Exercise Intolerance in Patients With Heart Failure

Lifestyle Interventions with a Focus on Nutritional Strategies to Increase Cardiorespiratory Fitness in Chronic Obstructive Pulmonary Disease, Heart Failure, Obesity, Sarcopenia, and Frailty

“…However, the changes in peak VO2 were significantly different between the L-carnosine group (+ 1.1 mL/kg/min) compared to the control, which, in fact, experienced a trend toward a reduction in peak VO2 (−1.4 mL/kg/min). Similarly, the changes of VO2 at the anaerobic threshold, a measure of submaximal effort [2] and peak ET workload on cycle ergometer CPET, favored the L-carnosine-supplemented group versus control (Figure 1) [81]. Of note, no significant changes in echocardiographic parameters occurred [81].…”

“…The clinical syndrome of HF is characterized by reduced CRF accompanied by dyspnea and fatigue [2]. Low CRF is a significant risk for HF, and improvements in peak VO 2 through ET are associated with decreases in CVD and all-cause mortality, as well as HF hospitalizations [100,101].…”

“…Low CRF is a significant risk for HF, and improvements in peak VO 2 through ET are associated with decreases in CVD and all-cause mortality, as well as HF hospitalizations [100,101]. A reduction in cardiac output is a major contributor to reduced CRF in HF patients, but individuals with HF also suffer malfunction throughout the oxygen transport chain in the form of pulmonary and SM abnormalities, as well as other exercise-limiting comorbidities such as obesity and anemia [2]. There are two major types of HF-HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF).…”

“…Cardiorespiratory fitness (CRF), often expressed as maximal oxygen consumption (VO 2 max) in healthy individuals or peak VO 2 in those with limitations to exercise, reflects the maximal amount of oxygen that can be taken up, perfused and transported in the blood, absorbed, and utilized during strenuous exercise [1]. The gold standard of VO 2 measurement is cardiopulmonary exercise testing (CPET), as it allows for the evaluation of the cardiovascular (CV), respiratory, and muscular responses to maximal exercise encompassed under the term CRF [2]. Recently, CRF has been proposed as a vital sign due to its strong inverse association with all-cause and CV disease (CVD) mortality, which is stronger than many traditional risk factors such as type 2 diabetes mellitus (T2DM) and smoking [1,3], and independent of sex and race [4].…”

Increased C-reactive protein is associated with the severity of thoracic radiotherapy-induced cardiomyopathy

“…When a nested case-control matched analysis was performed, the mean heart dose was higher in HF cases (3.3 ± 2.7 Gy) than controls (2.1 ± 2.0 Gy; P = 0.004), and the odds ratio (95% confidence interval) for HF per logchange in mean cardiac radiation dose was 9.1 (3.4-24.4), thus highlighting that even relatively small doses of radiotherapy to the heart have the potential to cause HF [9]. Moreover, exercise intolerance, a surrogate of impaired cardiac reserve and a strong predictor of allcause and cancer-related mortality [10,11], seems to appear early after radiotherapy and may contribute significantly to impairments in quality of life [12][13][14][15].…”