Caffeine

This review of peer‑reviewed literature (1975–2021) analyzes caffeine’s mechanisms of action in animal models. By blocking adenosine receptors, caffeine causes tachycardia with potential arrhythmogenic risk via unopposed β1 stimulation. In lung tissue, caffeine inhibits hyperoxia‑induced inflammation, decreasing pro‑inflammatory cytokine expression and preventing functional and structural changes. Beyond its well‑known central nervous system effects, caffeine provides tissue protection, particularly anti‑inflammatory actions in the lung.

Fig. 1 Effects of caffeine on pneumocytes. (Villanueva-García D, et al., 2021)

In 32 young males, the acute effects of caffeine (vs. placebo) on autonomic control and cardiorespiratory parameters were assessed after 30 minutes of treadmill exercise at 60% VO₂peak, followed by 60 minutes of recovery. Caffeine significantly delayed the recovery of RMSSD and SD1 (time‑domain parasympathetic indices) compared to placebo. Systolic blood pressure differences persisted longer with caffeine, and diastolic blood pressure was affected only in the caffeine protocol. However, caffeine did not influence respiratory rate, oxygen saturation, or frequency‑domain heart rate variability indices. The authors conclude that caffeine delays parasympathetic recovery but has limited overall impact on post‑exercise autonomic regulation.

Fig. 2 Flowchart sample loss during the study. (Gonzaga LA, et al., 2017)