Distinguishing science from pseudoscience in commercial respiratory interventions: an evidence-based guide for health and exercise professionals.

Respiratory function has become a global health priority. Not only is chronic respiratory disease a leading cause of worldwide morbidity and mortality, but the COVID-19 pandemic has heightened attention on respiratory health and the means of enhancing it. Subsequently, and inevitably, the respiratory system has become a target of the multi-trillion-dollar health and wellness industry. Numerous commercial, respiratory-related interventions are now coupled to therapeutic and/or ergogenic claims that vary in their plausibility: from the reasonable to the absurd. Moreover, legitimate and illegitimate claims are often conflated in a wellness space that lacks regulation. The abundance of interventions, the range of potential therapeutic targets in the respiratory system, and the wealth of research that varies in quality, all confound the ability for health and exercise professionals to make informed risk-to-benefit assessments with their patients and clients. This review focuses on numerous commercial interventions that purport to improve respiratory health, including nasal dilators, nasal breathing, and systematized breathing interventions (such as pursed-lips breathing), respiratory muscle training, canned oxygen, nutritional supplements, and inhaled L-menthol. For each intervention we describe the premise, examine the plausibility, and systematically contrast commercial claims against the published literature. The overarching aim is to assist health and exercise professionals to distinguish science from pseudoscience and make pragmatic and safe risk-to-benefit decisions.

Effects of inspiratory muscle training on respiratory muscle electromyography and dyspnea during exercise in healthy men.

Inspiratory muscle training (IMT) has consistently been shown to reduce exertional dyspnea in health and disease; however, the physiological mechanisms remain poorly understood. A growing body of literature suggests that dyspnea intensity can be explained largely by an awareness of increased neural respiratory drive, as measured indirectly using diaphragmatic electromyography (EMGdi). Accordingly, we sought to determine whether improvements in dyspnea following IMT can be explained by decreases in inspiratory muscle electromyography (EMG) activity. Twenty-five young, healthy, recreationally active men completed a detailed familiarization visit followed by two maximal incremental cycle exercise tests separated by 5 wk of randomly assigned pressure threshold IMT or sham control (SC) training. The IMT group (n = 12) performed 30 inspiratory efforts twice daily against a 30-repetition maximum intensity. The SC group (n = 13) performed a daily bout of 60 inspiratory efforts against 10% maximal inspiratory pressure (MIP), with no weekly adjustments. Dyspnea intensity was measured throughout exercise using the modified 0-10 Borg scale. Sternocleidomastoid and scalene EMG was measured using surface electrodes, whereas EMGdi was measured using a multipair esophageal electrode catheter. IMT significantly improved MIP (pre: -138 ± 45 vs. post: -160 ± 43 cmH2O, P < 0.01), whereas the SC intervention did not. Dyspnea was significantly reduced at the highest equivalent work rate (pre: 7.6 ± 2.5 vs. post: 6.8 ± 2.9 Borg units, P < 0.05), but not in the SC group, with no between-group interaction effects. There were no significant differences in respiratory muscle EMG during exercise in either group. Improvements in dyspnea intensity ratings following IMT in healthy humans cannot be explained by changes in the electrical activity of the inspiratory muscles.NEW & NOTEWORTHY Exertional dyspnea intensity is thought to reflect an increased awareness of neural respiratory drive, which is measured indirectly using diaphragmatic electromyography (EMGdi). We examined the effects of inspiratory muscle training (IMT) on dyspnea, EMGdi, and EMG of accessory inspiratory muscles. IMT significantly reduced submaximal dyspnea intensity ratings but did not change EMG of any inspiratory muscles. Improvements in exertional dyspnea following IMT may be the result of nonphysiological factors or physiological adaptations unrelated to neural respiratory drive.

Inspiratory muscle training enhances pulmonary O(2) uptake kinetics and high-intensity exercise tolerance in humans.

Fatigue of the respiratory muscles during intense exercise might compromise leg blood flow, thereby constraining oxygen uptake (Vo(2)) and limiting exercise tolerance. We tested the hypothesis that inspiratory muscle training (IMT) would reduce inspiratory muscle fatigue, speed Vo(2) kinetics and enhance exercise tolerance. Sixteen recreationally active subjects (mean + or - SD, age 22 + or - 4 yr) were randomly assigned to receive 4 wk of either pressure threshold IMT [30 breaths twice daily at approximately 50% of maximum inspiratory pressure (MIP)] or sham treatment (60 breaths once daily at approximately 15% of MIP). The subjects completed moderate-, severe- and maximal-intensity "step" exercise transitions on a cycle ergometer before (Pre) and after (Post) the 4-wk intervention period for determination of Vo(2) kinetics and exercise tolerance. There were no significant changes in the physiological variables of interest after Sham. After IMT, baseline MIP was significantly increased (Pre vs. Post: 155 + or - 22 vs. 181 + or - 21 cmH(2)O; P < 0.001), and the degree of inspiratory muscle fatigue was reduced after severe- and maximal-intensity exercise. During severe exercise, the Vo(2) slow component was reduced (Pre vs. Post: 0.60 + or - 0.20 vs. 0.53 + or - 0.24 l/min; P < 0.05) and exercise tolerance was enhanced (Pre vs. Post: 765 + or - 249 vs. 1,061 + or - 304 s; P < 0.01). Similarly, during maximal exercise, the Vo(2) slow component was reduced (Pre vs. Post: 0.28 + or - 0.14 vs. 0.18 + or - 0.07 l/min; P < 0.05) and exercise tolerance was enhanced (Pre vs. Post: 177 + or - 24 vs. 208 + or - 37 s; P < 0.01). Four weeks of IMT, which reduced inspiratory muscle fatigue, resulted in a reduced Vo(2) slow-component amplitude and an improved exercise tolerance during severe- and maximal-intensity exercise. The results indicate that the enhanced exercise tolerance observed after IMT might be related, at least in part, to improved Vo(2) dynamics, presumably as a consequence of increased blood flow to the exercising limbs.

Acute and chronic responses of the upper airway to inspiratory loading in healthy awake humans: an MRI study.

We assessed upper airway responses to acute and chronic inspiratory loading. In Experiment I, 11 healthy subjects underwent T(2)-weighted magnetic resonance imaging (MRI) of upper airway dilator muscles (genioglossus and geniohyoid) before and up to 10 min after a single bout of pressure threshold inspiratory muscle training (IMT) at 60% maximal inspiratory mouth pressure (MIP). T(2) values for genioglossus and geniohyoid were increased versus control (p<0.001), suggesting that these airway dilator muscles are activated in response to acute IMT. In Experiment II, nine subjects underwent 2D-Flash sequence MRI of the upper airway during quiet breathing and while performing single inspirations against resistive loads (10%, 30% and 50% MIP); this procedure was repeated after 6 weeks of IMT. Lateral narrowing of the upper airway occurred at all loads, whilst anteroposterior narrowing occurred at the level of the laryngopharynx at loads > or =30% MIP. Changes in upper airway morphology and narrowing after IMT were undetectable using MRI.

Dyspnoea in health and obstructive pulmonary disease : the role of respiratory muscle function and training.

A consistent finding of recent research on respiratory muscle training (RMT) in healthy humans has been an attenuation of respiratory discomfort (dyspnoea) during exercise. We argue that the neurophysiology of dyspnoea can be explained in terms of Cambell's paradigm of length-tension inappropriateness. In the context of this paradigm, changes in the contractile properties of the respiratory muscles modify the intensity of dyspnoea predominantly by changing the required level of motor outflow to these respiratory muscles. Thus, factors that impair the contractile properties of the respiratory muscles (e.g. the pattern of tension development, functional weakening and fatigue) have the potential to increase the intensity of dyspnoea, while factors that improve the contractile properties of these respiratory muscles (e.g. RMT) have the potential to reduce the intensity of dyspnoea. In patients with obstructive pulmonary disease, functional weakening of the inspiratory muscles in response to dynamic lung hyperinflation appears to be a central component of dyspnoea. A decrease in the intensity of respiratory effort sensation (during exercise and loaded breathing) has been observed in both healthy individuals and patients with obstructive pulmonary disease after RMT. We conclude that RMT has the potential to reduce the severity of dyspnoea in healthy individuals and in patients with obstructive pulmonary disease, and that this probably occurs via a reduction in the level of motor outflow. Further work is required to clarify the role of RMT in the management of other disease conditions in which the function of the respiratory muscles is impaired, or the loads that they must overcome are elevated (e.g. cardiorespiratory and neuromuscular disorders).

Specificity and reversibility of inspiratory muscle training.

PURPOSE: The purpose of this study was to evaluate the pressure-flow specificity of adaptations to inspiratory muscle training (IMT), in addition to the temporal effects of detraining and reduced frequency of training upon these adaptations. METHODS: Twenty-four healthy subjects were assigned randomly to one of four groups (A: low-flow-high-pressure IMT; B: high-flow-low-pressure IMT; C: intermediate flow-pressure IMT; and D: no IMT). Subjects performed IMT 6 d.wk(-1) for 9 wk, and inspiratory muscle function was evaluated at baseline and every 3 wk. Groups A, B, and C were then assigned randomly to either a maintenance group (M) (IMT 2 d.wk(-1) ) or a detraining group (DT) (no IMT). Inspiratory muscle function was reassessed at 9 and 18 wk post-IMT. RESULTS: At 9 wk, group A exhibited the largest increase in pressure, B a large increase in flow, C more uniform increases in pressure and flow, and D no changes in pressure or flow. Maximum inspiratory muscle power increased in groups A, B, and C by 48 +/- 3%, 25 +/- 3%, and 64 +/- 3%, respectively (mean +/- SEM, P < or = 0.01). Maximum rate of pressure development increased in groups A, B, and C by 59 +/- 1%, 10 +/- 1%, and 29 +/- 1%, respectively ( P < or = 0.01). A decrease in inspiratory muscle function was observed at 9 wk post-IMT in DT. Inspiratory muscle function plateaued between 9 and 18 wk but remained above pre-IMT values. Group M retained the improvements in inspiratory muscle function. CONCLUSION: These data support the notion of pressure-flow specificity of IMT. Detraining resulted in small but significant reductions in inspiratory muscle function. Reducing training frequency by two thirds allowed for the maintenance of inspiratory muscle function up to 18 wk post-IMT.

Effects of inspiratory muscle training on time-trial performance in trained cyclists.

We evaluated the effects of specific inspiratory muscle training on simulated time-trial performance in trained cyclists. Using a double-blind, placebo-controlled design, 16 male cyclists (VO2max = 64 +/- 2 ml x kg(-1) x min(-1); mean +/- s(x)) were assigned at random to either an experimental (pressure-threshold inspiratory muscle training) or sham-training control (placebo) group. Pulmonary function, maximum dynamic inspiratory muscle function and the physiological and perceptual responses to maximal incremental cycling were assessed. Simulated time-trial performance (20 and 40 km) was quantified as the time to complete pre-set amounts of work. Pulmonary function was unchanged after the intervention, but dynamic inspiratory muscle function improved in the inspiratory muscle training group (P < or = 0.05). After the intervention, the inspiratory muscle training group experienced a reduction in the perception of respiratory and peripheral effort (Borg CR10: 16 +/- 4% and 18 +/- 4% respectively; compared with placebo, P < or = 0.01) and completed the simulated 20 and 40 km time-trials faster than the placebo group [66 +/- 30 and 115 +/- 38 s (3.8 +/- 1.7% and 4.6 +/- 1.9%) faster respectively; P = 0.025 and 0.009]. These results support evidence that specific inspiratory muscle training attenuates the perceptual response to maximal incremental exercise. Furthermore, they provide evidence of performance enhancements in competitive cyclists after inspiratory muscle training.