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The influence of the cytochrome P450 enzymes, specifically a polymorphism of the CYP1A2 genotype, following caffeine ingestion has been shown to influence aerobic endurance; however, the effect on short‐term anaerobic performance is inconclusive. Individuals with the AA variant are responders to caffeine and those with the AC/CC variant are non‐responders.PURPOSETo examine the effects of caffeine and specific CYP1A2 genotype on anaerobic performance.METHODS10 subjects completed two 30 second Wingate Anaerobic Tests (WAnT30) (resistance = 0.075 kg•BW−1) on the Velotron that were separated by 2 to 7 days. Relative peak power (PP) and relative mean power (MP) were computed by the Velotron software. An oral bolus of caffeine (CAF), 5mg•kg−1, or placebo (PLA), maltodextrin, was given in a randomized and counterbalanced design 60 min prior to testing. Buccal epithelial cells were collected via a mouth rinse of 0.9% NaCl. Genomic extraction was obtained using QiAmp Mini spin columns and cell lysing with proteinase k, followed by PCR amplification with Fast Taq. The restriction enzyme (ApaI) was used to cut fragments. Cut and uncut samples underwent electrophoresis in 1% agarose gel and ultraviolet light photography identified genotype. The data was analyzed using a 2 (condition) × 2 (CYP) ANOVA with repeated measures (p>0.05).RESULTS5 people were AA and 5 people were AC/CC. The results revealed that CAF elicited no ergogenic effects. The main effect of condition, PLA versus CAF, showed no significant difference for PP or MP (p = 0.49). The main effect of CYP1A2, AA or AC/CC, did not reveal power differences for PP or MP (p = 0.96). Follow‐up pairwise comparisons between PLA to CAF for PP (W•kg−1) showed non‐significant D's of 1.17% in AA (10.3 and 10.42) and −0.38% for AC/CC (10.36 and 10.46, respectively). Likewise, MP resulted in non‐significant D's of 3.66% for AA (8.2 and 8.5 W•kg−1, respectively) and 2.24% for AC/CC (8.3 and 8.5, W•kg−1 respectively).CONCLUSIONCaffeine did not produce an ergogenic effect for anaerobic exercise, regardless of an individual's CYP1A2 variant. However, the larger percent increases, specifically in MP, suggest that further research should be conducted, such as increasing sample size and identifying confounding variables such as other receptor sites that may interact with caffeine.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
INTRODUCTION The supplementation of caffeine is often used to elicit an enhancement of focus, arousal, or performance; however, intra‐individual response to caffeine has been shown to vary the effects of caffeine. Genetic variation of the adenosine receptor, 1976T>C (ADORA2A), has been linked to caffeine sensitivity and is a potential target for understanding individual differences. The TT genotype demonstrates an increased sensitivity to caffeine compared to the TC/CC genotype. The anxiogenic effects, genetic influences, and pharmacological interactions play a role in the ergogenic effects of caffeine. PURPOSE To examine the effects of caffeine and ADORA2A genetic variants on anaerobic performance during a 30s Wingate test. METHODS Sixteen trained subjects (age=19.8±0.5 years, weight=70.5±10.3 kg, height=175.8±8.8 cm) volunteered for a randomized, counterbalanced, and double‐blind study. Sixty minutes prior to testing, the subjects ingested a gelatin capsule containing either caffeine (CAF), 5mg·kg−1 bodyweight (BW), or a proportional placebo (PLA) of maltodextrin. The 30‐second Wingate Test (WAnT30) trials were performed on a Velotron cycle ergometer at 0.075 kg·BW−1 resistance and were separated by a minimum of 48 hours. Anaerobic power (AP) (W·kg−1), anaerobic capacity (AC) (W·kg−1), and total power (TP) (W) were determined for each condition. Genotype was determined using a mouth rinse of 0.9% NaCl to obtain buccal epithelial cells, which were lysed using proteinase k. DNA was extracted using QiAmp Mini spin columns. The allelic determination of ADORA2A was identified using TaqMan® SNP Assay (rs5751876) and 40 thermocycles for amplification with a One‐Step qPCR (Life Technologies, Carlsbad, CA). The data was analyzed using a 2 (condition) × 2 (genotype) ANOVA with repeated measures, p < 0.05. RESULTS Genotypic distribution resulted in 6 TT and 10 TC/CC individuals. The main effect of condition, PLA vs CAF, produced no significant ergogenic effect for AP (P=0.52), AC (p=0.67), or TP (p=0.85). The main effect of ADORA2A, TT vs TC/CC, produced no significant difference for AP (p=0.95), AC (p=0.49), or TP (p=0.95). The interaction effect of condition x genotype showed no significant differences for AP (p=0.65), AC (p=0.94), or TP (p=0.95). Although follow up simple effect tests showed no significant differences for AP, individuals with the TT genotype showed a 4.5% (11.2±1.12 to 11.7±1.3), PLA to CAF, improvement compared to the 0.81% (11.4±1.4 to 11.5±1.3) improvement of the TC/CC individuals. Likewise, for TP (W), TT individuals improved by 1.8% (192975±25911 to 196525±21111) while TC/CC individuals increased only 0.94% (194787±48699 to 196635±44092). CONCLUSION Caffeine did not elicit a significant anaerobic ergogenic effect for the WAnt30. However, the results indicate that individuals with the TT genotype did experience larger percent improvement than their TC/CC counterparts. As such, future research should continue to investigate these inter‐individual differences by increasing sample size and identifying...
Obesity and long‐term exposure to high fat diet (HFD) are both associated with peripheral and central inflammation. Acute HFD exposure, however, is also associated with neuroinflammation in brainstem areas responsible for control of gastric functions and energy homeostasis prior to the development of obesity. Neuroinflammation and astroglial activation are known to modulate neuronal activity and physiological outcomes, such as gastric motility, emptying, and food intake. Following initial HFD exposure and a brief (24hr) period of hyperphagia, both humans and rodent models regulate their caloric intake within 3–5 days. The neuroinflammation observed within the brainstem during acute HFD exposure may, therefore, contribute to the homeostatic regulation of caloric intake. The aim of this study is to test the hypothesis that restoration of energy balance during acute HFD exposure requires brainstem astroglial activation. Sprague‐Dawley rats, 6–8 weeks of age, were fed a control or HFD (14% or 60% kcal from fat, respectively) throughout the study. Immunohistochemical techniques were used to examine astrocyte (GFAP and S100β) and microglia (Iba1 and CD11b) morphology and activity state within the dorsal vagal complex (DVC) after 1,3,5, and 14 days of HFD exposure. Confocal microscopy was used to quantify astrocyte and microglial density, staining intensity, and morphology. Chronic 4th ventricular cannulae were implanted for the administration the astrocyte metabolism inhibitor, fluoroacetate, the microglial activation inhibitor, minocycline (5 and 10mg/mL in 5μL, respectively), or vehicle (PBS) to assess the role of astrocytes and microglia in the regulation of caloric intake. Food intake and body weight were measured twice daily for 10 days prior to, and throughout, HFD exposure. The effects of 4th ventricular administration of fluoroacetate on gastric emptying rates were additionally assessed using the 13C octanoic acid breath test technique. Immunohistochemical characterization of DVC microglia and astrocytes demonstrated an increase in Iba1 and GFAP staining intensity on days 3 and 5 of HFD exposure, which recovered by day 14 (3 Day: 225%, 210%, 5 Day: 195%, 280%, 14 Day: 124%, 92% of control total fluorescence (CTF), respectively, N=2). 4th ventricular application of fluoroacetate and minocycline attenuated the homeostatic regulation of caloric intake observed following acute HFD exposure, compared to vehicle controls (AUC: 242±11.4 vs. 264±2.8 vs. 187±10.6, P<0.05 F=10.35, N=3–5) and preliminary data suggest that fluoroacetate also attenuates the homeostatic delay in gastric emptying observed in control conditions (t1/2: 102.5% vs 150.3% of baseline, respectively, N=1–2). The results from this study indicate that astrocyte and microglial activation occurs within 3–5 days of HFD exposure and is required for the homeostatic regulation of caloric intake and gastric emptying following acute HFD exposure. Understanding the physiological mechanisms responsible for energy homeostasis, and importantly, how this mechanism...
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