.3% of the total) than the acetone group (31.3% of the total, P = 0.029). In summary, oral treatment of mice with caffeine or green tea during chronic UVB irradiation changed the mutation profile of the p53 gene in early mutant p53 positive epidermal patches, and topical applications of caffeine after discontinuation of chronic UVB irradiation specifically eliminated patches harboring homozygous p53 mutations.

Administration, Oral↗