Diaphragm dysfunction in heart failure and chronic obstructive pulmonary disease: mechanisms, cardiopulmonary interactions, and inspiratory muscle training

The diaphragm integrates respiratory mechanics with cardiovascular function. In heart failure (HF) and chronic obstructive pulmonary disease (COPD), chronic mechanical loading, systemic inflammation, oxidative stress, and altered neural drive promote structural and metabolic remodeling of the inspiratory muscles, reducing force-generating capacity and contractile efficiency. As capacity declines, the relative ventilatory load increases, accelerating fatigue and promoting activation of the inspiratory muscle metaboreflex. This response contributes to sympathetic overactivity, impaired limb perfusion, and dyspnea, thereby limiting exercise tolerance. Despite distinct pathophysiological triggers, HF and COPD converge on a shared mechanism characterized by an imbalance between inspiratory load and muscle capacity. In HF, pulmonary congestion and reduced lung compliance increase the work of breathing, whereas in COPD, hyperinflation imposes mechanical constraints and increases inspiratory threshold loading. In both conditions, the diaphragm operates closer to its maximal capacity, predisposing to fatigue and ventilatory inefficiency. Inspiratory muscle training (IMT) targets this imbalance by increasing pressure-generating capacity and contractile reserve, thereby reducing the relative inspiratory load. These adaptations may delay fatigue, attenuate metaboreflex activation, and improve ventilatory efficiency, dyspnea, and exercise capacity. However, the magnitude of benefit varies across populations and depends on baseline impairment and training characteristics. This review integrates current evidence within a unified physiological framework centered on inspiratory load–capacity imbalance.