Interstitial lung diseases (ILD) constitute a group of disorders that diffusely affect the lungs, causing varying degrees of inflammation, fibrosis, and structural alterations in the lung parenchyma. These diseases may present with either acute or chronic progression and can involve not only the interstitium but also the alveoli, small airways, vascular structures, and pleura. The etiology of ILD is diverse and may be related to identifiable causes such as environmental or occupational exposures, medications, and radiation. Connective tissue diseases-including rheumatoid arthritis, systemic sclerosis, and systemic lupus erythematosus-along with several systemic disorders, may also lead to pulmonary damage and involvement. Systemic diseases can affect the lungs through infections, vasculitis, or inflammatory mechanisms. Globally, approximately two million individuals are affected by ILD, and in Türkiye, the incidence has been reported as 25.8 per 100,000. The most frequently encountered ILD subtypes include sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis .
Dyspnea is one of the most common and disabling symptoms in individuals with ILD, substantially reducing quality of life. Respiratory irregularities observed at rest become more pronounced during exercise. Chronic cough is another prevalent symptom in ILD that negatively impacts daily functioning, social interactions, and psychological well-being, and may also indicate disease progression. Impaired gas exchange and reduced lung elasticity lead to a significant decrease in exercise capacity in ILD, resulting in limitations in daily activities. Assessment of exercise capacity is essential for monitoring disease severity and evaluating treatment effectiveness.
In individuals with ILD, progressive circulatory limitations reduce oxygen consumption. Fibrotic changes in the pulmonary vascular bed restrict blood flow, compromising oxygen delivery during exertion and leading to a marked reduction in VO₂ capacity. Pulmonary hypertension and decreased cardiac output further exacerbate this mechanism. During exercise, the oxygen pulse shows limited increase and may plateau or even decrease in some patients. Consequently, heart rate rises disproportionately compared with healthy individuals, increasing peripheral hypoxia and exercise-induced desaturation. Monitoring muscle oxygenation is important for determining how exercise interventions can be optimized to reduce dyspnea and improve exercise capacity.
Blood flow restriction (BFR) exercise was first introduced in 1966; however, it gained more attention in the mid-1980s due to its potential to induce strength gains at low exercise intensities, thereby reducing orthopedic injury risk. The technique relies on applying controlled external pressure to restrict venous return without completely occluding arterial inflow. This results in a temporary hypoxic and metabolically stressful environment distal to the cuff. Accumulation of lactic acid within the ischemic and hypoxic muscle environment leads to a decrease in intramuscular pH. These metabolic stress responses, which are typically observed during high-intensity exercise, stimulate growth hormone release. Growth hormone-mediated IGF-1 secretion enhances protein synthesis within muscle cells, ultimately promoting muscle hypertrophy. A key advantage of restricting blood flow during aerobic exercise is the potential to increase muscle mass even during low-intensity training .
In recent years, the applicability of BFR exercise has been demonstrated across various populations, including older adults, individuals with obesity, and those with cardiovascular conditions. However, most studies have been conducted in athletes and healthy individuals, and research in clinical populations remains limited. For individuals with ILD, BFR training may offer a safe and practical method to enhance both muscle mass and exercise capacity while imposing minimal stress on the cardiovascular and musculoskeletal systems.