In elite athletes, exercise-induced bronchoconstriction (EIB) may respond to dietary modification, thereby reducing the need for pharmacologic treatment. Ten elite athletes with EIB and 10 elite athletes without EIB (control subjects) participated in a randomized, double-blind crossover study. Subjects entered the study on their normal diet, and then received either fish oil capsules containing 3.2 g eicosapentaenoic acid and 2.2 g docohexaenoic acid (n-3 polyunsaturated fatty acid [PUFA] diet; n = 5) or placebo capsules containing olive oil (placebo diet; n = 5) taken daily for 3 weeks. Diet had no effect on preexercise pulmonary function in either group or on postexercise pulmonary function in control subjects. However, in subjects with EIB, the n-3 PUFA diet improved postexercise pulmonary function compared with the normal and placebo diets. FEV1 decreased by 3 ± 2% on n-3 PUFA diet, 14.5 ± 5% on placebo diet, and 17.3 ± 6% on normal diet at 15 minutes postexercise. Leukotriene (LT)E4, 9α, 11β-prostaglandin F2, LTB4, tumor necrosis factor–α, and interleukin-1β, all significantly decreased on the n-3 PUFA diet compared with normal and placebo diets and after the exercise challenge. These data suggest that dietary fish oil supplementation has a markedly protective effect in suppressing EIB in elite athletes, and this may be attributed to their antiinflammatory properties.

Normalization of brachial artery flow-mediated dilation (FMD) to individual shear stress area under the curve (peak FMD:SSAUC ratio) has recently been proposed as an approach to control for the large inter-subject variability in reactive hyperemia-induced shear stress; however, the adoption of this approach among researchers has been slow. The present study was designed to further examine the efficacy of FMD normalization to shear stress in reducing measurement variability.

Because the anomalous respiratory characteristics of competitive swimmers have been suggested to be due to inspiratory muscle work, the respiratory muscle and pulmonary function of 30 competitively trained swimmers was assessed at the beginning and end of an intensive 12-week swim training (ST) program. Swimmers (n = 10) combined ST with either inspiratory muscle training (IMT) set at 80% sustained maximal inspiratory pressure (SMIP) with progressively increased work–rest ratios until task failure for 3-days per week (ST + IMT) or ST with sham-IMT (ST + SHAM-IMT, n = 10), or acted as controls (ST only, ST, n = 10). Measures of respiratory and pulmonary function were assessed at the beginning and end of the 12 week study period. There were no significant differences (P > 0.05) in respiratory and pulmonary function between groups (ST + IMT, ST + SHAM-IMT and ST) at baseline and at the end of the 12 week study period. However, within all groups significant increases (P < 0.05) were observed in a number of respiratory and pulmonary function variables at the end of the 12 week study, such as maximal inspiratory and expiratory pressure, inspiratory power output, forced vital capacity, forced expiratory and inspiratory volume in 1-s, total lung capacity and diffusion capacity of the lung. This study has demonstrated that there are no appreciable differences in terms of respiratory changes between elite swimmers undergoing a competitive ST program and those undergoing respiratory muscle training using the flow-resistive IMT device employed in the present study; as yet, the causal mechanisms involved are undefined.

The purpose of this study was to determine if inspiratory muscle training (IMT) alters the oxygen cost of breathing (V̇o_2RM) during voluntary hyperpnea. Sixteen male cyclists completed 6 wk of IMT using an inspiratory load of 50% (IMT) or 15% placebo (CON) of maximal inspiratory pressure (Pi_max). Prior to training, a maximal incremental cycle ergometer test was performed to determine V̇o₂and ventilation (V̇_E) at multiple workloads. Pre- and post-training, subjects performed three separate 4-min bouts of voluntary eucapnic hyperpnea (mimic), matching V̇_Ethat occurred at 50, 75, and 100% of V̇o_{2 max}. Pi_maxwas significantly increased ( P < 0.05) by 22.5 ± 8.7% from pre- to post-IMT and remained unchanged in the CON group. The V̇o_2RMrequired during the mimic trial corresponded to 5.1 ± 2.5, 5.7 ± 1.4, and 11.7% ± 2.5% of the total V̇o₂(V̇o_2T) at ventilatory workloads equivalent to 50, 75, and 100% of V̇o_{2 max}, respectively. Following IMT, the V̇o_2RMrequirement significantly decreased ( P < 0.05) by 1.5% (4.2 ± 1.4% of V̇o_2T) at 75% V̇o_{2 max}and 3.4% (8.1 ± 3.5% of V̇o_2T) at 100% V̇o_{2 max}. No significant changes were shown in the CON group. IMT significantly reduced the O₂cost of voluntary hyperpnea, which suggests that a reduction in the O₂requirement of the respiratory muscles following a period of IMT may facilitate increased O₂availability to the active muscles during exercise. These data suggest that IMT may reduce the O₂cost of ventilation during exercise, providing an insight into mechanism(s) underpinning the reported improvements in whole body endurance performance; however, this awaits further investigation.

The purpose of the study was to determine which of the active constituents of fish oil, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), is most effective in suppressing proinflammatory mediator generation and cytokine expression from LPS-stimulated human asthmatic alveolar macrophages (AMphi). The AMphi were obtained from twenty-one asthmatic adults using fiberoptic bronchoscopy. Cells were pretreated with DMEM, pure EPA, an EPA-rich media (45% EPA/10% DHA), pure DHA, a DHA-rich media (10% EPA/50% DHA) or Lipovenos (n-6 PUFA), and then exposed to Dulbecco's Modified Eagle's Medium (DMEM) (-) or LPS (+). Supernatants were analyzed for leukotriene (LT)B(4), prostaglandin (PG)D(2), tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta production. Detection of TNF-alpha and IL-1beta mRNA expression levels was quantified by reverse transcriptase polymerase chain reaction. 120 microM pure EPA and EPA-rich media significantly (p<0.05) suppressed TNF-alpha and IL-1beta mRNA expression and the production of LTB(4), PGD(2) and TNF-alpha and IL-1beta in LPS-stimulated primary AMphi cells obtained from asthmatic patients to a much greater extent than 120 microM pure DHA and DHA-rich media respectively. This study has shown for the first time that EPA is a more potent inhibitor than DHA of inflammatory responses in human asthmatic AMphi cells.