Exercise and postprandial lipemia: effects on vascular health in inactive adults
Metadatos
Mostrar el registro completo del ítemAutor
Ramírez-Vélez, Robinson; Correa Rodríguez, María; Tordecilla-Sanders, Alejandra; Aya-Aldana, Viviana; Izquierdo, Mikel; Correa-Bautista, Jorge Enrique; Álvarez, Cristian; Garcia Hermoso, AntonioEditorial
BioMed Central
Materia
Postprandial lipemia Endothelial function Exercise intensity High-intensity exercise Moderate continuous training
Fecha
2018-04-03Referencia bibliográfica
Ramírez-Vélez et al. Exercise and postprandial lipemia: effects on vascular health in inactive adults. Lipids in Health and Disease (2018) 17:69 [http://hdl.handle.net/10481/52237]
Patrocinador
This study as funded in part by the Center for Studies on Measurement of Physical Activity, School of Medicine and Health Sciences, Universidad del Rosario (Code N° FIUR DN-BG001). We declare that the results of the study are presented clearly, honestly, and without fabrication, falsification, or appropriate data manipulationResumen
Background: There is evidence to suggest that postprandial lipemia are is linked to the impairment of endothelial
function, which is characterized by an imbalance between the actions of vasodilators and vasoconstrictors. The aim
of this study was to determine the effects of a 12-week high-intensity training (HIT) and moderate continuous
training (MCT) protocol on postprandial lipemia, vascular function and arterial stiffness in inactive adults after
high-fat meal (HFM) ingestion.
Methods: A randomized clinical trial was conducted in 20 healthy, inactive adults (31.6 ± 7.1 years). Participants followed
the two exercise protocols for 12 weeks. To induce a state of postprandial lipemia (PPL), all subjects received a HFM.
Endothelial function was measured using flow-mediated vasodilation (FMD), normalized brachial artery FMD (nFMD),
aortic pulse wave velocity (PWV) and augmentation index (AIx). Plasma total cholesterol, high-density lipoprotein
cholesterol (HDL-c), triglycerides and glucose were also measured.
Results: The effects of a HFM were evaluated in a fasted state and 60, 120, 180, and 240 min postprandially. A significant
decrease in serum glucose between 0 min (fasted state) and 120 min postprandially was found in the HIT group (P= 0.
035). Likewise, FMD (%) was significantly different between the fasted state and 60 min after a HFM in the HIT group
(P = 0.042). The total cholesterol response expressed as area under curve (AUC)(0–240) was lower following HIT than
following MCT, but no significant differences were observed (8%, P > 0.05). Similarly, triglycerides AUC(0–240) was also
lower after HIT compared with MCT, which trended towards significance (24%, P= 0.076). The AUC(0–240) for the glucose
response was significantly lower following HIT than MCT (10%, P = 0.008). FMD and nFMD AUC(0–240) were significantly
higher following HIT than following MCT (46.9%, P = 0.021 and 67.3%, P = 0.009, respectively). PWV AUC(0–240) did not
differ following between the two exercise groups (2.3%, P > 0.05).
Conclusions: Supervised exercise training mitigates endothelial dysfunction and glucose response induced by PPL.
Exercise intensity plays an important role in these protective effects, and medium-term HIT may be more effective than
MCT in reducing postprandial glucose levels and attenuating vascular impairment.