Heart failure (HF) is a heterogeneous syndrome in which the heart is unable to handle a human’s metabolic needs due to its structural and/or functional abnormalities. The prevalence is 1–2% in the Western world [1], and it is accelerating due to the demographic trend of an aging population and an increase in risk factors [2]. Patients with HF are classified according to the left ventricular ejection fraction (LVEF) into HF with preserved (HFpEF: LVEF ≥ 50%), mildly reduced (HFmrEF: 41% < LVEF ≤ 49%), and reduced (HFrEF: LVEF ≤ 40%) ejection fraction [2], and they face various symptoms regardless of the disease severity. The limited exercise capacity [3], dyspnea, and poor quality of life (QoL) [4] are the most common expressions of the disease. Moreover, muscle weakness in both peripheral [5] and inspiratory muscles [6] is present in patients with HF regardless of LVEF magnitude. Inspiratory muscle weakness (IMW) is diagnosed when maximal inspiratory pressure (MIP) is reduced by less than 70% of predicted values [7]. Additionally, patients with HF demonstrated significantly reduced endurance capacity compared to healthy control subjects, indicating impaired respiratory muscle endurance in this population [8].

The skeletal muscle hypothesis, originally proposed by Coats et al. [9], describes the vicious cycle that contributes to the progression of HF and the generation of its characteristic symptoms. It emphasizes that HF is not solely a consequence of central cardiac dysfunction but also involves important peripheral abnormalities, particularly affecting skeletal and respiratory muscles. Although left ventricular dysfunction is a defining feature of the disease, it initiates a cascade of systemic effects. This dysfunction promotes a catabolic state, leading to structural and metabolic abnormalities in skeletal and respiratory muscles. Muscle alterations during physical exertion heighten ergoreflex activity, which sends signals to the central nervous system and increases sympathetic nervous system activity [9].

The resulting peripheral vasoconstriction and increased left ventricular afterload further impair cardiac performance. Through this mechanism, the skeletal muscle hypothesis explains why patients with HF experience symptoms such as exercise intolerance, early fatigue, and dyspnea, often out of the degree of left ventricular dysfunction [10]. Furthermore, it also provides a physiological basis for the beneficial effects of exercise training, which can improve muscle function and symptoms. This is why exercise training is highly recommended in clinical guidelines as a non-pharmacological therapy [11]. Aerobic exercise (AE) is the most common exercise modality in HF rehabilitation programs due to multiple benefits on patients’ exercise capacity, cardiac function [12], functional capacity, and QoL [13]. Furthermore, inspiratory muscle training (IMT) is recommended as an adjuvant exercise in the most severe patients, enriching the conventional exercise programs [14].

To date, there is a variety in training loads and modalities implemented in patients with HF. Therefore, a comprehensive patient evaluation of respiratory muscle status is essential to enable clinicians to implement appropriately tailored IMT interventions.

In light of these considerations, this entry provides a comprehensive overview of inspiratory muscle pathophysiology in patients with HF and further delineates the various modalities of IMT, outlining their theoretical rationale and mechanistic underpinnings. Additionally, it synthesizes current evidence regarding the effects of IMT and gives practical considerations supporting the structured and individualized implementation of IMT in clinical practice.