Decreased phrenic nerve compound muscle action potential, inspiratory muscle strength, and exercise capacity after COVID-19

Abstract

ObjectivesRespiratory muscle weakness with higher ventilatory demands were reported even in patients recovering from only mild COVID-19 symptoms. Aim of this study was to assess the function of phrenic nerve and inspiratory respiratory muscle as well as cardiopulmonary exercise capacity in patients with prolonged exertional dyspnea after COVID-19 infection.MethodsIn this observational exploratory study, electrophysiological examination of the phrenic nerve, inspiratory muscle capacity as well as lung function test, 6-min walk distance (6MWD) and cardiopulmonary exercise test, have been performed in 22 patients post COVID-19 diagnosis (post-CoV).ResultsExercise capacity (peak workload, Wpeak % predicted and peak oxygen uptake, VO2peak % predicted) were significantly affected in the post-CoV patients (61.8 ± 23.3 Wpeak % and 70.9 ± 22.3 VO2peak %). Maximum inspiratory pressure (MIP) was reduced (60.1 ± 25.5 mbar). In 6 of the 22 patients the electrophysiological response of the phrenic nerve was pathologically decreased (reduced compound muscle action potential, CMAP), while nerve conduction velocity (NCV) was normal, which corresponds to reduced muscle fiber contraction capacity. Positive relationships were demonstrated between 6MWD and MIP (rs = 0.88) as well as quality of life questionnaire (CRQ) and MIP (rs = 0.71) only in patients with reduced CMAP.DiscussionRespiratory muscle weakness and exercise capacity is associated with reduced phrenic nerve CMAP without signs of neuropathy. This indicates that muscle fiber pathology of the diaphragm may be one pathophysiological factor for the prolonged respiratory symptoms after COVID-19 infections.

A follow‐up study on respiratory outcomes, quality of life and performance perception of SARS‐CoV‐2 primary and reinfection in elite athletes: A 9‐month prospective study

“…As is known, SARS-CoV-2 severely affects the respiratory system and may cause predominant pathophysiological changes, which mostly result in abnormalities or dysfunctions. Furthermore, emerging evidences suggest that muscle fiber pathology of the diaphragm may be a pathophysiological factor contributing to reduced respiratory muscle strength and function post-SARS-CoV-2 (Anastasio et al, 2021;Regmi et al, 2023;Shi et al, 2021;Vonbank et al, 2024). Previous studies have found that most people who develop a primary infection begin to recover rapidly after the initial months; however, in some severe patients, persistent symptoms, impaired lung function, and radiographic abnormalities sustain for up to 8 months and even 12 months in certain conditions (Scaramuzzo et al, 2022;Wu et al, 2021;Zhang et al, 2021).…”