Combined endurance/resistance training reduces NT-proBNP levels in patients with chronic heart failure

Conraads, Viviane M.; Beckers, Paul; Vaes, Johan; Martin, M. De; Hoof, Viviane Van; Maeyer, Cathérine De; Possemiers, Nadine; Wuyts, Floris L.; Vrints, Christiaan J.

doi:10.1016/j.ehj.2004.07.022

Cited by 110 publications

(95 citation statements)

References 36 publications

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“…Moderate-intensity endurance exercise training has been shown to improve left ventricular function in individuals with non-BTHS heart failure as well as improve levels of plasma markers known to be associated with the severity of cardiac impairment (e.g., TNF-a and pro-BNP) (Adamopoulos et al 2002;Conraads et al 2004;Chen et al 2012). However, in the current study we did not observe improvements in resting nor exercise-stimulated left ventricular function, plasma pro-BNP, or plasma TNF-a following endurance exercise training in four participants with BTHS.…”

Section: Discussionmentioning

confidence: 99%

“…This is important because peak oxygen consumption (i.e., exercise tolerance) is the single best predictor of cardiovascular and all-cause mortality in individuals with cardiovascular disease (Myers et al 2002). In individuals with non-BTHS heart failure, endurance (aerobic) exercise training increases peak whole-body oxygen consumption, left ventricular function, skeletal muscle blood flow and oxidative function, plasma lactate concentration during exercise, and improves serum markers associated with the severity of the cardiac impairment (e.g., tumor-necrosis factor-a (TNF-a) and probrain natriuretic peptide(pro-BNP)) (Sullivan et al 1988;Minotti et al 1990;Coats et al 1992;Hambrecht et al 1997Hambrecht et al , 1998Adamopoulos et al 2002;Delagardelle et al 2002;Giannuzzi et al 2003;Conraads et al 2004;Bartlo 2007). Most importantly, endurance exercise training in patients with non-BTHS heart failure was safe, improved survival (Belardinelli et al 1999), decreased hospitalization (Belardinelli et al 1999), and increased quality of life (Coats et al 1992;Tyni-Lenne et al 1996;Belardinelli et al 1999).…”

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Endurance Exercise Training in Young Adults with Barth Syndrome: A Pilot Study

et al. 2016

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Background: Barth syndrome (BTHS) is a rare X-linked disorder that is characterized by mitochondrial abnormalities, cardio-skeletal myopathy, exercise intolerance, and premature mortality. The effect on endurance exercise training on exercise tolerance, cardio-skeletal function, and quality of life in BTHS is unknown.Methods: Four young adults (23 AE 5 years, n ¼ 4) with BTHS participated in a 12-week, supervised, individualized endurance exercise training program. Exercise training was performed on a cycle ergometer for 30-45 0 three times per week at a moderate intensity level.Exercise tolerance was measured by graded exercise testing and peak oxygen consumption, heart function via two-dimensional and M-mode echocardiography, skeletal muscle function by near-infrared spectroscopy, and quality of life through the Minnesota Living with Heart Failure questionnaire.Results: There were no adverse events during exercise testing or training for any participant. Peak oxygen consumption modestly (~5%) improved in three or four participants. Mean quality of life questions regarding dyspnea and side effects from medications significantly improved following exercise training. Mean resting heart function or skeletal muscle oxygen extraction during exercise did not improve after exercise training.Conclusion: Endurance exercise training is safe and appears to modestly improve peak exercise tolerance and certain measures of quality of life in young adults with BTHS. However, compared to improvements resulting from endurance exercise training seen in other non-BTHS mitochondrial myopathies and heart failure, these improvements appear blunted. Further research into the most beneficial mode, intensity and frequency of exercise training in BTHS is warranted.Barth syndrome (BTHS) is an X-linked disorder that results in cardio-skeletal myopathy, heart failure, fatigue, chronic/ cyclic neutropenia, growth delay, and premature mortality (Barth et al. 1983). The full scope of the pathological and clinical manifestations of BTHS is not fully understood, but involves a tafazzin gene defect that results in cardiolipin deficiency and severe mitochondrial dysfunction. BTHSassociated mitochondrial dysfunction is assumed to mediate the cardio-skeletal myopathy seen in the majority of those with BTHS (Spencer et al. 2006).

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confidence: 99%

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Endurance Exercise Training in Young Adults with Barth Syndrome: A Pilot Study

et al. 2016

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“…The pleiotropic stimulus of ET leaves room for mechanistic considerations regarding the beneficial effect of ET in HFpEF, including anti‐inflammation10 and reduced neuro‐hormonal activation 11. Hormonal alterations may play a pivotal role in mediating this process.…”

Section: Introductionmentioning

confidence: 99%

Ghrelin and hormonal markers under exercise training in patients with heart failure with preserved ejection fraction: results from the Ex‐DHF pilot study

et al. 2016

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BackgroundOver 50% of patients with symptomatic heart failure (HF) experience HF with preserved ejection fraction (HFpEF). Exercise training (ET) is effective in improving cardiorespiratory fitness and dimensions of quality of life in patients with HFpEF. A systemic pro‐inflammatory state induced by comorbidities as the cause of myocardial structural and functional alterations has been proposed in HFpEF. ET modifies myocardial structure and has been related to inflammatory state. We investigated Ghrelin, related adipokines, markers of inflammation, and neuro‐hormonal activation in patients undergoing a structured ET vs. usual care are with HFpEF. Methods and resultsEx‐DHF‐P was a prospective, controlled, randomized multi‐centre trial on structured and supervised ET in patients with HFpEF. We performed a post hoc analysis in 62 patients from Ex‐DHF‐P. Ghrelin, adiponectin, leptin, IL‐1ß, IL‐6, IL‐10, tumour necrosis factor‐alpha, MR‐proANP, MR‐proADM, CT‐proET1, and CT‐proAVP were assessed to seize the impact of ET on these markers in patients with HFpEF. Thirty‐six (58%) patients were female, mean age was 64 years, and median ghrelin was 928 pg/mL (interquartile range 755–1156). When stratified for high versus low ghrelin, groups significantly differed at baseline in presence obesity, waist circumference, and adiponectin levels (P < 0.05, respectively). Overall, ghrelin levels rose significantly to 1013 pg/mL (interquartile range 813–1182) (P < 0.001). Analysis of covariance modelling for change in ghrelin identified ET (P = 0.013) and higher baseline adiponectin levels (P = 0.035) as influencing factors.ConclusionsExercise training tended to increase ghrelin levels in Ex‐DHF‐P. This increase was especially pronounced in patients with higher baseline adiponectin levels. Future trials are needed to investigate the effect of ET on endogenous ghrelin levels in regard to interactions with cardiac structure and clinically meaningful surrogate parameters.

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“…Rodrigues et al [21], Park et al [18] reported no significantly change in the end diastolic diameter and end systolic diameter after aerobic exercise. Conraads et al [2] showed a decrease in left ventricular end-systolic diameter in the trained heart failure group. Aerobic activities bring about a volume overload which increases the initial diastolic filling at rest and exercise.…”

Section: Discussionmentioning

confidence: 99%

The effect of aerobic continuous training and detraining on left ventricular structure and function in male students

Mahdiabadi

Toba

2017

PES

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Purpose:Regular exercise training induces cardiac physiological hypertrophy. The aim of this study was to determine the effect of aerobic continuous training and a detraining period on left ventricular structure and function in non-athlete healthy men. Material:Ten untrained healthy male students (aged 18-22 years) were volunteered and participated in countryside continuous jogging programme (3days/week, at 70% of Maximum Heart Rate for 45 min, 8-weeks) and four weeks detraining afterwards. M-mode, 2-dimensional, colour and Doppler transthoracic echocardiography were performed, during resting conditions, before and after the training and after detraining period. Results:Using t-test, we found significant difference in end systolic diameter and the posterior wall thickness, percentage shortening and ejection fraction after eight weeks training compared to before training. It was found no significant difference in end diastolic diameter, interventricular septum thickness, left atrium diameter, aortic root diameter, heart rate, systolic and diastolic blood pressures. Following four weeks detraining after training, compared with eight weeks of training was a significant difference in end diastolic diameter, percentage shortening and ejection fraction and no significant difference in end systolic diameter, posterior wall thickness, interventricular septum thickness, left atrium diameter, aortic root diameter, heart rate, systolic and diastolic blood pressures. Conclusions:In general, eight-week aerobic continuous training and a detraining period can affect left ventricular structure and function.

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Combined endurance/resistance training reduces NT-proBNP levels in patients with chronic heart failure

Cited by 110 publications

References 36 publications

Endurance Exercise Training in Young Adults with Barth Syndrome: A Pilot Study

Endurance Exercise Training in Young Adults with Barth Syndrome: A Pilot Study

Ghrelin and hormonal markers under exercise training in patients with heart failure with preserved ejection fraction: results from the Ex‐DHF pilot study

The effect of aerobic continuous training and detraining on left ventricular structure and function in male students

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