Randomized Controlled Trial of Fish Oil and Montelukast and Their Combination on Airway Inflammation and Hyperpnea-Induced Bronchoconstriction

Both fish oil and montelukast have been shown to reduce the severity of exercise-induced bronchoconstriction (EIB). The purpose of this study was to compare the effects of fish oil and montelukast, alone and in combination, on airway inflammation and bronchoconstriction induced by eucapnic voluntary hyperpnea (EVH) in asthmatics. In this model of EIB, twenty asthmatic subjects with documented hyperpnea-induced bronchoconstriction (HIB) entered a randomized double-blind trial. All subjects entered on their usual diet (pre-treatment, n = 20) and then were randomly assigned to receive either one active 10 mg montelukast tablet and 10 placebo fish oil capsules (n = 10) or one placebo montelukast tablet and 10 active fish oil capsules totaling 3.2 g EPA and 2.0 g DHA (n = 10) taken daily for 3-wk. Thereafter, all subjects (combination treatment; n = 20) underwent another 3-wk treatment period consisting of a 10 mg active montelukast tablet or 10 active fish oil capsules taken daily. While HIB was significantly inhibited (p0.017) between treatment groups; percent fall in forced expiratory volume in 1-sec was −18.4±2.1%, −9.3±2.8%, −11.6±2.8% and −10.8±1.7% on usual diet (pre-treatment), fish oil, montelukast and combination treatment respectively. All three treatments were associated with a significant reduction (p0.017) in these biomarkers between treatments. While fish oil and montelukast are both effective in attenuating airway inflammation and HIB, combining fish oil with montelukast did not confer a greater protective effect than either intervention alone. Fish oil supplementation should be considered as an alternative treatment for EIB

Inspiratory loading and limb locomotor and respiratory muscle deoxygenation during cycling exercise

The aim of this study was to determine the effect of inspiratory loading on limb locomotor (LM) and respiratory muscle (RM) deoxygenation ([deoxy (Hb+Mb)]) using NIRS during constant-power cycling exercise. Sixteen, male cyclists completed three, 6-min trials. The intensity of the first 3-min of each trial was equivalent to ~80% V(O(2max)) (EX(80%)); during the final 3-min, subjects received an intervention consisting of either moderate inspiratory loading (Load(mod)), heavy inspiratory loading (Load(heavy)), or maximal exercise (Load(EX)). Load(heavy) significantly increased LM [deoxy(Hb+Mb)] from 12.2±9.0 μm during EX(80%) to 15.3±11.7 μm, and RM [deoxy(Hb+Mb)] from 5.9±3.6 μm to 9.5±6.6 μm. LM and RM [deoxy(Hb+Mb)] were significantly increased from EX(80%) to Load(EX); 12.8±9.1 μm to 16.4±10.3 μm and 5.9±2.9 μm to 11.0±6.4 μm, respectively. These data suggest an increase in respiratory muscle load increases muscle deoxy(Hb+Mb) and thus may indicate a reduction in oxygen delivery and/or increased oxygen extraction by the active muscles

Inspiratory muscle training lowers the oxygen cost of voluntary hyperpnea

The purpose of this study was to determine if inspiratory muscle training (IMT) alters the oxygen cost of breathing (VO(2RM)) during voluntary hyperpnea. Sixteen male cyclists completed 6 wks of inspiratory muscle training (IMT) using an inspiratory load of 50% (IMT) or 15% [placebo] (CON) of maximal inspiratory pressure (PImax). Prior to training, a maximal incremental cycle ergometer test was performed to determine VO(2) and ventilation (V(E)) at multiple workloads. Pre- and post- training, subjects performed three separate 4-min bouts of voluntary eucapnic hyperpnea (mimic), matching V(E) that occurred at 50%, 75% and 100% of VO(2max). PI(max) was significantly increased (p0.05) were shown in the CON group. IMT significantly reduced the O(2) cost of voluntary hyperpnea, which suggests that a reduction in the O(2) requirement of the respiratory muscles following a period of IMT may facilitate increased O(2) availability to the active muscles during exercise. These data may provide an insight into the mechanism(s) underpinning the reported improvements in endurance performance following IMT, however, this awaits further investigation

Effect of Inspiratory Muscle Training on Exercise Tolerance in Asthmatic Individuals

The aim of this study was to determine the effects of inspiratory muscle training (IMT) on exercise tolerance, inspiratory muscle fatigue, and the perception of dyspnea in asthmatic individuals. Using a matched double-blind placebo-controlled design, 15 clinically diagnosed asthmatic individuals underwent either 6 wk of IMT (n = 7) consisting of 30 breaths twice daily at 50% maximum inspiratory pressure (PImax) or sham-IMT (placebo; PLA, n = 8) consisting of 60 breaths daily at 15% PImax. Time to the limit of exercise tolerance (Tlim) was assessed using constant-power output (70% peak power) cycle ergometry. Inspiratory muscle fatigue was determined by comparing the pre- to postexercise reduction in PImax. Dyspnea during the Tlim test was evaluated at 2-min intervals using the Borg CR-10 scale. There were no significant changes (P > 0.05) in Tlim, inspiratory muscle fatigue, or perception of dyspnea in the PLA group after the intervention. In contrast, in the IMT group, PImax increased by 28%, and Tlim increased by 16% (P < 0.05). Dyspnea during exercise was also reduced significantly by 16% (P < 0.05). The exercise-induced fall in PImax was reduced from 10% before IMT to 6% after IMT (P < 0.05), despite the longer Tlim. Pulmonary function remained unchanged in both the IMT and PLA groups. These data suggest that IMT attenuates inspiratory muscle fatigue, reduces the perception of dyspnea, and increases exercise tolerance. These findings suggest that IMT may be a helpful adjunct to asthma management that has the potential to improve participation and adherence to exercise training in this group. However, the perception of breathlessness is also an important signal of bronchoconstriction, and thus, caution should be exercised if this symptom is abnormally low