scholarly journals Unraveling the Role of Respiratory Muscle Metaboloreceptors under Inspiratory Training in Patients with Heart Failure

Author(s):  
Hugo Fernández-Rubio ◽  
Ricardo Becerro-de-Bengoa-Vallejo ◽  
David Rodríguez-Sanz ◽  
César Calvo-Lobo ◽  
Davinia Vicente-Campos ◽  
...  

Exercise intolerance may be considered a hallmark in patients who suffer from heart failure (HF) syndrome. Currently, there is enough scientific evidence regarding functional and structural deterioration of skeletal musculature in these patients. It is worth noting that muscle weakness appears first in the respiratory muscles and then in the musculature of the limbs, which may be considered one of the main causes of exercise intolerance. Functional deterioration and associated atrophy of these respiratory muscles are related to an increased muscle metaboreflex leading to sympathetic–adrenal system hyperactivity and increased pulmonary ventilation. This issue contributes to increased dyspnea and/or fatigue and decreased aerobic function. Consequently, respiratory muscle weakness produces exercise limitations in these patients. In the present review, the key role that respiratory muscle metaboloreceptors play in exercise intolerance is accurately addressed in patients who suffer from HF. In conclusion, currently available scientific evidence seems to affirm that excessive metaboreflex activity of respiratory musculature under HF is the main cause of exercise intolerance and sympathetic–adrenal system hyperactivity. Inspiratory muscle training seems to be a useful personalized medicine intervention to reduce respiratory muscle metaboreflex in order to increase patients’ exercise tolerance under HF condition.

2014 ◽  
Vol 20 (10) ◽  
pp. S136
Author(s):  
Yoshiharu Kinugasa ◽  
Kensaku Yamada ◽  
Takeshi Sota ◽  
Mari Miyaki ◽  
Shinobu Sugihara ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Paolo Formenti ◽  
Michele Umbrello ◽  
Martin Dres ◽  
Davide Chiumello

Abstract Although mechanical ventilation is a lifesaving treatment, abundant evidence indicates that its prolonged use (1 week or more) promotes respiratory muscle weakness due to both contractile dysfunction and atrophy. Along with the diaphragm, the intercostal muscles are one of the most important groups of respiratory muscles. In recent years, muscular ultrasound has become a useful bedside tool for the clinician to identify patients with respiratory muscle dysfunction related to critical illness and/or invasive mechanical ventilation. Images obtained over the course of illness can document changes in muscle dimension and can be used to estimate changes in function. Recent evidence suggests the clinical usefulness of ultrasound imaging in the assessment of intercostal muscle function. In this narrative review, we summarize the current literature on ultrasound imaging of the parasternal intercostal muscles as used to assess the extent of muscle activation and muscle weakness and its potential impact during discontinuation of mechanical ventilation. In addition, we proposed a practical flowchart based on recent evidence and experience of our group that can be applied during the weaning phase. This approach integrates multiple predictive parameters of weaning success with respiratory muscle ultrasound.


Amyloid ◽  
2008 ◽  
Vol 15 (2) ◽  
pp. 129-136
Author(s):  
Arnt V. Kristen ◽  
Thomas J. Dengler ◽  
J. H. Kristen ◽  
Stefan O. Schonland ◽  
Ute Hegenbart ◽  
...  

2020 ◽  
Vol 35 (2) ◽  
pp. 123-130
Author(s):  
J. L. Begrambekova ◽  
N. A. Karanadze ◽  
V. Yu. Mareev ◽  
E. A. Kolesnikova ◽  
Ya. A. Orlova

Respiratory system remodeling plays an important role in the progression of congestive heart failure (CHF). Decreased oxygenation of the respiratory muscles during intense physical exertion in patients with CHF may aggravate respiratory failure and provoke hyperactivation of the inspiratory metaborefl ex, thereby aggravating exercise intolerance due to a decrease in muscular system perfusion. Respiratory muscle training can minimize the eff ects of inspiration metaborefl ex activation and prolong the duration of exercise.Trial design. This is a prospective randomized trial with a sham control. The trial will include 40 adult patients of both genders with NYHA II-III CHF and with ejection fraction (EF) ≤ 49%. Patients will be randomized in a 1:1 ratio to either Active or Control group. Active group will receive four-week guided respiratory muscles training followed by 12-week guided aerobic training (treadmill walking). Control group will receive four-week sham respiratory muscles training (THRESHOLD® IMT breathing trainer with level slightly above 0), followed by 12 weeks guided aerobic training (treadmill walking). The primary aim is to compare the eff ect of diff erent training modalities on functional capacity (peak VO2 ). Secondary outcome measures include changes in respiratory muscle strength, serum biomarkers (NT-proBNP and ST2) and Angiotensin II. Health-related quality of life (MLwHFQ.23) and psycho-emotional state of patients also will be assessed.The study also planned an additional analysis with a suitable group of patients who were screened but refused to participate in the study.Conclusion. Heart failure patients often give up exercise due to symptoms of shortness of breath and muscle weakness. We suggest that the training technique based on the inclusion of respiratory muscle training as the fi rst stage of cardiac rehabilitation will positively aff ect the eff ectiveness of subsequent aerobic training in patients with heart failure, by reducing the activity of RAAS and SAS and increasing respiratory effi ciency. 


2018 ◽  
Vol 314 (1) ◽  
pp. H11-H18 ◽  
Author(s):  
Jasdeep Kaur ◽  
Danielle Senador ◽  
Abhinav C. Krishnan ◽  
Hanna W. Hanna ◽  
Alberto Alvarez ◽  
...  

When oxygen delivery to active muscle is insufficient to meet the metabolic demand during exercise, metabolites accumulate and stimulate skeletal muscle afferents, inducing a reflex increase in blood pressure, termed the muscle metaboreflex. In healthy individuals, muscle metaboreflex activation (MMA) during submaximal exercise increases arterial pressure primarily via an increase in cardiac output (CO), as little peripheral vasoconstriction occurs. This increase in CO partially restores blood flow to ischemic muscle. However, we recently demonstrated that MMA induces sympathetic vasoconstriction in ischemic active muscle, limiting the ability of the metaboreflex to restore blood flow. In heart failure (HF), increases in CO are limited, and metaboreflex-induced pressor responses occur predominantly via peripheral vasoconstriction. In the present study, we tested the hypothesis that vasoconstriction of ischemic active muscle is exaggerated in HF. Changes in hindlimb vascular resistance [femoral arterial pressure ÷ hindlimb blood flow (HLBF)] were observed during MMA (via graded reductions in HLBF) during mild exercise with and without α1-adrenergic blockade (prazosin, 50 µg/kg) before and after induction of HF. In normal animals, initial HLBF reductions caused metabolic vasodilation, while reductions below the metaboreflex threshold elicited reflex vasoconstriction, in ischemic active skeletal muscle, which was abolished after α1-adrenergic blockade. Metaboreflex-induced vasoconstriction of ischemic active muscle was exaggerated after induction of HF. This heightened vasoconstriction impairs the ability of the metaboreflex to restore blood flow to ischemic muscle in HF and may contribute to the exercise intolerance observed in these patients. We conclude that sympathetically mediated vasoconstriction of ischemic active muscle during MMA is exaggerated in HF. NEW & NOTEWORTHY We found that muscle metaboreflex-induced vasoconstriction of the ischemic active skeletal muscle from which the reflex originates is exaggerated in heart failure. This results in heightened metaboreflex activation, which further amplifies the reflex-induced vasoconstriction of the ischemic active skeletal muscle and contributes to exercise intolerance in patients.


PLoS ONE ◽  
2015 ◽  
Vol 10 (2) ◽  
pp. e0118218 ◽  
Author(s):  
Pedro Verissimo ◽  
Karina T. Timenetsky ◽  
Thaisa Juliana André Casalaspo ◽  
Louise Helena Rodrigues Gonçalves ◽  
Angela Shu Yun Yang ◽  
...  

2007 ◽  
Vol 30 (3) ◽  
pp. 45
Author(s):  
Sergio Pulici ◽  
Piergiorgio Schiavoni

Background: Patients in cardiopulmonary rehabilitation often complain of exercise intolerance. While ventilatory limitation is often present, other factors are also important: cardiovascular deconditioning, respiratory muscle dysfunction, gas exchange abnormalities and ventricular dysfunction. Methods: Forty patients, hospitalized for a consecutive 6 month-period, with persistent exercise intolerance due to cardiopulmonary pathologies were included. 90% were COPD II to IV GOLD stage; 5% had chronic cardiac decompensation; 5% had undergone surgery for coronary bypass and/or cardiac valve prosthesis. Patients were excluded who were clinically unstable, unable to cooperate correctly, had arrythmia due to atrial fibrillation and/or receiving beta-blocking therapy. We have, furthermore, measured parameters of ventilatory dysfunction (ventilatory reserve, dynamic inspiratory capacity), the parameters of cardiovascular limitation (peak heart rate and recovery heart rate at the first minute), parametes of respiratory muscles dysfunction (maximal inspiratory pressure and at the end of the 6 min walking test). Afterwards we classified patients into three groups: ventilatory-limited, cardiovascular-limited, respiratory muscles-limited. Results: Exercise performance limitation resulted from ventilatory limitation in 60% of the patients, second by cardiovascular limitation in 30% of the patients and also by respiratory muscle limitation in 10% of the patients. Conclusions: Based on admission diagnosis of 40 patients, 90% were defined as subject to pulmonary rehabilitation and in 10% were receiving cardiac rehabilitation. They divided into three specific functional recovery programs: ventilatory function recovery program (60%), cardiac function recovery program (30%), respiratory muscles recovery program (10%).


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