Key result
Respiratory muscle fatigue, defined by a decrease in maximal inspiratory pressure after exercise, was associated with significantly lower peak VO2 (14.2 vs 17.4 mL/kg/min) in patients with cardiovascular disease.
Why the study?
Patients with cardiovascular diseases frequently experience exertional dyspnea, but the relationship between respiratory muscle strength, including fatigue, and cardiovascular dysfunctions remains unclear.
Does respiratory muscle fatigue correlate with exercise capacity and renal function in patients with cardiovascular disease?
Observational (n=44)
No
Does respiratory muscle fatigue correlate with exercise capacity and renal function in patients with cardiovascular disease?
Absolute Event Rate: 14.2% vs 17.4%
p-value: p=0.020
Respiratory muscle fatigue, indicated by a decrease in maximal inspiratory pressure after exercise, is significantly associated with reduced exercise capacity and worse renal function in patients with cardiovascular disease.
May explain part of exercise intolerance; hypothesis-generating and requires prospective trials before any clinical role.
Patients with cardiovascular diseases frequently experience exertional dyspnea. However, the relationship between respiratory muscle strength including its fatigue and cardiovascular dysfunctions remains to be clarified.The maximal inspiratory pressure/maximal expiratory pressure (MIP/MEP) before and after cardiopulmonary exercise testing (CPX) in 44 patients with heart failure and ischemic heart disease were measured. Respiratory muscle fatigue was evaluated by calculating MIP (MIPpost/MIPpre) and MEP (MEPpost/MEPpre) changes.The mean MIPpre and MEPpre values were 67.5 ± 29.0 and 61.6 ± 23.8 cm H2O, respectively. After CPX, MIP decreased in 25 patients, and MEP decreased in 22 patients. We evaluated the correlation relationship between respiratory muscle function including respiratory muscle fatigue and exercise capacity evaluated by CPX such as peak VO2 and VE/VCO2 slope. Among MIP, MEP, change in MIP, and change in MEP, only the value of change in MIP had an association with the value of VE/VCO2 slope (R = -0.36, P = .017). In addition, multivariate analysis for determining factor of change in MIP revealed that the association between the change in MIP and eGFR was independent from other confounding parameters (beta, 0.40, P = .017). The patients were divided into 2 groups, with (MIP change < 0.9) and without respiratory muscle fatigue (MIP change > 0.9), and a significant difference in peak VO2 (14.2 ± 3.4 [with fatigue] vs 17.4 ± 4.7 [without fatigue] mL/kg/min; P = .020) was observed between the groups.Respiratory muscle fatigue demonstrated by the change of MIP before and after CPX significantly correlated with exercise capacity and renal function in patients with cardiovascular disease.
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Taya et al. (2020) conducted an observational in Cardiovascular disease (heart failure and ischemic heart disease) (n=44). Respiratory muscle fatigue (MIP change < 0.9) vs. No respiratory muscle fatigue (MIP change > 0.9) was evaluated on Peak VO2 (p=0.020). Respiratory muscle fatigue, defined by a decrease in maximal inspiratory pressure after exercise, was associated with significantly lower peak VO2 (14.2 vs 17.4 mL/kg/min) in patients with cardiovascular disease.
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