Comparison of Two Fluid Replacement Protocols During a 20-km Trail Running Race in the Heat.

Lopez, RM, Casa, DJ, Jensen, K, Stearns, RL, DeMartini, JK, Pagnotta, KD, Roti, MW, Armstrong, LE, and Maresh, CM. Comparison of two fluid replacement protocols during a 20-km trail running race in the heat. J Strength Cond Res 30(9): 2609-2616, 2016-Proper hydration is imperative for athletes striving for peak performance and safety, however, the effectiveness of various fluid replacement strategies in the field setting is unknown. The purpose of this study was to investigate how two hydration protocols affect physiological responses and performance during a 20-km trail running race. A randomized, counter-balanced, crossover design was used in a field setting (mean ± SD: WBGT 28.3 ± 1.9° C). Well-trained male (n = 8) and female (n = 5) runners (39 ± 14 years; 175 ± 9 cm; 67.5 ± 11.1 kg; 13.4 ± 4.6% BF) completed two 20-km trail races (5 × 4-km loop) with different water hydration protocols: (a) ad libitum (AL) consumption and (b) individualized rehydration (IR). Data were analyzed using repeated measures ANOVA. Paired t-tests compared pre-race-post-race measures. Main outcome variables were race time, heart rate (HR), gastrointestinal temperature (TGI), fluid consumed, percent body mass loss (BML), and urine osmolality (Uosm). Race times between groups were similar. There was a significant condition × time interaction (p = 0.048) for HR, but TGI was similar between conditions. Subjects replaced 30 ± 14% of their water losses in AL and 64 ± 16% of their losses in IR (p < 0.001). Ad libitum trial experienced greater BML (-2.6 ± 0.5%) compared with IR (-1.3 ± 0.5%; p < 0.001). Pre-race to post-race Uosm differences existed between AL (-273 ± 146 mOsm) and IR (-145 ± 215 mOsm, p = 0.032). In IR, runners drank twice as much fluid than AL during the 20-km race, leading to > 2% BML in AL. Ad libitum drinking resulted in 1.3% greater BML over the 20-km race, which resulted in no thermoregulatory or performance differences from IR.

Differential elemental distribution of retained particles along the respiratory tract.

CONTEXT: Prolonged exposure to ambient particles is associated with premature mortality due to cardio-respiratory diseases and lung cancer. The size and composition of these particles determine their toxicity, which is aggravated by their long-term retention in the lungs. OBJECTIVE: To compare the elemental profile of particles retained along the bronchial tree and lymph nodes by combining laser capture microdissection (LCM) and elemental composition analysis through energy dispersive x-ray (EDX) and scanning electron microscopy (SEM). MATERIAL AND METHODS: Twenty-four right lung middle lobes from autopsied cases were obtained from two cities with different pollution backgrounds. Lung samples were collected from three distinct sites within the lung at the time of autopsy: peribronchial tissue, peripheral parenchyma and hilar lymph nodes. Areas of potentially increased particle deposition were microdissected using LCM and analyzed for elemental composition through EDX "allied" with SEM. RESULTS: Elemental analyses of the particles retained along the bronchial tree showed two groups of distribution: peribronchiolar or lymph node deposition. The elemental profile of peribronchial areas were significantly different between the two cities and were better discriminators of past air pollution exposure. CONCLUSION: Our data suggest that particle uptake varies along the bronchial tree and human lung tissue retains particles indicative of regional air pollution background.

Concentrated ambient air particles induce vasoconstriction of small pulmonary arteries in rats.

The objective of this study was to determine whether short-term exposures to concentrated ambient particles (CAPs) alter the morphology of small pulmonary arteries in normal rats and rats with chronic bronchitis (CB). Sprague-Dawley male rats were exposed to CAPs, using the Harvard Ambient Particle Concentrator, or to particle-free air (sham) under identical conditions during 3 consecutive days (5 hr/day) in six experimental sets. CB was induced by exposure to 276 +/- 9 ppm of sulfur dioxide (5 hr/day, 5 days/week, 6 weeks). Physicochemical characterization of CAPs included measurements of particle mass, size distribution, and composition. Rats were sacrificed 24 hr after the last CAPs exposure. Histologic slides were prepared from random sections of lung lobes and coded for blinded analysis. The lumen/wall area (L/W) ratio was determined morphometrically on transverse sections of small pulmonary arteries. When all animal data (normal and CB) were analyzed together, the L/W ratios decreased as concentrations of fine particle mass, silicon, lead, sulfate, elemental carbon, and organic carbon increased. In separate univariate analyses of animal data, the association for sulfate was significant only in normal rats, whereas silicon was significantly associated in both CB and normal rats. In multivariate analyses including all particle factors, the association with silicon remained significant. Our results indicate that short-term CAPs exposures (median, 182.75 micro g/m3; range, 73.50-733.00 micro g/m3) can induce vasoconstriction of small pulmonary arteries in normal and CB rats. This effect was correlated with specific particle components and suggests that the pulmonary vasculature might be an important target for ambient air particle toxicity.

Lung inflammation induced by concentrated ambient air particles is related to particle composition.

The objectives of this study were (1) to determine whether short-term exposures to concentrated air particles (CAPs) cause pulmonary inflammation in normal rats and rats with chronic bronchitis (CB); (2) to identify the site within the lung parenchyma where CAPs-induced inflammation occurs; and (3) to characterize the component(s) of CAPs that is significantly associated with the development of the inflammatory reaction. Four groups of animals were studied: (1) air treated, filtered air exposed (air-sham); (2) sulfur dioxide treated (CB), filtered air exposed (CB-sham); (3) air treated, CAPs exposed (air-CAPs); and (4) sulfur dioxide treated, CAPs exposed (CB-CAPs). CB and normal rats were exposed by inhalation either to filtered air or CAPs during 3 consecutive days (5 hours/day). Pulmonary inflammation was assessed by bronchoalveolar lavage (BAL) and by measuring the numerical density of neutrophils (Nn) in the alveolar walls at the bronchoalveolar junction and in more peripheral alveoli. CAPs (as a binary exposure term) and CAPs mass (in regression correlations) induced a significant increase in BAL neutrophils and in normal and CB animals. Nn in the lung tissue significantly increased with CAPs in normal animals only. Greater Nn was observed in the central compared with peripheral regions of the lung. A significant dose-dependent association was found between many CAPs components and BAL neutrophils or lymphocytes, but only vanadium and bromine concentrations had significant associations with both BAL neutrophils and Nn in CAPs-exposed groups analyzed together. Results demonstrate that short-term exposures to CAPs from Boston induce a significant inflammatory reaction in rat lungs, with this reaction influenced by particle composition.