BACKGROUND: In recent years, there has been increased interest in the subjective quality of life (QoL) of patients with bronchial asthma. QoL is a significant indicator guiding the efforts of professionals caring for patients, especially chronically ill ones. The identification of factors affecting the QoL reported by patients, despite their existing condition, is important and useful to provide multidisciplinary care for these patients.
AIM: To investigate the clinical factors affecting asthma patients' QoL.
METHODS: The study comprised 100 patients (73 female, 27 male) aged 18-84 years (mean age was 45.7) treated in the Allergy Clinic of the Wroclaw Medical University Department and Clinic of Internal Diseases, Geriatrics and Allergology. All asthma patients meeting the inclusion criteria were invited to participate. Data on sociodemographic and clinical variables were collected. In this study, we used medical record analysis and two questionnaires: the Asthma Quality of Life Questionnaire (AQLQ) to assess the QoL of patients with asthma and the Asthma Control Test to measure asthma control.
RESULTS: Active smokers were shown to have a significantly lower QoL in the "Symptoms" domain than nonsmokers (P=0.006). QoL was also demonstrated to decrease significantly as the frequency of asthma exacerbations increased (R=-0.231, P=0.022). QoL in the domain "Activity limitation" was shown to increase significantly along with the number of years of smoking (R=0.404; P=0.004). Time from onset and the dominant symptom of asthma significantly negatively affected QoL in the "Activity limitation" domain of the AQLQ (R=-0.316, P=0.001; P=0.029, respectively). QoL scores in the "Emotional function" and "Environmental stimuli" subscale of the AQLQ decreased significantly as time from onset increased (R=-0.200, P=0.046; R=-0.328, P=0.001, respectively).
CONCLUSION: Patients exhibiting better symptom control have higher QoL scores. Asthma patients' QoL decreases as time from onset increases. A lower QoL is reported by patients who visit allergy clinics more often, and those often hospitalized due to asthma. Smoking also contributes to a lower QoL in asthma patients.
KEYWORDS: bronchial asthma; clinical factors; quality of life
PMID: 27143863 PMCID: PMC4844459 DOI: 10.2147/PPA.S103043

To the Editor:
Dyspnoea is typically the main symptom limiting exercise capacity in patients with chronic obstructive pulmonary disease (COPD) [1–3]. Exertional dyspnoea has been linked to dynamic hyperinflation (DH), when lung expansion critically encroaches upon the inspiratory reserve volume (IRV) [4]. Consequently, patients develop a rapid and shallow breathing pattern, which is energetically opposite to the pattern required to minimise the work of breathing [5]. Furthermore, the restriction of tidal volume (VT) expansion has recently been linked to daily physical activity limitation [6].
Besides mechanical factors, the limitation on VT expansion might also be related to an imbalance between the load and capacity relationship of the inspiratory muscles. The inspiratory muscles are functionally weakened by DH during exercise. Furthermore, they are also forced to contract at higher velocities, whilst working against elevated elastic loads [7, 8]. These factors might exacerbate restriction of VT expansion and exacerbate exertional dyspnoea.
Inspiratory muscle training (IMT) is applied in COPD patients during pulmonary rehabilitation (PR) to improve inspiratory muscle function, exertional dyspnoea, and exercise tolerance [9, 10]. Wanke et al. [10] previously studied the effects of mechanical threshold loading (MTL) IMT in addition to general exercise training and observed additional improvements in exercise capacity and larger VT expansion at peak exercise in the IMT group. We have reported recently that high intensity tapered flow resistive loading (TFRL) IMT resulted in significantly larger increases in respiratory muscle strength and endurance, as well as changes in breathing pattern during loaded breathing, compared with conventional MTL-IMT [11]. We were led to speculate that the specific characteristics of TFRL-IMT might result in beneficial changes in breathing pattern during whole body exercise [11].
We hypothesised that the addition of TRFL-IMT to a PR programme would have the following effects: 1) enhancement of inspiratory muscle function might result in improvements in VT expansion, by providing a training stimulus within the range of IRV; and 2) enhancement of the velocity of shortening of the inspiratory muscles against high resistances might enable patients to shorten their inspiratory time and leave more time for expiration.
This historically controlled study was approved by the University Hospital Leuven's Institutional Review Board (Approval Number ML7489) and registered at www.clinicaltrials.gov (NCT02186340). 25 clinically stable COPD patients with inspiratory muscle weakness (maximal inspiratory pressure (PImax <100% predicted) gave their written informed consent, and were offered IMT during the final 8 weeks of a 12-week multidisciplinary PR programme. A historical control group including patients who participated in an identical PR programme without IMT was recruited from the PR database of the University Hospital Leuven. These patients were individually matched to the participants of the combined intervention for the following baseline characteristics upon entry into the programme: age, sex, pulmonary function, PImax, and exercise capacity.
Patients performed daily high intensity TFRL-IMT (POWERbreathe KH1; HaB International Ltd., Southam, UK) consisting of two cycles of 30 breaths at the highest tolerable intensity according to a recently published protocol [11].
All repeated measures analyses of changes in breathing pattern at different levels of ventilation were performed in SAS 9.3 Software (SAS, Cary, NC, USA). Levels of ventilation were defined as percentages of baseline maximal ventilation (V′Emax) (40, 60, 80, and 100% of peak ventilation of the baseline cycling test). Outcomes between groups were compared with a mixed models analysis. The Tukey method was used to correct post hoc comparisons between groups at cut-off levels of minute ventilation (V′E) for multiple testing.
Patients in the IMT group exhibited significantly larger improvements in PImax in comparison to the control group (29±15 versus 1±12 cmH2O, p<0.001). The IMT group completed 94±5% of sessions (based on data stored by the TFRL devices) and increased their training load from 45±2% to 81±4% of their baseline PImax (p<0.001).
A significantly larger increase in peak exercise cycle capacity was observed in the IMT group, which is consistent with a previous study [10]. Significantly higher levels of peak V′E (3±6 versus −2±7 L·min−1, p=0.013) and peak work rate (13±14 versus 2±12 W, p=0.004) were obtained in the IMT group, but dyspnoea intensity at peak exercise was not different between groups.
At 80% and 100% of baseline V′Emax significant differences in the interaction effects of group by ventilation interaction were found, between groups for both VT and fR, between post intervention and baseline (p=0.047 and p=0.004, respectively) (figure 1). However, the deeper and slower breathing pattern adopted only by participants in the TFRL-IMT group was not accompanied by changes in inspiratory flow rates. The VT/inspiratory time (tI) remained constant, with tI and expiratory time (tE) time increasing proportionately, leaving duty cycle (tI/period of respiratory cycle (tTOT)) unchanged. In the IMT group, there were significant correlations between changes in PImax and changes in breathing pattern (VT (r=0.448, p=0.001), and fR (r=−0.417, p=0.003)) at 80% of baseline V′Emax. This supports a possible causal link between inspiratory muscle weakness and breathing pattern. In contrast with Wanke et al. [10] who observed changes in breathing pattern only at peak exercise, we also observed changes in breathing pattern at iso-ventilation. The larger improvements in breathing pattern that we found at iso-ventilation after IMT, did not, however, translate into larger improvements in breathing pattern at peak exercise. Improvements in peak exercise capacity were comparable between studies. Our second hypothesis was that patients would be able to perform faster contractions with their inspiratory muscles during exercise; resulting in reductions in inspiratory time and leaving more time for expiration, which in turn might ameliorate DH. However, the previously observed increased capacity to perform fast contractions [11], did not result in significant between-group changes in inspiratory flow rates during exercise. This is consistent with previous data from Petrovic et al. [12], who reported a similarly small within group difference (5% as compared to 7% in our study) in VT/tI, which also did not result in a significant between group difference after 8 weeks of inspiratory flow resistive loading (IFRL). It is possible that longer training durations are needed to achieve significance. Another possibility might be that specific breathing retraining strategies, during exercise, in combination with IMT might be needed to teach patients how to use their increased capacity to perform faster inhalations during exercise. Collins et al. [13] previously observed that the combination of ventilation feedback and exercise training changed tI/tTOT, decreased exercise-induced DH, and increased exercise tolerance.
Based on the observed differences in results and differences in training methods in our study in comparison with the studies of Wanke et al. [10], and Petrovic et al. [12], a prospective study would be worthwhile comparing the specific effects of each training method on exercise capacity and breathing pattern head-to-head. In contrast to Wanke et al. [10] who used maximal isometric contractions performed at residual volume and high intensity MTL training, both TFRL-IMT, and IFRL-IMT (used by us and by Petrovic et al. [12], respectively) allow end-inspiratory lung volume (EILV) to enter the IRV, and permit higher inspiratory flow rates (i.e. higher shortening velocities) at high training intensities (i.e. resistances >50% PImax) [11, 12]. According to muscle length (lung volume) and pressure-flow specificity of IMT, this should provide a training stimulus that is more specific to the operating range and the contraction pattern of the inspiratory muscles during exercise, since the largest improvements in function should occur at the volumes over which IMT is performed and larger increases in inspiratory flow are expected with high velocity training [14, 15].
The main limitation of this study is the study design. Since a historical group of patients who participated in an identical PR programme served as control subjects, a prospective randomised controlled study design will be needed to corroborate our findings. It also remains uncertain whether our observed effects on breathing pattern occurred due to a reduction in mechanical restriction on VT expansion (reaching higher EILV) or due to a reduction in DH (reducing end-expiratory lung volume (EELV)). However, it seems most likely that the higher VT would be due to higher EILV, and not to a lowering EELV, because tI increased in proportion to tE and tI/ttot remained unchanged; however, more elaborate measurement techniques will be required to evaluate the effects of IMT on operating lung volumes.
In conclusion, the addition of IMT to a PR programme in COPD patients with inspiratory muscle weakness resulted in a deeper and slower breathing pattern during exercise. Patients could achieve significantly higher peak work rate and exercise ventilation without increasing dyspnoea sensation. Our findings provide encouraging preliminary evidence supporting an additional benefit of adjunctive TFRL-IMT on exercise breathing pattern.
PMID: 26917617 DOI: 10.1183/13993003.01574-2015

Respiratory muscle dysfunction may develop rapidly in critically ill ventilated patients and is associated with increased morbidity, length of intensive care unit stay, costs, and mortality. This review briefly discusses the pathophysiology of respiratory muscle dysfunction in intensive care unit patients and then focuses on strategies that prevent the development of muscle weakness or, if weakness has developed, how respiratory muscle function may be improved. We propose a simple strategy for how these can be implemented in clinical care.
PMID: 27091359 PMCID: PMC4835880 DOI: 10.1186/s13054-016-1280-y

Asthma is a pathological condition comprising of a variety of symptoms which affect the ability to function in daily life. Due to the high prevalence of asthma and associated healthcare costs, it is important to identify low-cost alternatives to traditional pharmacotherapy. One of these low cost alternatives is the use of inspiratory muscle training (IMT), which is a technique aimed at increasing the strength and endurance of the diaphragm and accessory muscles of respiration. IMT typically consists of taking voluntary inspirations against a resistive load across the entire range of vital capacity while at rest. In healthy individuals, the most notable benefits of IMT are an increase in diaphragm thickness and strength, a decrease in exertional dyspnea, and a decrease in the oxygen cost of breathing. Due to the presence of expiratory flow limitation in asthma and exercise-induced bronchoconstriction, dynamic lung hyperinflation is common. As a result of varying operational lung volumes, due in part to hyperinflation, the respiratory muscles may operate far from the optimal portion of the length-tension curve, and thus may be forced to operate against a low pulmonary compliance. Therefore, the ability of these muscles to generate tension is reduced, and for any given level of ventilation, the work of breathing is increased as compared to non-asthmatics. Evidence that IMT is an effective treatment for asthma is inconclusive, due to limited data and a wide variation in study methodologies. However, IMT has been shown to decrease dyspnea, increase inspiratory muscle strength, and improve exercise capacity in asthmatic individuals. In order to develop more concrete recommendations regarding IMT as an effective low-cost adjunct in addition to traditional asthma treatments, we recommend that a standard treatment protocol be developed and tested in a placebo-controlled clinical trial with a large representative sample.
KEYWORDS: Respiratory muscles; asthma treatment; exercise tolerance; lung hyperinflation; pulmonary function
PMID: 27094568 DOI: 10.1080/00913847.2016.1176546

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).
PMID: 14965190 DOI: 10.2165/00007256-200434020-00005