The aim of this study was to characterize the pattern of inspiratory muscle fatigue and to assess the resistance to fatigue of the diaphragm (D), parasternal (PS), sternocleidomastoid (SCM), and scalene (SC) muscles. Nine healthy, untrained male subjects participated in this study. Electromyographic activity (EMG) of D, PS, SCM, and SC was recorded during an incremental cycling test to exhaustion (workload of 1.0 W/kg with 0.5 W/kg increments every 5 min). The before-to-after exercise measurements of maximal inspiratory pressure (MIP) and EMG power spectrum changes were performed. The maximal inspiratory pressure declined about 8.1 % after exercise compared with that in the control condition (124.3 ± 8.5 vs. 114.2 ± 8.9 cmH2O) (P > 0.05), whereas the peak magnitude of integrated electrical activity of D, PS, SCM, and SC during the post-exercise Müller maneuver was significantly greater in all subjects than that pre-exercise. The extent of inspiratory muscles fatigue was evaluated by analysis of a shift in centroid frequency (fc) of EMG power spectrum. Exercise-induced D fatigue was present in three subjects and PS fatigue was another in two; whereas both D and PC fatigue were observed in four subjects. All subjects demonstrated a significant reduction in fc of SCM and SC. Results indicate that early signs of the fatiguing process might be detected in the D, PS, SCM, and SC muscles during exercise to exhaustion. Fatigue of either D or PS muscles develops selectively or together during exhaustive exercise, depending on the recruitment pattern of respiratory muscles. Accessory inspiratory muscles of the neck are less resistant to fatigue compared with the D and PS muscles.

The aim of this study was to assess the effect of inspiratory muscle training (IMT) on resistance to fatigue of the diaphragm (D), parasternal (PS), sternocleidomastoid (SCM) and scalene (SC) muscles in healthy humans during exhaustive exercise. Daily inspiratory muscle strength training was performed for 3 weeks in 10 male subjects (at a pressure threshold load of 60% of maximal inspiratory pressure (MIP) for the first week, 70% of MIP for the second week, and 80% of MIP for the third week). Before and after training, subjects performed an incremental cycle test to exhaustion. Maximal inspiratory pressure and EMG-analysis served as indices of inspiratory muscle fatigue assessment. The before-to-after exercise decreases in MIP and centroid frequency (fc) of the EMG (D, PS, SCM, and SC) power spectrum (P<0.05) were observed in all subjects before the IMT intervention. Such changes were absent after the IMT. The study found that in healthy subjects, IMT results in significant increase in MIP (+18%), a delay of inspiratory muscle fatigue during exhaustive exercise, and a significant improvement in maximal work performance. We conclude that the IMT elicits resistance to the development of inspiratory muscles fatigue during high-intensity exercise.

The global pandemic of a new coronavirus disease (COVID-19) has posed challenges to public health specialists around the world associated with diagnosis, intensive study of epidemiological and clinical features of the coronavirus infection, development of preventive approaches, therapeutic strategies and rehabilitation measures. However, despite the successes achieved in the study of COVID-19 pathogenesis, many aspects that aggravate the severity of the disease and cause high mortality of patients remain unclear. The main clinical manifestation of the new variant of SARS-CoV-2 virus infection is pneumonia with massive parenchymal lesions of lung tissue, diffuse alveolar damage, thrombotic manifestations, disruption of ventilation-perfusion relationships, etc. However, symptoms in patients hospitalized with COVID pneumonia show a broad diversity: the majority has minimal manifestations, others develop severe respiratory failure complicated by acute respiratory distress syndrome (ARDS) with rapidly progressing hypoxemia that leads to high mortality. Numerous clinical data publications report that some COVID pneumonia patients without subjective signs of severe respiratory failure (dyspnea, “air hunger”) have an extremely low saturation level. As a result, there arises a paradoxical condition (called “silent hypoxia” or even “happy hypoxia”) contradicting the very basics of physiology, as it essentially represents a severe life-incompatible hypoxemia which lacks respiratory discomfort. All this raises numerous questions among professionals and has already ignited a discussion in scientific publications concerned with the pathogenesis of COVID-19. Respiratory failure is a complex clinical problem, many aspects of which remain controversial. However, according to the majority of authors, one of the first objective indicators of the clinical sign of respiratory failure are hypoxemia-associated changes in external respiration. This review addresses some possible causes of hypoxemia in COVID-19.

A pressing issue of the day is the identification of therapeutic targets to suppress the “cytokine storm” in COVID-19 complicated by acute respiratory distress syndrome (ARDS) with concomitant hypoxemia. However, the key cytokine and its relative contribution to the pathogenesis of ARDS, which leads to high mortality, are unknown. A comparative assessment of the effect of elevated systemic levels of pro-inflammatory cytokines IL-1β, TNF-1α and IL-6 on the respiratory patterns and survival rate in rats was carried out under progressively increasing acute hypoxia. Increasing hypoxia was simulated by a rebreathing method (from normoxia to apnea). The recorded parameters were the breathing pattern components (tidal volume and respiratory rate), minute ventilation (MV), oxygen saturation, apnea onset time, and posthypoxic survival rate. A comparative analysis was carried out under mild, moderate and severe hypoxia (at F I O 2 = 15, 12 and 8%, respectively). It was shown that increasing hypoxia was accompanied by an acute suppression of the compensatory elevation of MV in rats with increased systemic levels of IL-1β and TNF-1α. By contrast, IL-6 caused an intensive elevation of MV with increasing hypoxia. Acute hypoxia (F I O 2 < 8%), in all experimental series, was accompanied by an impairment of the respiratory rhythm up to the development of apnea. Posthypoxic breathing restoration (survival rate) was 50% with IL-1β and TNF-1α and only 10% with IL-6. The obtained results indicate that the elevated IL-6 level, despite the absence of respiratory disorders at the initial stage of the developing pathologic process, leads to a higher mortality in rats compared to IL-1β and TNF-1α. This allows considering IL-6 as an early prognostic biomarker of a high risk of mortality under severe hypoxemia.

We studied the dependence of parameters of lung volumes and the elastic properties of the lungs on changes in the central hemodynamics occurring in the initial period of passive postural changes in cats. It was found that transition from the horizontal to head-up and head-down tilting was accompanied by opposite hemodynamic changes in the cranial and caudal parts of the body. Changes in lung compliance and functional residual capacity of the lungs were opposite and linearly depended on the intensity of hemodynamic shifts, which indicates passive character of the primary disorders primarily determined by a physical factor, gravity-dependent redistribution of body fluids.

The compensatory responses of the respiratory system to simulated central hypervolemia (CHV) were investigated in 14 normal subjects. The central hypervolemia was caused by a short-time passive head-down tilt (HDT, -30°, 30 min). The results show that CHV increased the mechanical respiratory load and the airway resistance, slowed the inspiratory flow, increased the duration of the inspiratory phase, reduced the respiratory rate, but not changed the minute ventilation. CHV induced a significant rise in inspiratory swings of alveolar pressure (184%), based on the inspiratory occlusion pressure measurement. These changes indicate a compensatory increase in the inspiratory muscle contraction force. A stable level of minute ventilation during CHV was an effect of increased EMG activity of parasternal muscles more than twice (P<0.01). A contribution of the diaphragm and scalene muscles to ventilation during spontaneous breathing in HDT was reduced. An increase of genioglossus contractile activity during HDT contributed to the stabilization of airway patency. These results suggest that a coordinated modulation of inspiratory muscles activity allows preserving a constant level of minute ventilation during a short-time intrathoracic blood volume expansion. The mechanisms of respiratory load compensation seem to be mediated by afferent information from the lung and respiratory muscle receptors and from the segmentary reflexes and intrinsic properties of the muscle fibers.

As a part of the multi-disciplinary "SELENA-T"-2015 Bed Rest Study, we investigated the pattern of inspiratory muscles fatigue in 22 healthy male subjects during incremental exercise test to exhaustion before and after 21 days of hypokinesia evoked by bed rest. Hypokinesia consisted of head-down bed rest (HDBR) at a minus 6° angle, simulating microgravity present on orbiting spacecraft, in 10 subjects. The remaining 12 subjects spent the first 5 days of hypokinesia in HDBR position and the subsequent 16 days in head-up bed rest (HUBR) at a plus 9.6° angle, as a presumed analog of lunar gravity that is six times less than Earth's gravity. Maximal inspiratory pressure (MIP) and electromyograms (EMG) of the diaphragm (D), parasternal (PS), sternocleidomastoid (SCM), and scalene (S) muscles served as indices of inspiratory muscle function. Before both HDBR and HUBR, exercise decreased MIP and centroid frequency (fc) of EMG (D, PS, SCM, and S) power spectrum (p < 0.05). After 3 weeks of HDBR, but not HUBR, inspiratory muscles fatigue was more expressed compared with control (p < 0.05). We conclude that HDBR lowers inspiratory muscles resistance to fatigue during high-intensity exercise while HUBR has no such effect. These changes may limit maximal ventilation and may contribute to exercise intolerance observed after prolonged simulated microgravity. The physiological mechanisms of respiratory muscle dysfunction after HDBR consist primarily of postural effects, and are not due only to hypokinesia.

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