The No-Caffeine Pre-Workout

Nitric oxide without caffeine

Background: Caffeine is known to inhibit phosphodiesterases, to mobilise intracellular calcium, and to act as an antagonist at adenosine receptors, all of which can potentially alter nitric oxide (NO) production. It was therefore hypothesised that caffeine may alter exhaled NO (eNO) levels.

Methods: In a randomised, single blind, crossover manner, 12 normal subjects consumed either (1) coffee and a placebo capsule, (2) decaffeinated coffee and a capsule of 200 mg caffeine, or (3) decaffeinated coffee and a placebo capsule. Serum caffeine levels were measured at baseline and 1 hour later. Exhaled NO levels were also measured at baseline and each hour for 4 hours.

Results: A significant percentage fall in mean (SE) eNO from baseline was seen 1 hour after either caffeinated coffee or a caffeine capsule when compared with placebo (13.5 (4.0)%, p=0.009 and 19.0 (3.8)%, p=0.001, respectively).

Conclusion: Caffeine causes a significant decrease in eNO which will need to be considered when designing trials to measure eNO levels. The mechanism may be via adenosine receptor antagonism or by altering levels of cGMP.

Nitric oxide (NO) is generated from l-arginine by constitutive NO synthases (ecNOS and nNOS) and inducible NO synthase (iNOS). It has become apparent that a number of exogenous factors affect levels of exhaled NO. Cigarette smoking and alcohol decrease exhaled NO levels via effects upon constitutive and iNOS, respectively, while asthmatic inflammation and upper respiratory tract infections increase exhaled NO (eNO) via iNOS induction.

Caffeine is widely consumed as coffee, tea, and cola. Coffee also contains numerous other substances such as minerals, lipids, proteins, carbohydrates, aliphatic acids, glycosides, and contaminants formed during the roasting process including nitrosamines, heterocyclic amines, and paraffins. In high doses caffeine inhibits phosphodiesterases, leading to elevation of cyclic AMP (cAMP) and cyclic GMP (cGMP) which may be the mechanism for its weak bronchodilatory effect in mild asthmatic subjects. It can also mobilise intracellular calcium stores and, at lower concentrations, caffeine antagonises adenosine receptors (A1, A2a). In addition, an increase in intracellular cGMP upregulates ecNOS expression and an increase in intracellular cAMP downregulates it. Stimulation of adenosine receptors leads to differential effects, with A2a receptor stimulation increasing NO generation while A1 receptor stimulation leads to decreased NO production by endothelial cells. This led us to test the hypothesis that caffeine may have an effect on eNO levels in normal subjects.

Study sample and protocol

Twelve normal healthy habitual caffeine drinkers (four men) of mean age of 33.2 (9.3) years were recruited to the study. All were non-smoking non-asthmatic subjects with normal spirometric parameters and no recent history of respiratory tract infections. Subjects abstained from dietary methylxanthines for at least 8 hours before the study. The study was approved by the institutional ethics committee and all subjects gave written informed consent.

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