Chronic obstructive pulmonary disease is a common, preventable and treatable disease characterized by persistent respiratory symptoms and airway limitation due to airway and/or alveolar abnormality, which is affected by many factors that cause abnormal lung development resulting from exposure to harmful gases or particles. Chronic obstructive pulmonary disease is known as the fourth most common cause of death in the world and is expected to rise to third place by the end of 2020. Physiopathological changes such as airflow limitation, bronchial fibrosis, increased airway resistance, ciliary dysfunction, gas exchange abnormalities and air trapping occur in Chronic obstructive pulmonary disease. While smoking is the most common risk factor in chronic obstructive pulmonary disease; Occupational dust and chemicals, air pollution, lung growth and development, genetic predisposition such as age and gender, and exposure to environmental effects. Symptoms such as shortness of breath (dyspnea), cough and sputum are common in chronic obstructive pulmonary disease. In addition to pulmonary changes such as increased respiratory workload, there are also extrapulmonary changes such as respiratory muscle dysfunction in individuals with chronic obstructive pulmonary disease.~Respiratory muscle dysfunction; It is a decrease in respiratory muscle strength, endurance, or both, caused by factors such as elongated diaphragm fibers, increased respiratory workload, changes in muscle mass and abdominal weight. Strength is defined as the muscle's capacity to produce power, while endurance is defined as the muscle's ability to sustain a given force over time (the capacity to resist fatigue). Loss of strength and/or endurance contributes to diaphragm weakness and impaired performance.~Neural respiratory impulse, indirectly measured by electromyogram of respiratory muscles, has attracted attention as a potential physiological marker of clinical deterioration due to imbalance between workload and capacity of respiratory muscles. The neural respiratory drive is the output of the brainstem respiratory centers. Neural respiratory drive is not affected by the patient's will, is associated with symptoms such as dyspnea, and is usually increased in chronic obstructive pulmonary disease patients.~Mechanical abnormalities such as airflow obstruction, static and dynamic hyperinflation, and intrinsic positive end-expiratory pressure increase the load on respiratory muscles in individuals with chronic obstructive pulmonary disease. Inspiratory muscle contraction is impaired as a result of pressure changes, muscle shortening, increased contraction rate, change in geometry, and decreased compliance of the respiratory system. As a result, an increase in muscle activation and neural respiratory drive is observed. Those with severe chronic obstructive pulmonary disease require significantly higher muscle activations, both electrical and mechanical, to breathe and overcome the respiratory workload than those with mild to moderate chronic obstructive pulmonary disease. In individuals with chronic obstructive pulmonary disease, neural respiratory drive increases when the load on the respiratory muscles increases as a result of an increase in respiratory workload, a decrease in capacity, or a combination of both. Studies have shown that in addition to respiratory workload, workloads given with respiratory muscle training devices lead to an increase in the activation of respiratory muscles.~In addition to pulmonary changes, extrapulmonary changes occur in individuals with chronic obstructive pulmonary disease. Loss of respiratory muscle strength and endurance; The effect of the inappropriate position of the diaphragm on length-tension due to hyperinflation are among the most common extrapulmonary changes resulting from the use of corticosteroids, hypoxemia and hypercapnia. Weakness of respiratory muscles in chronic obstructive pulmonary disease patients leads to hypoxemia, hypercapnia, dyspnea and reduces exercise capacity. Inspiratory muscle training reduces type 2 fibers, shortens the inspiratory time, prolongs the expiratory time, and reduces dynamic hyperinflation. Inspiratory muscle training has been proposed as one of the non-pharmacological treatment modalities because it can delay worsening of lung function by increasing inspiratory muscle strength and endurance. In chronic obstructive pulmonary disease, inspiratory muscle training improves respiratory muscle strength and exercise capacity and reduces dyspnea and is widely used in therapy.
It has been observed in the literature that respiratory muscle electromyography activations at certain threshold loads have been examined in individuals with chronic obstructive pulmonary disease. However, no study has been found in the literature examining the acute effects of respiratory muscle training given at low, medium and high threshold loads on respiratory muscle activations. With this planned study, it is aimed to examine the electromyography activations of respiratory muscles before and after respiratory muscle training and to contribute to the literature by comparing the acute effects of respiratory muscle training applied at low, medium and high intensity on respiratory muscle electromyography activations.