Liverpool Hope University

Low energy availability (LEA) signifies a condition where the body lacks sufficient energy to support essential physiological functions crucial for maintaining optimal health (1). This energy insufficiency can be exacerbated by the demands of sports and exercise, resulting in negative impacts on various physiological, psychological, and sports performance (11, 8, 2). While LEA is commonly associated with cardiovascular abnormalities, such as early atherosclerosis, endothelial dysfunction, and lower blood pressure, the existing body of research faces limitations, including small sample sizes and primarily exploratory approaches (2). Additionally, despite a growing body of evidence suggesting a strong link between DNA methylation (an epigenetic modification influencing gene expression by tagging specific parts of the DNA code) and cardiovascular disease (9, 6), there has been no prior investigation exploring the interplay between DNA methylation, cardiovascular disease, and LEA. To better understand LEA and its effects on cardiovascular health, it is imperative to address these limitations through further research. Utilising more comprehensive markers of cardiovascular disease and expanding the scope of investigations will contribute to a great understanding of LEA and its implications on cardiovascular health (10).

In the United Kingdom, heart failure (HF) affects about 900,000 people with 60,000 new cases annually. Up to 60% of people living with HF also experience sarcopenia, known as loss of muscle mass and strength. Sarcopenia contributes significantly to low physical capacity and exercise intolerance and worsens the prognosis of the disease and quality of life.
In comparison to primary sarcopenia (age-related sarcopenia), secondary sarcopenia occurs if other factors, including malignancy or organ failure, are evident in addition to aging. Secondary sarcopenia is highly common in patients with heart failure (Sarc-HF) (prevalence is 35%-69%), and has a significantly negative impact on exercise capacity, weight-adjusted peak maximal oxygen consumption, left ventricular function, and re-hospitalization rates and mortality.
In this integrated study of NHS patients with HF, the investigators aim is to identify the underlying mechanisms of muscle weakness in HF utilizing including body composition, circulating metabolites (metabolic profile), and functional tests for (1) early detection of otherwise subclinical HF, (2) diagnostic assessment of clinically manifest HF-sarcopenia, (3) the risk stratification of subjects with a suspected or confirmed diagnosis, and (4) selection of an appropriate therapeutic intervention.