Effect Of Acute Caffeine Ingestion Research Articles

Acute Caffeine Ingestion and Glucose Tolerance in Women With or Without Gestational Diabetes Mellitus

ObjectiveRecent work showing that caffeine impairs glucose tolerance may be of particular concern in pregnancy because of a possible negative effect on fetal outcome. The current study sought to assess the effect of acute caffeine ingestion on glucose tolerance in women with or without gestational diabetes mellitus (GDM). MethodsNineteen women whose routine GDM test was negative (control) and eight women with an initial positive GDM screen completed two trials one week apart in a double-blind randomized crossover study. Following an overnight fast, subjects ingested caffeine (3 mg/kg pre-pregnancy body weight) or an identical-appearing placebo (gelatin) capsule and one hour later began a 75 g 2-hour oral glucose tolerance test. ResultsIn the control group, caffeine did not significantly affect blood glucose, insulin, or C-peptide. In the GDM group, glucose area under the curve (AUC) was greater (P < 0.01), C-peptide AUC was greater (P < 0.05), and insulin sensitivity index was lower (18%, P < 0.05) after caffeine than after placebo. ConclusionCaffeine impaired insulin sensitivity in women with GDM. Additional research regarding more specific dietary caffeine recommendations for women with GDM is warranted.

Caffeine-Induced Changes in Cardiovascular Function during Resistance Training

Caffeine (CAF) exerts a pressor effect both at rest and during exercise, as blood pressure is higher than with placebo. The effect of acute CAF ingestion combined with intense resistance training on cardiovascular function is unknown, however. The primary aim of the study was to examine changes in cardiovascular function after completion of fatiguing bench-press and leg-press exercise after CAF or placebo ingestion. Twenty-two resistance-trained men ingested CAF (6 mg/kg) or placebo 1 h preexercise in a randomized, double-blind crossover design. They refrained from CAF intake and strenuous exercise 48 and 24 h pretrial, respectively. Heart rate and blood pressure were measured preexercise. After a standardized warm-up, 1-repetition-maximum (1-RM) on the barbell bench press and leg press was tested. When it had been determined, a load equivalent to 60% of 1-RM was placed on the bar, and the subject completed repetitions to failure. Measurements of heart rate and blood pressure were immediately completed, and mean arterial pressure and rate-pressure product were calculated. Results showed significant (P < 0.05) increases in heart rate (+ 10 beats/min), systolic blood pressure (+ 8-10 mmHg), and rate-pressure product with acute CAF ingestion versus placebo. No change (P > 0.05) in diastolic blood pressure across time or treatment was shown. To prevent elevated blood pressure and potential enhanced risk of heart disease, CAF intake should be monitored in at-risk men who participate in resistance training.

Effects of Caffeine on Prolonged Intermittent-Sprint Ability in Team-Sport Athletes

Caffeine can be a powerful ergogenic aid for the performance of prolonged, submaximal exercise. Little evidence, however, supports an ergogenic effect of caffeine on intermittent-sprint performance. Hence, this study was conducted to examine the effects of acute caffeine ingestion on prolonged intermittent-sprint performance. Using a double-blind, placebo-controlled design, 10 male team-sport athletes (amateur level, VO2peak 56.5 +/- 8.0 mL x kg(-1) x min(-1)) completed two exercise trials, separated by 7 d, 60 min after ingestion of either 6 mg x kg(-1) caffeine or placebo. The exercise trial was performed on a front-access cycle ergometer and consisted of 2 x 36-min halves, each composed of 18 x 4-s sprints with 2-min active recovery at 35% VO2peak between each sprint. Urinary caffeine levels were measured after exercise. The total amount of sprint work performed during the caffeine trial was 8.5% greater than that performed during the placebo trial in the first half (75,165.4 +/- 3,902.9 vs 69,265.6 +/- 3,719.7 J, P < 0.05), and was 7.6% greater in the second half (73,978.7 +/- 4,092.6 vs 68,783.2 +/- 3,574.4 J, P < 0.05). Similarly, the mean peak power score achieved during sprints in the caffeine trial was 7.0% greater than that achieved during the placebo trial in the first half (1330.9 +/- 68.2 vs 1244.2 +/- 60.7 W, P < 0.05), and was 6.6% greater in the second half (1314.5 +/- 68.4 vs 1233.2 +/- 59.9 W, P < 0.05). Urinary caffeine levels following the caffeine trial ranged from 3.5 to 9.1 microg x mL(-1) (6.9 +/- 0.6 microg x mL(-1)). This study revealed that acute caffeine ingestion can significantly enhance performance of prolonged, intermittent-sprint ability in competitive, male, team-sport athletes.

Acute effects of caffeine on heart rate variability

Caffeine ingestion has been found to increase sympathetic nervous system activity (SNSA).1 This observation may underlie the finding of short-term increases in systolic blood pressure and arterial stiffness after caffeine ingestion.2 There have been few studies on the effects of caffeine on the cardiac parasympathetic nervous system activity (PNSA).3 PNSA is an independent risk factor for future cardiovascular events, in particular sudden cardiac death,4 at least in patients with existing disease. The present study therefore sought to determine the effect of acute caffeine ingestion on PNSA in nonhabitual caffeine users. Because of putative direct effects of caffeine on the autonomic nervous system, we hypothesised that, in addition to increased SNSA, acute caffeine ingestion would be associated with reduced PNSA.

Acute effects of caffeine ingestion on signal-averaged electrocardiograms

Background Although moderate caffeine ingestion has not been shown to be arrhythmogenic, caffeine toxicity can cause severe cardiac arrhythmias, including atrial fibrillation and ventricular tachycardia. Atrial fibrillation and ventricular tachycardia have been associated with prolongation of P-wave and QRS complex durations on signal-averaged electrocardiograms. This study investigated acute effects of caffeine ingestion on signal-averaged P-wave and QRS complexes. Methods and Results Signal-averaged electrocardiograms were obtained from 12 normal subjects (6 men, 6 women; ages 21 to 26 years) before and after ingestion of caffeine (5 mg/kg body weight) or placebo in a randomized, double-blind, crossover fashion. Electrocardiograms for signal averaging were recorded from electrodes left in a constant location. After bandpass filtering (30 to 300 Hz) and amplification, signals were sampled over 7.2 minutes at 2000 Hz. Signal-averaged P-wave and QRS complex durations did not significantly change after placebo ingestion. After caffeine ingestion QRS duration prolonged in 9 of 11 subjects at 90 minutes (mean ± SEM = 0.8 ± 0.3 ms, P < .02) and in 8 of 9 after 3 hours (1.1 ± 0.2 ms, P < .001). No significant change in P-wave duration or heart rate was found after caffeine ingestion at any test interval. Average caffeine level in saliva 90 minutes after ingestion was 6.6 ± 1.6 (SD) μg/dL. Conclusions Although probably not arrhythmogenic in normal subjects, moderate caffeine ingestion does produce a small but statistically significant prolongation of signal-averaged QRS complexes. Further prolongation caused by excessive caffeine intake may be a factor in the genesis of arrhythmias associated with caffeine toxicity. (Am Heart J 1998;136:643-6.)

Hemodynamic effects of acute caffeine ingestion in young adults

In summary, the inotropic effect of caffeine on the heart was significant in our study. These data suggest the importance of further investigation into the effects of caffeine on patients with known heart disease.

Acute effects of caffeine ingestion at rest in humans with impaired epinephrine responses.

Caffeine ingestion has been demonstrated to increase circulating epinephrine (Epi) and norepinephrine (NE), elevate free fatty acids (FFAs), and alter heart rate, blood pressure (BP), and ventilation in humans. Whether these physiological responses are a result of caffeine acting through direct stimulation of specific tissues via adenosine receptors or secondary to Epi increases is not known. In the present experiment, six tetraplegics (level of spinal cord lesions C4-C6) were tested at rest for 3 h to investigate the effects of 6 mg/kg caffeine in capsule form on subjects with impaired Epi responses. Ventilatory, cardiovascular, metabolic, and hormonal data were collected every 15-20 min after caffeine ingestion. There were no significant (P > 0.05) increases in plasma Epi after caffeine ingestion [0.19 +/- 0.04 (SE) nM (preingestion); 0.20 +/- 0.04 nM (80 min postingestion)] or in plasma NE [0.53 +/- 0.16 nM (preingestion); 0.49 +/- 0.09 nM (80 min postingestion; P > 0.05)]. However, significant increases were found in serum FFAs [0.53 +/- 0.08 nM (preingestion); 1.03 +/- 0.20 mM (40 min postingestion; P < 0.05] and in glycerol. These concentrations remained elevated throughout the experiment. BP increased in the first hour postingestion. These data demonstrate that caffeine in physiological doses directly stimulates specific tissues, i.e., adipose and peripheral vascular tissue, and these effects are not secondary to increases in Epi after caffeine ingestion.

Effects of acute caffeine ingestion and menopause on sulfate homeostasis in women

Inorganic sulfate is a physiological anion which is utilized in the metabolism of both endogenous compounds and xenobiotics. Its homeostasis is maintained predominantly by facilitated reabsorptive processes in the kidneys. The objectives of the present investigation were to evaluate the effects of menopausal status and caffeine ingestion on the serum concentrations and clearance of inorganic sulfate. Thirty-nine women who were classified as premenopausal, postmenopausal with or without estrogen treatment, and postmenopausal with osteoporosis participated in the study. The women were studied on two separate occasions following the ingestion of a decaffeinated beverage to which 6 mg caffeine/kg lean body mass or no caffeine was added. All women were habitual caffeine users (mean ingestion of 588 mg caffeine per day) but abstained from all caffeine sources for 2 weeks prior to the control study day. Postmenopausal women with estrogen supplementation exhibited significantly lower sulfate serum concentrations (0.24 ± 0.02 mM vs. 0.32 ± 0.04 mM in premenopausal women, mean ± SD, p < 0.05) and a decreased renal reabsorption of sulfate for the control (no caffeine) period. There was no difference in serum sulfate or sulfate reabsorption in estrogen supplemented postmenopausal women, compared with women not taking estrogen. Postmenopausal women with osteoporosis had significantly lower creatinine and sulfate clearances than postmenopausal women with estrogen supplementation which may be related to their older age, or factors related to the disease process. The 6 mg/kg dose of caffeine caused a diuresis, but no change in GFR, as indicated by urine volume and creatinine clearance values, respectively. Caffeine administration resulted in an increase in the sulfate excretion rate; there was no change in sulfate serum concentrations. The results of this investigation indicate that menopause results in decreased sulfate serum concentrations that may be the consequence of a decreased renal reabsorption of sulfate. Secondly, this investigation demonstrated that caffeine ingestion increases the urinary excretion of sulfate, an effect that may be related to the diuretic effect of caffeine or due to a caffeine-induced alteration in the renal reabsorption of sulfate.

123 Maternal and Fetal Cardiovascular Effects of Acute Caffeine Ingestion

123 Maternal and Fetal Cardiovascular Effects of Acute Caffeine Ingestion