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Background: To examine the effects of varying doses of caffeine on autonomic reactivation following anaerobic exercise., Methods: Recreationally active males (N = 20; 24 ± 2y) participated in a randomized, double-blind, placebo-controlled, crossover study where participants ingested: [1] Control (CON; no supplement), [2] a non-caffeinated placebo (PLA), [3] 3-mg∙kg - 1 of caffeine (CAF3) or [4] 6-mg∙kg - 1 of caffeine (CAF6) prior to Wingate testing. Parasympathetic (lnRMSSD, primary outcome) and global HRV (lnSDNN, secondary outcome) were assessed at rest (i.e., pre-ingestion), 45-min post-ingestion, and 5-min and 35-min post-exercise recovery. We used a GLM to assess mean (95% CI) changes from pre-ingestion baseline., Results: Overall, we observed a significant trend for lnRMSSD and lnSDNN (both, p = 0.001, ηp 2  = 0.745). Forty-five minutes after treatment ingestion, we observed a significant increase in lnRMSSD for CAF3 (0.15 ms, 95%CI, 0.07,0.24) and CAF6 (0.16 ms, 95%CI, 0.06,0.25), both being significant (both, p <  0.004) vs. CON (- 0.02 ms, 95%CI, - 0.09,0.04). Five-minutes after exercise, all treatments demonstrated significant declines in lnRMSSD vs. baseline (all, p <  0.001). After 35-min of recovery, lnRMSSD returned to a level not significantly different than baseline for CAF3 (0.03 ms, 95%CI, - 0.05, 0.12) and CAF6 (- 0.03 ms, 95%CI, - 0.17, 0.10), while PLA (- 0.16 ms, 95%CI, - 0.25, - 0.06) and CON (- 0.17 ms, 95%CI, - 0.28, - 0.07) treatments remained significantly depressed. A similar pattern was also observed for SDNN., Conclusion: Caffeine ingestion increases resting cardiac autonomic modulation and accelerates post-exercise autonomic recovery after a bout of anaerobic exercise in recreationally active young men. However, no differences between caffeine doses on cardiac autonomic reactivity were observed.

The sympathicotonic effect of caffeine is strongly evidenced in the literature. However, the effects of caffeine or caffeine expectancy on the cardiac parasympathetic modulation remain obscure. Thus, the aim of this study was to investigate the effects of caffeine consumption and expectancy of caffeine consumption on the cardiac parasympathetic modulation under different stress conditions. Twenty-one physically active men (22.3 ± 2.9 years, 25.2 ± 2.7 kg/m 2 ) consumed ∼3 mg/kg of caffeine received as caffeine, caffeine as placebo, placebo as placebo and placebo as caffeine. Parasympathetic modulation was assessed by heart rate variability (HRV-Poincaré SD1 index) at supine and orthostatic positions, during a submaximal exercise (HRV threshold-HRV T ) and during each 60 seconds (s) within 300 s of post-exercise active recovery. A factorial ANOVA for repeated measures (p < 0.05) was used to assess the effect of caffeine, expectancy and resting time after caffeine intake on the HRV. No significant effect of caffeine or expectancy was observed on the SD1 value at supine or standing positions (p = 0.47-0.53; p = 0.57-0.31, respectively), despite an increase in this variable after resting periods in both positions (p < 0.001). During exercise, caffeine and expectancy do not alter the HRV T (p = 0.51-0.39). However, higher SD1 values were observed after caffeine administration from 60 to 300 s post-exercise recovery (p = 0.01-0.05) but not for the effects of expectancy (p = 0.19-0.94). We concluded that low doses of caffeine or expectancy do not alter the resting cardiac parasympathetic modulation or HRV T . However, caffeine, but not expectancy, increases parasympathetic reactivation after a submaximal exercise test in young men.