Exercise alters cardiac function independent of acute systemic inflammation in healthy men

• Published in: American journal of physiology. Heart and circulatory physiology Vol. 320; no. 5; pp. H1762 - H1773
• Main Authors: Coates, Alexandra M., Petrick, Heather L., Millar, Philip J., Burr, Jamie F.
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.05.2021
• Subjects: Adaptation, Physiological; Adult; Aorta; Bicycling; Cardiac function; Cardiovascular System - diagnostic imaging; Cardiovascular System - metabolism; Cardiovascular System - physiopathology; Carotid-Femoral Pulse Wave Velocity; Cross-Over Studies; Cycles; Cytokines; Cytokines - blood; Echocardiography; Echocardiography, Stress; Exercise; Exercise Test; Femur; Healthy Volunteers; Heart; Humans; Inflammation; Inflammation - blood; Inflammation - diagnostic imaging; Inflammation - physiopathology; Inflammation Mediators - blood; Influenza; Influenza Vaccines - administration & dosage; Interleukin 6; Male; Random Allocation; Sex Factors; Stiffness; Stroke; Stroke volume; Time Factors; Tumor necrosis factor-α; Vaccination; Vaccines; Vascular Stiffness; Ventricle; Ventricular Function, Left; Wave velocity; Young Adult; arterial stiffness; influenza vaccine; flow-mediated dilation; echocardiography; exercise-induced cardiac fatigue
• ISSN: 0363-6135; 1522-1539; 1522-1539
• DOI: 10.1152/ajpheart.00809.2020

This experimental investigation sought to determine the role of inflammation on the occurrence of cardiovascular alterations following exercise. Despite successfully stimulating systemic inflammation via vaccination, vascular and cardiac functions were largely unaltered. Prolonged exercise itself reduced cardiac function assessed via echocardiography performed during light exercise stress. This demonstrates a potential advantage to using stress-echocardiography for measuring exercise-induced cardiac fatigue, as typical resting measures following similar exercise exposures commonly suggest no effect. Acute elevations in inflammatory cytokines have been demonstrated to increase aortic and left ventricular stiffness and reduce endothelial function in healthy subjects. As vascular and cardiac functions are often transiently reduced following prolonged exercise, it is possible that cytokines released during exercise may contribute to these alterations. The a priori aims of this study were to determine whether vaccine-induced increases in inflammatory cytokines would reduce vascular and left ventricular function, whether vascular alterations would drive cardiac impairments, and whether this would be potentiated by moderate exercise. In a randomized crossover fashion, 16 male participants were tested under control (CON) and inflammatory (INF) conditions, wherein INF testing occurred 8 h following administration of an influenza vaccine. On both days, participants underwent measures of echocardiography performed during light cycling (stress-echocardiography), carotid-femoral pulse wave velocity (cf-PWV), and superficial femoral flow-mediated dilation (FMD) before and after cycling for 90 min at ∼85% of their first ventilatory threshold. IL-6 increased significantly (Δ1.9 ± 1.3 pg/mL, P < 0.001), whereas TNFα was nonsignificantly augmented (Δ0.05 ± 0.11 pg/mL, P = 0.09), 8 h following vaccination. Vascular function was unaltered following cycling or inflammation (all P > 0.05). The use of echocardiography during light cycling revealed cardiac alterations traditionally expected to occur only with greater exercise loads, with reduced systolic (e.g., longitudinal strain CON: Δ3.3 ± 4.4%, INF: Δ1.7 ± 2.7%, P = 0.002) and diastolic function (e.g., E/ A ratio CON: Δ−0.32 ± 0.34 a.u., INF:Δ−0.25 ± 0.27 a.u., P = 0.002) following cycling, independent of inflammation. The vaccine reduced stroke volume (SV) (main effect of condition P = 0.009) before-and-after cycling. These findings indicate that reduced cardiac function following exercise occurs largely independent of additional inflammatory load. NEW & NOTEWORTHY This experimental investigation sought to determine the role of inflammation on the occurrence of cardiovascular alterations following exercise. Despite successfully stimulating systemic inflammation via vaccination, vascular and cardiac functions were largely unaltered. Prolonged exercise itself reduced cardiac function assessed via echocardiography performed during light exercise stress. This demonstrates a potential advantage to using stress-echocardiography for measuring exercise-induced cardiac fatigue, as typical resting measures following similar exercise exposures commonly suggest no effect.