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
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

Auteurs

Joshua E Gonzalez (JE)

Oregon Institute of Occupational Health Sciences, Oregon Health and Science University Hospital (Portland, Oregon, United States), Portland, OR, United States.

William H Cooke (WH)

Kinesiology and Integrative Physiology, Michigan Technological University, Houghton, MI, United States.

Classifications MeSH