Ventilatory Assistance Improves Exercise Endurance  in Stable Congestive Heart Failure

O’Donnell, Denis E.; D’Arsigny, Christine L.; Raj, Satish R.; Abdollah, Hoshiar; Webb, Katherine A.

doi:10.1164/ajrccm.160.6.9808134

Cited by 109 publications

(114 citation statements)

References 30 publications

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“…Cycle exercise tests were carried out as previously described [1,6,17], using a cardiopulmonary exercise testing system (Vmax 299d). All exercise tests consisted of a steady-state resting period and a 1-min warm-up of loadless pedalling followed by an immediate increase in work-rate; pedalling frequencies were maintained at 50-70 revolutions per minute.…”

Section: Methodsmentioning

confidence: 99%

Effect of salmeterol on the ventilatory response to exercise in chronic obstructive pulmonary disease

O’Donnell¹,

Voduc²,

Fitzpatrick³

et al. 2004

European Respiratory Journal

330

273

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This study examined the effects of bronchodilator-induced reductions in lung hyperinflation on breathing pattern, ventilation and dyspnoea during exercise in chronic obstructive pulmonary disease (COPD). Quantitative tidal flow/volume loop analysis was used to evaluate abnormalities in dynamic ventilatory mechanics and their manipulation by a bronchodilator.In a randomised double-blind crossover study, 23 patients with COPD (mean¡SEM forced expiratory volume in one second 42¡3% of the predicted value) inhaled salmeterol 50 mg or placebo twice daily for 2 weeks each. After each treatment period, 2 h after dose, patients performed pulmonary function tests and symptom-limited cycle exercise at 75% of their maximal work-rate.After salmeterol versus placebo at rest, volume-corrected maximal expiratory flow rates increased by 175¡52%, inspiratory capacity (IC) increased by 11¡2% pred and functional residual capacity decreased by 11¡3% pred. At a standardised time during exercise, salmeterol increased IC, tidal volume (VT), mean inspiratory and expiratory flows, ventilation, oxygen uptake (V9O 2 ) and carbon dioxide output. Salmeterol increased peak exercise endurance, V9O 2 and ventilation by 58¡19, 8¡3 and 12¡3%, respectively. Improvements in peak V9O 2 correlated best with increases in peak VT; increases in peak VT and resting IC were interrelated. The reduction in dyspnoea ratings at a standardised time correlated with the increased VT.Mechanical factors play an important role in shaping the ventilatory response to exercise in chronic obstructive pulmonary disease. Bronchodilator-induced lung deflation reduced mechanical restriction, increased ventilatory capacity and decreased respiratory discomfort, thereby increasing exercise endurance. Several recent studies have shown that improvements in exertional dyspnoea following bronchodilator therapy in chronic obstructive pulmonary disease (COPD) correlate well with reductions in lung hyperinflation, as indicated by increases in inspiratory capacity (IC) [1][2][3][4][5]. However, the relationship between bronchodilator-induced increases in IC and improvements in symptoms and exercise performance is complex and poorly understood. Given the multifactorial nature of dyspnoea and exercise limitation in COPD, it remains unclear why small increases in resting IC (in the order of 0.3 L) appear to be clinically important. The current study extends previous studies conducted in the present authors9 laboratory using ipratropium bromide by, in addition, examining the effect of a bronchodilator (salmeterol) on plethysmographic lung volume components at rest and on breathing pattern and ventilatory capacity during exercise. Moreover, the study was designed to advance understanding of the mechanisms of bronchodilatorinduced dyspnoea relief, especially the role of reduced mechanical restriction.It has previously been shown that acute-on-chronic hyperinflation during exercise severely constrains tidal volume (VT) expansion, and that this dynamic mechanical restriction makes ...

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Section: Methodsmentioning

confidence: 99%

Effect of salmeterol on the ventilatory response to exercise in chronic obstructive pulmonary disease

O’Donnell¹,

Voduc²,

Fitzpatrick³

et al. 2004

European Respiratory Journal

330

273

View full text Add to dashboard Cite

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“…Therefore, the first set of postexercise twitch measurements were obtained 10 min after exercise and subsequent sets of unpotentiated twitches were obtained o15 min after any potentiation manoeuvre. End-expiratory lung volume is known to increase during exercise in patients with CHF [26]. It rapidly returns to baseline after stopping exercise in patients with COPD [27].…”

Section: Critique Of Methodsmentioning

confidence: 99%

Diaphragmatic function after intense exercise in congestive heart failure patients

Kufel¹,

Pineda²,

Junega³

et al. 2002

Eur Respir J

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Respiratory muscle strength and endurance is reduced in patients with congestive heart failure, making these patients susceptible to diaphragmatic fatigue during exercise.In order to determine whether or not contractile fatigue of the diaphragm occurs in patients with congestive heart failure following intense exercise, twitch transdiaphragmatic pressures (twitch Ptdi) were measured during unpotentiated and potentiated cervical magnetic stimulation (CMS) of the phrenic nerves before and at intervals after cycle endurance exercise.Ten patients aged 65.7 ¡ 6.0 yrs (mean ¡ SD) with an ejection fraction of 31.2 ¡ 9.8% performed a constant-load symptom-limited exercise test at 60% of their peak work capacity. Twitch Ptdi at baseline were 15.9¡6.3 cmH 2 O (unpotentiated CMS) and 28.8¡ 10.7 cmH 2 O (potentiated CMS) and at 10 min postexercise were 16.4¡4.7 cmH 2 O (unpotentiated CMS) and 27.6¡10.1 cmH 2 O (potentiated CMS). One patient demonstrated a sustained fall in twitch Ptdi of o15%, considered potentially indicative of diaphragmatic fatigue.Contractile diaphragmatic fatigue is uncommon in untrained patients with congestive heart failure following high-intensity constant-workload cycle exercise. Therefore, diaphragmatic fatigue is an unlikely cause of exercise-limitation during activities of daily living in heart failure patients.

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“…Heliox has been shown to be beneficial in relieving symptoms and improving exercise tolerance in patients with COPD (63, 100) or CHF (74). Mechanical ventilation during an acute bout of exercise has also been shown to reduce exertional symptoms and increase exercise tolerance in patients with COPD (62,144) or CHF (95). When mechanical ventilation was used during routine exercise training, patients with advanced disease were able to exercise at higher intensities and for longer such that the training stimulus was increased to severely deconditioned locomotor muscles (32,43,130).…”

Section: Overcoming the Respiratory Limitations To Exercisementioning

confidence: 99%

Exercise-induced respiratory muscle fatigue: implications for performance

Romer

Polkey²

2008

Journal of Applied Physiology

256

212

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Romer LM, Polkey MI. Exercise-induced respiratory muscle fatigue: implications for performance. J Appl Physiol 104: 879 -888, 2008. First published December 20, 2007 doi:10.1152/japplphysiol.01157.2007.-It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O 2 and CO2 transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exerciseinduced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles. respiratory muscles; exercise; diaphragm; abdominals; magnetic stimulation; metaboreflex THE PURPOSE OF THIS MINIREVIEW is to address the question of whether the respiratory demands of exercise contribute significantly toward exercise limitation, either directly through limitations of the respiratory muscle pump or indirectly through effects on limb blood flow and locomotor muscle fatigue. We describe the mechanical and metabolic costs of meeting the ventilatory requirements of exercise. We then ask whether the respiratory muscles fatigue with exercise, what factors contribute to any such fatigue, and what the implications of these factors are for exercise tolerance. Finally, we deal with the potential mechanisms by which respiratory muscle fatigue could compromise exercise tolerance and whether it is possible to overcome this potential respiratory limitation. Our review focuses on the healthy young adult exercising near sea level. However, we also consider special circumstances that determine the balance between metabolic demand and respiratory system capacity in the highly trained endurance ...

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Ventilatory Assistance Improves Exercise Endurance in Stable Congestive Heart Failure

Cited by 109 publications

References 30 publications

Effect of salmeterol on the ventilatory response to exercise in chronic obstructive pulmonary disease

Effect of salmeterol on the ventilatory response to exercise in chronic obstructive pulmonary disease

Diaphragmatic function after intense exercise in congestive heart failure patients

Exercise-induced respiratory muscle fatigue: implications for performance

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