Acute fasting reduces tolerance to progressive central hypovolemia in humans.
fasting
food deprivation
hemorrhage
lower body negative pressure
Journal
Journal of applied physiology (Bethesda, Md. : 1985)
ISSN: 1522-1601
Titre abrégé: J Appl Physiol (1985)
Pays: United States
ID NLM: 8502536
Informations de publication
Date de publication:
21 Dec 2023
21 Dec 2023
Historique:
medline:
21
12
2023
pubmed:
21
12
2023
entrez:
21
12
2023
Statut:
aheadofprint
Résumé
Potential health benefits of an acute fast include reductions in blood pressure and increases in vagal cardiac control. These purported health benefits could put fasted humans at risk for cardiovascular collapse when exposed to central hypovolemia. The purpose of this study was to test the hypothesis that an acute 24-hour fast (vs 3-hours postprandial) would reduce tolerance to central hypovolemia induced via lower body negative pressure (LBNP). We measured blood ketones (β-OHB) to confirm a successful fast (N=18). We recorded the ECG, beat-to-beat arterial pressure, muscle sympathetic nerve activity (MSNA; N=7), middle cerebral artery blood velocity (MCAv), and forearm blood flow. Following a 5-min baseline, LBNP was increased by 15 mmHg until -60 mmHg and then increased by 10 mmHg every 5-min in a stepwise manner until onset of presyncope. Data are expressed as means ± SE. P-values ≤ 0.05 were considered statistically significant. β-OHB increased (β-OHB; 0.12±.04 fed vs. 0.47±.11, p<0.01 mmol/L fast). Tolerance to central hypovolemia was decreased by ~10% in the fasted condition measured via total duration of negative pressure (1370 89 fed vs. 1229±94 s fast, p=0.04), and was negatively associated with fasting blood ketones (R =-0.542, P = 0.02). During LBNP, heart rate and MSNA increased similarly, but in the fasted condition forearm vascular resistance was significantly reduced. Our results suggest that acute fasting reduces tolerance to central hypovolemia by blunting increases in peripheral resistance, indicating that prolonged fasting may hinder an individual's ability to compensate to a loss of blood volume.
Identifiants
pubmed: 38126086
doi: 10.1152/japplphysiol.00622.2023
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Michigan Space Grant Consortium (MSGC)
Organisme : Portage Health Foundation (PHF)
Organisme : Oregon Health and Science University Fellowship for Diversity in Research
Organisme : HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)
ID : T32HL083808