Home‐Based Inspiratory Muscle Training Can Restore Cardiac Autonomic Balance and Improve Spontaneous Breathing Pattern in Post‐ COVID Individuals

While the acute phase of the COVID-19 pandemic has receded, its legacy endures in the form of post-COVID condition, a complex syndrome affecting multiple organ systems. Beyond the well-characterized pulmonary sequelae, autonomic nervous system (ANS) dysfunction has emerged as a common and debilitating feature 1. A hallmark of this ANS dysfunction is reduced cardiac vagal tone, quantified as decreased heart rate variability (HRV), which is linked to poorer prognosis 1, dysregulated inflammatory responses 2, and blunted chemoreflexes 3. These symptoms raise the important question as to whether we can target this autonomic imbalance with a simple, accessible intervention? Breathing is a powerful modulator of cardiovascular function through intricate cardiorespiratory coupling. The rhythmic pressure changes in the thorax during respiration influence heart rate, a phenomenon known as respiratory sinus arrhythmia (RSA), which is predominantly vagally mediated 4. Furthermore, the pattern of breathing, specifically the timing of inspiration and expiration within each breath cycle (the duty cycle), directly impacts this coupling. A shorter inspiratory time (Ti) and a longer expiratory time (Te) prolong the phase of vagal-mediated heart rate slowing, thereby enhancing overall cardiac vagal modulation 4, 5. Inspiratory muscle training (IMT) is a well-established regimen to strengthen the diaphragm and accessory inspiratory muscles with clear benefits for respiratory strength and endurance. Intriguingly, emerging evidence suggests that the beneficial effects of IMT's extend beyond the respiratory system, improving blood pressure regulation and, notably, increasing HRV in older adults and cardiopulmonary patients 6. The proposed mechanism is elegantly physiological: by strengthening inspiratory muscles, IMT may lead to a more efficient and less effortful breathing pattern at rest. This adaptation could shorten Ti and lengthen Te, thereby creating a physiological window for enhanced vagal outflow to the heart with each breath 5, 6. Consequently, we hypothesize that IMT will improve inspiratory muscle strength, modify the respiratory pattern by shortening inspiratory time and prolonging expiratory time during the duty cycle, and increase cardiac vagal modulation at rest. We recruited 24 participants with a prior COVID-19 infection and randomized them to a 5-week, home-based protocol: true IMT (training at 50%–80% of maximal inspiratory pressure, MIP) or sham training (at 5% of MIP, minimal load). MIP, HRV, and respiratory patterns (recorded via respiratory belt) were assessed before and after the intervention. HRV was recorded using a three-lead electrocardiogram and analyzed in the frequency domain. As expected, the IMT group significantly increased their MIP, demonstrating improved respiratory muscle strength. The novel finding lay in the spontaneous breathing pattern and HRV indices. Only the IMT group significantly altered their breathing duty cycle, decreasing the relative inspiratory time (Ti/Ttot) and increasing the relative expiratory time (Te/Ttot) (Figure 1). Regarding cardiac autonomic control, the high-frequency (HF) power of HRV, a spectral component tightly coupled to the respiratory rhythm and a direct marker of vagal modulation 4-6, increased significantly after IMT (t0 21 ± 5 vs. t1 30 ± 20; p = 0.04), with no such change in the sham group (t0 34 ± 16 vs. t1 26 ± 21). These findings support a compelling physiological cascade. IMT, by strengthening the inspiratory pump, likely reduces the neural drive and mechanical effort required for each breath at rest 6. This leads to a faster, more efficient inspiration and a relative prolongation of expiration. The longer Te provides an extended period for vagal-mediated deceleration of the heart rate, amplifying the RSA effect, which is reflected in the increased vagal-mediated HRV 5. Essentially, IMT shifts the cardiorespiratory coupling toward a state of greater vagal predominance. Since breathing is a key external modulator of cardiovascular variability, it is plausible that the IMT-induced increase in vagally mediated HRV, particularly in the HF band synchronized with respiration, may be partially attributed to mechanical adaptations in thoracic dynamics that enhance respiratory influence on heart rate modulation 7. While the contribution of non-neural mechanisms to heart rate modulation is typically minimal, it becomes more relevant in conditions characterized by reduced cardiovascular variability 4. However, a central adaptation cannot be excluded, considering that a reduction in inspiratory relative time, beyond being more efficient, reduces the duration of the diaphragm twitch within the respiratory cycle, which consequently reduces inspiratory feedback to the brainstem 4. Given that changes in breathing depth and patterns influence autonomic activity, the complex interplay of breathing-related regulatory mechanisms may directly or indirectly modulate heart rate. Therefore, further investigation is warranted to explore potential IMT-induced adaptations in autonomic pathways. Enhancing vagal modulation is particularly important in post-COVID individuals, as the vagus nerve innervates key organs, including the heart and lungs, both commonly affected by post-COVID conditions 1. Additionally, the vagus nerve modulates inflammation through the cholinergic anti-inflammatory reflex 2. Ultrasound-based studies indicate potential vagus and phrenic nerve dysfunction, which may explain persistent dyspnea in post-COVID individuals without lung damage 8. If post-COVID conditions impair both respiratory muscles and autonomic regulation 1, enhanced cardiac vagal modulation following IMT could offer a protective effect, potentially mitigating subclinical inflammation and autonomic dysfunction. IMT may reduce inflammation 9, while slow breathing training has been shown to lower systemic inflammation in COVID-19 pneumonia patients 10, reinforcing the role of respiratory strategies in vagal stimulation and inflammation control. However, the specific effects of IMT on cardiac autonomic control and inflammation in post-COVID individuals remain unclear and warrant further investigation. In conclusion, 5 weeks of a home-based IMT program improves inspiratory muscle strength, modifies the spontaneous breathing pattern, and enhances cardiac vagal modulation in post-COVID individuals. These adaptations suggest that IMT may serve as a non-pharmacological strategy to optimize respiratory muscle strength and cardiac autonomic control. Given that autonomic dysfunction persists in post-COVID individuals, even in asymptomatic cases, IMT may offer protective effects against subclinical autonomic imbalances. Thus, IMT emerges as an accessible and promising intervention for restoring autonomic balance in post-COVID individuals, warranting further studies to elucidate its mechanisms and clinical impact. The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.