Inspiratory muscle training in heart failure

There is robust evidence suggesting that the weakness of inspiratory muscles is one of the main factors that lead to low exercise tolerance in patients with HF. ^, In fact, randomized clinical trials have shown several benefits of IMT in patients with this syndrome, namely: significant improvement in oxygen uptake efficiency, functional capacity and quality of life scores. These results were confirmed by meta-analyses, such as that carried out by Smart et al. When compared to the control group, patients undergoing IMT achieved an important improvement in maximum oxygen consumption (VO₂max): 1.83 mL.kg^-1.min^-1(95%CI, 1.33 for 2.32 mL.kg^-1.min^-1, p <0.00001), as well as in the 6-minute walking test: 34.35 m (95%CI, 22.45 to 46.24 m, p <0.00001). In turn, inspiratory muscle strength seems to have a significant correlation with VO₂max, which is an independent predictor of survival in individuals with HF. IMT should therefore be an integral part of these patients’ care whenever possible.

In this issue of the Arquivos Brasileiros de Cardiologia , a randomized, placebo-controlled trial evaluated the implications of an acute session of different intensities of IMT on the central hemodynamic response (CHR) of individuals with HF, using a non-invasive monitoring method. For this purpose, 20 patients with reduced ejection fraction (37.2% ± 6.3%), a mean age of 65 years, and the vast majority in New York Heart Association (NYHA) functional class II were included in the study. The IMT protocol consisted of 3 sessions lasting 15 minutes each. All participants underwent the training with an intensity of 30% and 60% of maximum inspiratory pressure (MIP), in addition to sham intervention (placebo), with a 1-hour washout between them. It was observed that CHR behaved in a heterogeneous way between intensities. For instance, there was an increase in heart rate with intensities of 30% and 60% of MIP (64 ± 15 to 69 ± 15 beats per minute; and 67 ± 14 to 73 ± 14 beats per minute, respectively). Regarding stroke volume, there was a tendency to decrease with a 30% load of MIP (73 ± 26 mL to 64 ± 20 mL). The cardiac output increased only in the group with the highest intensity (4.6 ± 1.5 L / min to 5.3 ± 1.7 L / min), a behavior that was similar in relation to the systolic blood pressure response. In fact, the increase in cardiac output observed at the highest applied intensity can be partially explained by the increase in heart rate in this group. These findings should not be ignored, since patients with HF tend to have impaired blood flow to the active muscles, secondary to reductions in cardiac output and peripheral vasodilator capacity. These changes are harmful, causing important intolerance to effort, being associated with reduced vasodilator capacity and increased sympathetic stimulation, common in these individuals.

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