Influence of caffeine upon tolerance to a simulated hemorrhagic challenge in habituated users
Authors: Pizzey Faith K , Tourula Erica N , Theorin Tyler J , Pearson James 
Published: June 2021

Caffeine is an adenosine receptor antagonist and its consumption in caffeine naïve individuals is associated with increased blood pressure. However, the influence of caffeine consumption upon blood pressure in individuals habituated to caffeine is less clear. Approximately 300mg of caffeine is consumed daily by 80% of the United States active duty military yet the influence of caffeine upon tolerance to a simulated hemorrhagic challenge in habituated users is unknown. Our aim was to examine the influence of caffeine consumption upon tolerance to a simulated hemorrhagic challenge (Lower Body Negative Pressure; LBNP) in habitual caffeine consumers. Eight healthy participants (age: 27 ± 6 yrs, Ht: 179 ± 10 cm, Wt: 76.0 ± 14.4 kg) completed three double blinded, counterbalanced trials (Caffeine, Decaffeinated and Water). Following baseline measures of cardiovascular control (including mean arterial pressure, MAP; mmHg and total peripheral resistance, TPR; mmHg/l/min) participants drank (6.25ml/kg body mass) either water (Water; volume control), decaffeinated coffee (Decaffeinated; placebo control) or caffeinated coffee (Caffeine; 4 mg caffeine/kg body mass). Participants were measured again following the ingestion of the drink (pre LBNP) and then underwent a graded LBNP protocol (−20mmHg, −30mmHg, etc.) until pre‐syncope. LBNP tolerance was quantified as cumulative stress index (CSI; mmHg*min). Data are presented at baseline (pre drink), prior to LBNP (pre LBNP and post drink), a common time point during LBNP tolerated by all individuals in all trials (−30mmHg) and at pre syncope. MAP increased from baseline to pre LBNP in all trials (Caffeine: from 84 ± 7 to 98 ± 7 mmHg; Decaffeinated: from 90 ± 10 to 94 ± 7 mmHg and Water: from 89 ± 9 to 97 ± 6 mmHg; P < 0.05 in all trials). MAP was reduced at pre syncope in all trials (Caffeine: 59 ± 4 mmHg; Decaffeinated: 57 ± 4 and Water: 60 ± 7 mmHg; all P < 0.05 relative to pre LBNP). MAP was not different between trials at any time point (P > 0.05). TPR was not different from baseline during LBNP in the Water and Decaffeinated trials (from: 13 ± 2 and 14 ± 2 to −30mmHg: 16 ± 3 and 16 ± 2 mmHg/l/min, respectively both P > 0.05 vs. baseline) but increased during LBNP in the Caffeine trial (from: 13 ± 2 to −30mmHg: 18 ± 3 mmHg/l/min; P = 0.004 vs. baseline). LBNP Tolerance was greater in the Caffeine trial (941 ± 376 mmHg*min, 19.2 ± 4.8 min) relative to the Decaffeinated trial (686 ± 382 mmHg*min, 15.7 ± 5.1 min; CSI: P = 0.021), but was not different relative to the Water trial (Water: 816 ± 383 mmHg*min, 17.5 ± 5.0 min; CSI: P = 0.093). Caffeine consumption alters cardiovascular control during a simulated hemorrhagic challenge and may influence LBNP tolerance in habitual caffeine users, although this affect appears to be small. This may have implications for the treatment of a hemorrhagic insult in individuals who are habitual caffeine users and whom have an elevated risk of hemorrhagic injury (e.g. soldiers).

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.