Forskning
October 26, 2020
Caffeine ingestion alters central hemodynamics following aerobic exercise in middle-aged men
M P Harber et al, 2020. Caffeine ingestion alters central hemodynamics following aerobic exercise in middle-aged men, European Journal of Applied Physiology, published online.
ABSTRACT:
Purpose: To examine the acute influence of caffeine on post-exercise central blood pressures, arterial stiffness, and wave reflection properties.
Methods: In a double-blind randomized placebo-controlled crossover study design, ten middle-aged males (55 ± 5 year) completed two exercise trials after ingestion of caffeine (400 mg) or placebo. Measurements were taken before and 30 min post-ingestion via cuff-based pulse wave analysis (PWA) and carotid-femoral pulse wave velocity (PWV). Participants performed a 40-min cycling bout at 70% HRmax with matched workloads between trials. PWA and PWV were reassessed 30 min post-exercise.
Results: Prior to exercise, compared to placebo, caffeine increased brachial systolic blood pressure (bSBP) (+ 12.3 ± 2.4 mmHg; p = 0.004), brachial diastolic blood pressure (bDBP) (+ 7.7 ± 0.9 mmHg; p = 0.011), central systolic blood pressure (cSBP) (+ 11.1 ± 2.1 mmHg; p = 0.005) and central diastolic blood pressure (cDBP) (+ 7.6 ± 1.0 mmHg; p = 0.012). PWV was higher 30 min after pill ingestion (p = 0.021 for time) with a trend for a greater increase in caffeine (p = 0.074 for interaction). bSBP (p = 0.036) and cSBP (p = 0.007) were lower after exercise but remained higher (both p < 0.001) in caffeine compared to placebo. PWV remained higher (p = 0.023) after exercise in caffeine compared to placebo but was not influenced by exercise. At rest, augmentation pressure (AP) and index (AIx) were not influenced by caffeine ingestion. Conversely, AIx was lower (p = 0.009) after exercise in placebo only.
Conclusion: In healthy and active middle-aged men, pre-exercise caffeine ingestion led to higher central and peripheral systolic blood pressures, PWV and AIx at 30 min post-exercise, indicating an increased left ventricular workload which may have implications for cardiovascular event risk.
