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Ergogenic Aids
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Caffeine is yet another ergogenic aid that is among the most widely used in the sport community. Though it appears in many beverages (e.g., coffee, tea), it is not essential for health. Furthermore, it is probably the most complementary ingredient in supplements and other nutritional products, so understanding its mechanisms and efficacy is extremely valuable for the sportsperson and supporting practitioners. Several mechanisms for the action of caffeine have been identified, but the most important physiologically is the inhibition of adenosine receptors. Caffeine is able to elicit this inhibition by holding a very similar structure to that of adenosine and can therefore bind to the receptors (adenosine A2A receptors) and block its action. Adenosine receptors are ubiquitous, appearing on tissues of the brain, heart, smooth muscle, adipocytes, and even skeletal muscle (45). Furthermore, caffeine may have intracellular actions. These are not well understood, but likely include direct effects on enzymes or influence post-receptor events (45). Collectively, this implies that caffeine can have a relatively pervasive effect and therefore have a variety of cooperating responses that are both primary and secondary actions.
Biochemistry of Caffeine's Influence On Exercise Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Jane Shearer, Robyn F. Madden, Jill A. Parnell
As previously mentioned, caffeine is a non-specific adenosine receptor antagonist. Adenosine receptors are a group of G protein–coupled receptors that mediate the physiological actions of adenosine. There are four main subtypes of adenosine receptors (A1, A2A, A2B, and A3) classified by their differential coupling to adenylyl cyclase that regulate cyclic AMP (cAMP) levels (26, 69). Receptors are distributed throughout the body, with different tissues expressing specific subtypes. Adenosine A1 and A3 receptors are coupled to Gi/o proteins, while adenosine A2A and A2B receptors act upon Gs/olf proteins (25, 69). Binding of adenosine to its receptors results in changes in cAMP levels that initiate a host of cell responses, including ion channels and enzymes. Caffeine has a similar structure to adenosine and therefore binds to the same receptors, essentially blocking the normal effects of adenosine (antagonist). However, caffeine has different affinities for each type of adenosine receptor, explaining why caffeine can produce distinct impacts on tissues depending on the type and level of adenosine receptors present (Table 24.1).
Caffeine in the modulation of brain function
Published in B.S. Gupta, Uma Gupta, Caffeine and Behavior, 2020
J. Patrick Myers, David A. Johnson, Devon E. McVey
The antagonism of adenosine receptors by caffeine is currently the most widely accepted mechanism of its action. The elucidation of this mechanism stemmed from a discovery by Sattin and Rall,11 who noticed that theophylline often reduced the accumulation of cAMP in cerebral slices rather than increasing it, as would be expected from a phosphodiesterase inhibitor. Furthermore, it was noted that adenosine itself produces effects opposite to those of caffeine, and it was later determined that methylxanthines act as competitive antagonists at adenosine receptors at concentrations well within the therapeutic range (less than 100 µg, which can be attained by drinking 1 to 3 cups of coffee).
Sleep-promoting activity of lotus (Nelumbo nucifera) rhizome water extract via GABAA receptors
Published in Pharmaceutical Biology, 2022
Yejin Ahn, Singeun Kim, Chunwoong Park, Jung Eun Kim, Hyung Joo Suh, Kyungae Jo
Furthermore, to evaluate the sleep-promoting activity of LE, caffeine was administered to rats to develop the insomnia model. Caffeine has been used with methylxanthine compounds to increase arousal and induce cortical activation (Bonnet and Arand 1992; Nehlig et al. 1992). Caffeine has been reported to induce arousal by blocking the action of adenosine receptors and lead to insomnia by reducing slow waves (Bonnet and Arand 1992; Panagiotou et al. 2020). In this study, the delta power in NREM corresponding to the slow wave was significantly decreased in the group treated with caffeine alone compared to the NC group (Figure 5). However, administration of 120 and 150 mg/kg LE significantly increased the NREM sleep time in the respective LE-group compared to the caffeine control group. In the caffeine-induced insomnia model, oral administration of LE increased sleep time, which can be attributed to an increase in NREM sleep time.
Istradefylline, an adenosine A2a receptor antagonist, inhibits the CD4+ T-cell hypersecretion of IL-17A and IL-8 in humans
Published in Immunological Medicine, 2022
Mieko Tokano, Masaaki Kawano, Rie Takagi, Sho Matsushita
Adenosine binds to the adenosine receptors expressed on the cell surface. There are four subtypes of adenosine receptors (A1, A2a, A2b, and A3), all of which belong to the G protein-coupled receptor family. A2aR and A2bR signal the Gs protein, whereas A1R and A3R signal the Gi protein [1]. A1R, A2bR, and A3R are widely expressed in vivo, whereas A2aR is expressed at high levels in only a few regions of the body, such as the striatum, olfactory tubercle, nucleus accumbens, endothelial cells, vascular smooth muscle cells, platelets, and immune cells [2]. A1R and A2aR are high-affinity receptors, whereas A2bR and A3R are low-affinity receptors [3,4]. Adenosine also plays a role as a neurotransmitter [5], and istradefylline is a selective A2aR antagonist used for the treatment of Parkinson's disease [6]. Adenosine is also a potent endogenous regulator of inflammation and immune reactions [1]. However, the molecular mechanisms underlying these effects are largely unknown. In a previous study, adenosine was reported to induce T-helper (Th)17 differentiation by activating A2bR [7].
Remedial effects of caffeine against depressive-like behaviour in mice by modulation of neuroinflammation and BDNF
Published in Nutritional Neuroscience, 2022
Sanchari Basu Mallik, Jayesh Mudgal, Susan Hall, Manas Kinra, Gary D. Grant, Madhavan Nampoothiri, Shailendra Anoopkumar-Dukie, Devinder Arora
CAF is a well established non-specific antagonist of adenosine A1 and A2A receptors. Both adenosine receptors are involved in providing neuroprotection during noxious brain conditions. Adenosine A1 receptors inhibit adenylyl cyclase via inhibitory G-protein, and CAF by blocking this receptor increases the cyclic AMP (cAMP) levels and activates the downstream pathways through protein kinase A (PKA) signalling. Chronic treatment of animals with CAF has been shown to cause upregulation of these A1 receptors [36], and this increased expression of receptors suppresses the proinflammatory cytokines [37]. Furthermore, increased adenosine levels within the CNS due to neuroinflammation promotes neuroglial activation [38] via adenosine A2A receptors. Blockage of these receptors by CAF significantly impacts the initiation and propagation of inflammatory cascade [39,40]. Adenosine A2A receptors are also involved in upregulation of pERK pathway and MAPK activation leading to increased oxidative stress, as observed by increased lipid peroxidation and CAF reduces lipid peroxidation and scavenges hydroxyl radicals [38,41].