Exercise alters Cardiac Function Independent of Acute Systemic Inflammation in Healthy Men

Author(s):  
Alexandra M. Coates ◽  
Heather L. Petrick ◽  
Philip J. Millar ◽  
Jamie F. Burr

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 function 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 if 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 cross-over fashion, sixteen male participants were tested under control (CON) and inflammatory (INF) conditions, wherein INF testing occurred 8h 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 90min at ~85% of their first ventilatory threshold. IL-6 increased significantly (∆1.9±1.3pg/mL, P<0.001), while TNFα was non-significantly augmented (∆0.05±0.11pg/mL, P=0.09), 8h 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:∆3.3±4.4%, INF:∆1.7±2.7%, P=0.002) and diastolic function (e.g. E/A ratio CON:∆-0.32±0.34a.u., INF:∆-0.25±0.27a.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.

2007 ◽  
pp. 605-616
Author(s):  
Tatsushi Tokuyasu ◽  
Akito Ichiya ◽  
Tadashi Kitamura ◽  
Genichi Sakaguchi ◽  
Masashi Komeda

1988 ◽  
Vol 62 (10) ◽  
pp. 745-750 ◽  
Author(s):  
Bruno Trimarco ◽  
Nicola De Luca ◽  
Bruno Ricciardelli ◽  
Giovanni Rosiello ◽  
Massimo Volpe ◽  
...  

2007 ◽  
Vol 103 (5) ◽  
pp. 1655-1661 ◽  
Author(s):  
Takanobu Okamoto ◽  
Mitsuhiko Masuhara ◽  
Komei Ikuta

Aerobic exercise training combined with resistance training (RT) might prevent the deterioration of vascular function. However, how aerobic exercise performed before or after a bout of RT affects vascular function is unknown. The present study investigates the effect of aerobic exercise before and after RT on vascular function. Thirty-three young, healthy subjects were randomly assigned to groups that ran before RT (BRT: 4 male, 7 female), ran after RT (ART: 4 male, 7 female), or remained sedentary (SED: 3 male, 8 female). The BRT and ART groups performed RT at 80% of one repetition maximum and ran at 60% of the targeted heart rate twice each week for 8 wk. Both brachial-ankle pulse wave velocity (baPWV) and flow-mediated dilation (FMD) after combined training in the BRT group did not change from baseline. In contrast, baPWV after combined training in the ART group reduced from baseline (from 1,025 ± 43 to 910 ± 33 cm/s, P < 0.01). Moreover, brachial artery FMD after combined training in the ART group increased from baseline (from 7.3 ± 0.8 to 9.6 ± 0.8%, P < 0.01). Brachial artery diameter, mean blood velocity, and blood flow in the BRT and ART groups after combined training increased from baseline ( P < 0.05, P < 0.01, and P < 0.001, respectively). These values returned to the baseline during the detraining period. These values did not change in the SED group. These results suggest that although vascular function is not improved by aerobic exercise before RT, performing aerobic exercise thereafter can prevent the deteriorating of vascular function.


PEDIATRICS ◽  
1992 ◽  
Vol 89 (4) ◽  
pp. 722-729
Author(s):  
Ranae L. Larsen ◽  
Gerald Barber ◽  
Charles T. Heise ◽  
Charles S. August

Cardiac toxicity is a potential complication of bone marrow transplantation because recipients frequently receive cardiotoxic chemotherapy and/or irradiation before transplantation. Most studies indicate that transient cardiac toxicity occurs within weeks of transplantation, but few studies have evaluated either cardiac status before or late after transplantation. Cardiac performance was assessed via cycle ergometry in 20 children and young adults before transplantation and 31 other children and young adults after transplantation. Mean survival time in the group post-transplantation was 3.9 years with a range of 11 months to 12.1 years. Left ventricular size and shortening fraction at rest were assessed via echocardiography. Data were compared to those of 70 healthy subjects from our laboratory. Patients before and after transplantation had normal oxygen consumptions and cardiac indices at rest. During exercise, however, patients treated for cancer both before and after bone marrow transplantation had reduced exercise times, reduced maximal oxygen consumptions, and reduced ventilatory anaerobic thresholds. Cardiac reserve, as judged by the response of the cardiac output during exercise, was reduced severely. There were no significant differences between the groups tested before and after transplantation. Patients who had been treated for aplastic anemia, who had received less intensive therapy before transplantation, performed significantly better than did patients treated for cancer. Despite these findings, only four patients had abnormalities by echocardiography. In conclusion, before transplantation patients with oncologic diagnoses had serious limitations in exercise performance, most likely as a result of the effects of the cardiotoxic therapy given as part of their conventional cancer therapy. Long-term survivors of bone marrow transplantation also had similar abnormalities. Since the same patients were not studied before and after transplantation, one cannot draw definite conclusions about the effect of the transplantation itself upon cardiac function. However, exercise testing is a sensitive, noninvasive method of assessing patients at risk for cardiac dysfunction secondary to potentially cardiotoxic agents.


2004 ◽  
Vol 2004.5 (0) ◽  
pp. 69-70
Author(s):  
Tatsushi TOKUYASU ◽  
Akito ICHIYA ◽  
Tadashi KITAMURA ◽  
Genichi SAKAGUCHI ◽  
Masashi KOMEDA

2021 ◽  
Vol 8 ◽  
Author(s):  
Carolyn L. Lekavich ◽  
Jason D. Allen ◽  
Daniel R. Bensimhon ◽  
Lori A. Bateman ◽  
Cris A. Slentz ◽  
...  

Background: The goal was studying the differential effects of aerobic training (AT) vs. resistance training (RT) on cardiac and peripheral arterial capacity on cardiopulmonary (CP) and peripheral vascular (PV) function in sedentary and obese adults.Methods: In a prospective randomized controlled trial, we studied the effects of 6 months of AT vs. RT in 21 subjects. Testing included cardiac and vascular ultrasoundography and serial CP for ventricular-arterial coupling (Ees/Ea), strain-based variables, brachial artery flow-mediated dilation (BAFMD), and peak VO2 (pVO2; mL/kg/min) and peak O2-pulse (O2p; mL/beat).Results: Within the AT group (n = 11), there were significant increases in rVO2 of 4.2 mL/kg/min (SD 0.93) (p = 0.001); O2p of 1.9 mL/beat (SD 1.3) (p = 0.008) and the brachial artery post-hyperemia peak diameter 0.18 mm (SD 0.08) (p = 0.05). Within the RT group (n = 10) there was a significant increase in left ventricular end diastolic volume 7.0 mL (SD 9.8; p = 0.05) and percent flow-mediated dilation (1.8%) (SD 0.47) (p = 0.004). Comparing the AT and RT groups, post exercise, rVO2 2.97, (SD 1.22), (p = 0.03), O2p 0.01 (SD 1.3), (p = 0.01), peak hyperemic blood flow volume (1.77 mL) (SD 140.69) (p = 0.009), were higher in AT, but LVEDP 115 mL (SD 7.0) (p = 0.05) and Ees/Ea 0.68 mmHg/ml (SD 0.60) p = 0.03 were higher in RT.Discussion: The differential effects of AT and RT in this hypothesis generating study have important implications for exercise modality and clinical endpoints.


2018 ◽  
Vol 315 (5) ◽  
pp. R986-R993 ◽  
Author(s):  
Saurabh S. Thosar ◽  
Alec M. Berman ◽  
Maya X. Herzig ◽  
Sally A. Roberts ◽  
Michael R. Lasarev ◽  
...  

Adverse cardiovascular events, such as myocardial infarction and sudden cardiac death, occur more frequently in the morning. Prior studies have shown that vascular endothelial function (VEF), a marker of cardiovascular disease, is attenuated during physical inactivity and declines across the night. We sought to determine whether a morning attenuation in VEF is a result of prior sleep or the inactivity that inevitably accompanies sleep. After 1 wk of a rigorously controlled sleep-wake schedule and behaviors, 10 healthy participants completed a randomized crossover protocol in dim light and constant conditions, incorporating a night of 6 h of sleep opportunity and a night of immobility while they were supine and awake. VEF was measured in the dominant brachial artery as flow mediated dilation (FMD) before and after each 6-h trial. To avoid disturbing sleep and posture of the participants, blood was drawn using a 12-ft catheter from an adjoining laboratory room before, during, and after each 6-h trial, and plasma was analyzed for markers of oxidative stress [malondialdehyde adducts (MDA)], and endothelin-1. Contrary to expectation, both nocturnal sleep and nocturnal inactivity significantly increased FMD ( P < 0.05). There was no significant change in MDA or endothelin-1 within and between trials. Contrary to expectations based on prior studies, we found that overnight sleep or the inactivity that accompanies sleep did not result in attenuation in VEF in the morning hours in healthy people. Thus, it is plausible that the endogenous circadian system, a remaining factor not studied here, is responsible for the commonly observed decline in VEF across the night.


Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Benard O Ogola ◽  
Bruna Visniauskas ◽  
Isabella Kilanowski-doroh ◽  
Caleb M Abshire ◽  
Alec Horton ◽  
...  

Aging is a nonmodifiable risk factor for cardiovascular mortality and is associated with arterial stiffening and cardiac dysfunction. In this study, we hypothesized that aging would decrease vascular compliance and cardiac function in male mice. Tail-cuff plethysmography was used to measure blood pressure, pulse wave velocity (PWV) for arterial stiffness, echocardiography for systolic and diastolic cardiac function, and wire myography for vessel reactivity in mature adult (25 weeks) and middle-aged (57 weeks) C57Bl/6 mice. Data was analyzed by t-test or 2-way ANOVA, and P<0.05 was considered significant. While there was no difference in blood pressure, PWV was higher in middle-aged male mice (1.8 ± 0.04 m/s vs. 1.2 ± 0.05 m/s; P<0.001) and associated with increased left ventricular (LV) posterior wall thickness (1.4 ± 0.07 mm vs. 1.1 ± 0.13 mm; P=0.03), and LV mass (172 ± 8 mg vs. 158 ± 20 mg; P=0.04). The ratio of early to late filling velocities, a measure of diastolic function, was lower in middle-age (1.6 ± 0.07 vs. 2.7 ± 0.37; P<0.001). Carotid artery histological analysis indicated that middle-aged mice had a greater collagen-to-elastin ratio along with decreased amounts of smooth muscle and thin collagen (P<0.05). Mesenteric artery contraction to PGF2α (446 ± 15% vs. 378 ± 14%; P=0.02) as well as relaxation to sodium nitroprusside (55 ± 7% vs. 31 ± 7%; P<0.01) were both blunted in the middle-aged group. The current study demonstrates that aging in male mice increases arterial stiffening and LV remodeling while decreasing diastolic and vascular function, independent of increased blood pressure. Future studies will investigate whether strategies that counteract arterial stiffness in the absence of changes in blood pressure can protect from cardiovascular aging.


Obesities ◽  
2021 ◽  
Vol 1 (1) ◽  
pp. 58-71
Author(s):  
Bryant H. Keirns ◽  
Samantha M. Hart ◽  
Christina M. Sciarrillo ◽  
Kara L. Poindexter ◽  
Stephen L. Clarke ◽  
...  

The cardiovascular disease (CVD) risk of metabolically healthy obesity (MHO) remains controversial. We sought to further characterize the CVD risk profile in MHO by evaluating postprandial triglycerides, vascular function, and systemic inflammatory markers. Control individuals that were normal-weight and metabolically healthy (Con), MHO, and metabolic syndrome (MetS) were recruited (n = 10–11/group). Each participant underwent an abbreviated fat tolerance test, fasting and postprandial flow-mediated dilation (FMD), and had a panel of inflammatory cytokines measured. MHO displayed postprandial triglycerides similar to those in Con and both MHO and Con had lower values than those for MetS (p < 0.01). Fasting FMD was lower in MHO and MetS compared to that of Con (p < 0.01), but during the postprandial period the vasodilatory response of MHO was similar to that while fasting (p = 0.39), while FMD in Con and MetS decreased after the high-fat meal (p values < 0.01). MHO displayed a number of inflammatory cytokines greater than those of Con and MetS (all p values < 0.05), while MetS and MHO had higher TNF-α than did Con (p < 0.05). In conclusion, MHO was associated with lower fasting FMD and a greater inflammatory burden but did not suffer the same negative postprandial effects as did MetS.


2002 ◽  
Vol 25 (11) ◽  
pp. 1074-1081 ◽  
Author(s):  
D. Modersohn ◽  
S. Eddicks ◽  
I. Ast ◽  
S. Holinski ◽  
W. Konertz

The mechanism of an indirect revascularization in ischemic myocardium by transmyocardial laser revascularization (TMLR) is not yet fully understood. An improvement of clinical symptoms caused by TMLR is reported in many clinical trials with patients in which a direct revascularization is not possible. An increase of myocardial perfusion through laser channels is doubtful, because the myocardial pressure in the wall is higher than in the cavum. Therefore we measured the local cardiac function (intramyocardial pressure, wall thickness, pressure-length curves) and acute metabolic changes (tissue lactate content, tissue pO2) in ischemic and non-ischemic regions before and after TMLR in isolated hemoperfused pig hearts. An isolated heart was chosen because it enabled us to separate coronary flow from flow through ventricular channels. The ischemia was induced by coronary occlusion or microembolization (eight hearts each). It should be noted that microembolization leads to conditions which are more comparable with those found in patients selected for TMLR. In the isolated working heart, the coronary perfusion can be controlled independently from perfusion through the ventricular cavum. Under the ischemic conditions mentioned above, we observed that the intramyocardial pressure in the ischemic region decreased below the left ventricular pressure, so one premise for indirect perfusion was met. TMLR after microembolization led to a significant improvement of regional cardiac work and the tissue oxygen pressure. These acute effects demonstrate the possibility of functional and metabolic amelioration by TMLR after ischemia induced by microembolization in an isolated hemoperfused pig heart.


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