Medicine and science in sports and exercise · 2026
Caffeine Increases Core Temperature without Altering Markers of Kidney or Gut Injury after Physical Work in the Heat in Caffeine-Habituated Adults.
СтатьяРандомизированное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Specht Jonathan W, Ramirez Marissa R, Quintana Amber, Bailly Alyssa R, Peña Ariel, Schmidt Ethan, DE Castro Magalhães Flávio, McKenna Zachary J, Schlader Zachary J, Amorim Fabiano T
Аннотация
METHODS: Using a double-blind, crossover design, 14 (6 male) active, caffeine-habituated adults ingested 5 mg/kg of bodyweight (up to 400 mg) of caffeine or placebo 30 min before a 2-h heat trial (35°C dry bulb, 50% relative humidity) involving walking (40% peak) and box-lifting. Bodyweight was measured pre- and post-trial. Core temperature (Tcore) and heart rate (HR) were recorded every 10 min. Blood and urine samples were collected pre-, post-, and 1-h post-trial to assess markers of AKI, intestinal injury, and endotoxemia.
RESULTS: Caffeine increased peak Tcore (38.2 ± 0.4 vs 38.0 ± 0.3°C; P = 0.02), peak HR (147 ± 18 vs 138 ± 17 bpm; P = 0.02), and bodyweight loss (1.7% ± 1.0% vs 1.5% ± 1.1%, P = 0.04) compared with placebo. There were no differences in markers of AKI (urinary insulin-like growth factor-binding protein 7• tissue inhibitor of metalloproteinase 2, neutrophil gelatinase-associated lipocalin) ( P > 0.05). Serum cystatin C increased from pre- to post-trial in the caffeine (∆0.24 ± 0.43 mg/L, P = 0.03) but not placebo (∆-0.07 ± 0.17 mg/L, P = 0.81) condition, suggesting a reduction in glomerular filtration. There were no differences in markers of intestinal injury (intestinal fatty acid binding protein) or endotoxemia (lipopolysaccharide-binding protein, soluble cluster of differentiation 14) ( P > 0.05).
CONCLUSIONS: Caffeine ingestion before work in the heat exacerbated increases in Tcore but did not affect biomarkers of kidney or intestinal injury. Workers performing labor in hot environmental conditions should consider that caffeine during work in the heat may increase the rate of Tcore rise.
RESULTS: Caffeine increased peak Tcore (38.2 ± 0.4 vs 38.0 ± 0.3°C; P = 0.02), peak HR (147 ± 18 vs 138 ± 17 bpm; P = 0.02), and bodyweight loss (1.7% ± 1.0% vs 1.5% ± 1.1%, P = 0.04) compared with placebo. There were no differences in markers of AKI (urinary insulin-like growth factor-binding protein 7• tissue inhibitor of metalloproteinase 2, neutrophil gelatinase-associated lipocalin) ( P > 0.05). Serum cystatin C increased from pre- to post-trial in the caffeine (∆0.24 ± 0.43 mg/L, P = 0.03) but not placebo (∆-0.07 ± 0.17 mg/L, P = 0.81) condition, suggesting a reduction in glomerular filtration. There were no differences in markers of intestinal injury (intestinal fatty acid binding protein) or endotoxemia (lipopolysaccharide-binding protein, soluble cluster of differentiation 14) ( P > 0.05).
CONCLUSIONS: Caffeine ingestion before work in the heat exacerbated increases in Tcore but did not affect biomarkers of kidney or intestinal injury. Workers performing labor in hot environmental conditions should consider that caffeine during work in the heat may increase the rate of Tcore rise.