Compartmental chest wall volume changes during volitional hyperpnoea with constant tidal volume in healthy individuals

Abstract

Prolonged high-intensity ventilation is associated with the development of rapid shallow breathing with decreased end-inspiratory volumes of all chest wall compartments. During respiratory muscle endurance training using normocapnic hyperpnoea, tidal volume (V(T)) is normally kept constant. The aim of this study was to investigate possible changes in muscle recruitment during constant-V(T) hyperpnoea, to assess potential mechanisms related to rapid shallow breathing. Ten healthy subjects performed 1h of normocapnic hyperpnoea at 70% of maximal voluntary ventilation. Chest wall volume changes were assessed by optoelectronic plethysmography. End-inspiratory (1.08 ± 0.18 versus 0.96 ± 0.27 l, p=0.017) and end-expiratory volumes (-0.13 ± 0.15 versus -0.31 ± 0.19 l, p=0.007) of the pulmonary ribcage decreased significantly and lung function and respiratory muscle strength were reduced (all p<0.05). Since with forced, constant V(T) only the inspiratory rib cage muscles were unable to sustain end-inspiratory volume of their compartment, inspiratory rib cage muscles are the most likely candidate responsible for the development of rapid shallow breathing. KEYWORDSRespiratory muscle recruitment, respiratory muscle fatigue, rapid shallow breathing 2

Air Stacking: A Detailed Look Into Physiological Acute Effects on Cough Peak Flow and Chest Wall Volumes of Healthy Subjects

“…On the other hand, the increase in ⌬V ab /T E mainly occurred from a decrease in T E throughout application of the protocol, in addition to a higher amount of volume displaced by the compartment. In contrast to diaphragm and expiratory muscles, the inspiratory muscles of the rib cage develop more passive tension for active force development when stretched beyond their optimal size, 40 and perhaps this is why a greater shortening velocity was seen in ⌬V rcp /T I in relation to the other indexes. In general, the increase in shortening velocity could be explained by the activation and recruitment of motor units in addition to the change in neural drive.…”

Similar Airway Function after Volitional Hyperpnea in Mild-Moderate Asthmatics and Healthy Controls

“…–2 to –7%) in FEV 1 , FVC, and increases (approx. 20%) in R5 were previously reported in healthy subjects following 30 min [11, 32] and 60 min [9, 10] of continuous HYP with similar or higher intensity, while no decline was reported after 30 min of HYP with unmeasured but likely lower ventilation [33]. …”

“…A potential cause of the changes in lung function observed after HYP might be HYP-induced respiratory muscle fatigue [9, 10, 32, 40, 41] since flow generation is effort dependent, at high lung volumes [42, 43] affecting PEF and to a lesser extent FEV 1 [44], and at very low lung volumes [42] potentially affecting FEF 25 − 75% and FVC. Although asthmatics showed reduced respiratory muscle strength, possibly rendering them more prone to the development of respiratory muscle fatigue, and although FEV 1 and PEF were indeed reduced early during HYP 1 – consistent with early development of fatigue [40] – respiratory muscle fatigue as a cause of changes in lung function seems unlikely since changes resolved already during the course of HYP 1 .…”

“…However, a potential problem with HYP might be HYP-induced bronchoconstriction since decreases in lung function, i.e., declines in forced expiratory volume in 1 s (FEV 1 ) in the range of –3 to –7%, were observed already in healthy subjects in the context of HYP training where subjects performed intense normocapnic HYP via partial rebreathing of expired air for 30–60 min [9-11]. Whether these changes would be more pronounced in asthmatics remains unclear since factors unrelated to airway narrowing might have caused these alterations in healthy subjects.…”

Optoelectronic Plethysmography in Clinical Practice and Research: A Review

“…The latter study showed that the end-inspiratory lung volume (EIV) increase in V CW was mainly achieved by increasing endinspiratory volumes of the RCp and RCa, reflecting the inspiratory RC muscle contribution to recruit the inspiratory reserve volume. Findings reported by Illi et al [75] likely indicate that all inspiratory muscles fatigued simultaneously rather than in succession and that inspiratory RC muscles did not take over diaphragmatic work in the course of prolonged normocapnic hyperpnoea.…”