<p>Heart failure (HF) management increasingly requires multimodal assessment beyond cardiac function. Although echocardiography remains central, skeletal muscle and diaphragmatic dysfunction—key drivers of exercise intolerance—are underdiagnosed. This review synthesizes two critical aspects: (1) the pathophysiological heterogeneity of muscle involvement across HF subtypes [HF with reduced ejection fraction (HFrEF), HF with mildly reduced ejection fraction (HFmrEF), and HF with preserved ejection fraction (HFpEF)] and (2) the clinical utility of muscle ultrasound as a dynamic, bedside-compatible tool for risk stratification and personalized interventions. Emerging evidence reveals distinct mechanisms: HFrEF predominantly associates with diaphragmatic atrophy and mitochondrial dysfunction, whereas HFpEF is characterized by reduced diaphragmatic motion and skeletal muscle fat infiltration. Ultrasound-derived parameters, such as echo intensity for quadriceps fat quantification and diaphragm thickness ratio for inspiratory weakness, strongly correlate with functional outcomes (e.g., 6-min walk distance and peak VO₂). Notably, a quadriceps echo intensity &gt; 28 dB in HFrEF or a diaphragmatic excursion &lt; 2.5 cm in HFpEF independently predicts adverse prognosis, guiding targeted interventions such as inspiratory muscle training or anti-inflammatory therapies. However, critical gaps persist, including the lack of standardized cutoff values for HF subtypes and insufficient data on ultrasound-guided therapeutic monitoring. Future research should prioritize subtype-specific protocols and validate cost-effective ultrasound algorithms against standard modalities. By bridging pathophysiology and clinical application, this review underscores muscle ultrasound’s transformative potential in refining HF phenotyping, ultimately enhancing exercise capacity and reducing hospitalizations.</p>