Lung function responses to cold water ingestion: A randomised controlled crossover trial.

This study tested the hypothesis that cold water ingestion would reduce lung function and thereby confound its measurement in a way that is mediated by both temperature and volume. In a randomised crossover trial, 10 healthy adults performed spirometry before and 5, 10, 15, and 30-minutes after consuming one-of-four drinks: 500 mL or 1000 mL refrigerated water (∼2 °C); identical water volumes at ambient temperature (∼18 °C). Ingesting 1000 mL cold water significantly reduced forced vital capacity (FVC) for at least 10 min (mean difference =0.28 L, p < 0.05, d=1.19) and forced expiratory volume in 1 s (FEV1) for at least 15 min (0.20-0.30 L, p < 0.05, d=1.01). Ingesting 500 mL cold water reduced FEV1 for 5 min (0.09 L, p < 0.05, d=1.05). Room-temperature water had no influence on lung function. To avoid confounding the measurement of lung function, we conclude that individuals should avoid drinking cold water, especially in large volumes, immediately prior to a given test.

Calcium ingestion suppresses appetite and produces acute overcompensation of energy intake independent of protein in healthy adults.

BACKGROUND: Prior evidence suggests that high-calcium intake influences postprandial appetite and insulinemia, possibly due to elevated incretins. In vitro and ex vivo models demonstrate that extracellular calcium and protein synergistically enhance secretion of incretins. This is yet to be shown in humans. OBJECTIVE: This study was designed to assess energy intake compensation in response to protein and calcium ingestion. METHODS: Twenty healthy adults (13 men; 7 women) completed 4 trials in a randomized, double-blind crossover design separated by ≥48 h. During the trials, each participant consumed a low-calcium and low-protein control preload [(CON); 4 g and 104 mg, respectively], a high-protein preload (PRO; 29 g), a high-calcium preload (CAL; 1170 mg), or a high-protein and high-calcium preload (PROCAL). Blood samples were collected at baseline and 15, 30, 45, and 60 min after preload ingestion to determine insulin and incretin hormone concentrations. Energy intake was assessed by a homogenous test meal 60 min after the preload. Visual analog scales were completed immediately before blood sampling to assess subjective appetite sensations. RESULTS: Relative to the CON, the PRO produced 100% (95% CI: 85%, 115%) energy compensation, whereas the CAL produced significant overcompensation [118% (95% CI: 104%, 133%)], which was significantly more positive than with the PRO (P < 0.05). The PROCAL resulted in energy compensation of 109% (95% CI: 95%, 123%), which tended to be greater than with the PRO (P = 0.06). The mean difference in appetite sensations relative to the CON was not significantly different between the PRO (-3 mm; 95% CI: -8, 3 mm), CAL (-5 mm; 95% CI: -9, 0 mm), and PROCAL (-5 mm; 95% CI: -10, -1 mm) (P > 0.05). CONCLUSIONS: The addition of protein to a preload results in almost perfect energy compensation, whereas the addition of calcium, with or without protein, suppresses appetite and produces overcompensation of subsequent energy intake. The role of circulating insulin and incretin concentrations in these responses, however, remains unclear. This trial was registered at clinicaltrials.gov as NCT01986036.

Randomized controlled trial of fish oil and montelukast and their combination on airway inflammation and hyperpnea-induced bronchoconstriction.

BACKGROUND: 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. METHODS: 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. RESULTS: While HIB was significantly inhibited (p<0.05) by montelukast, fish oil and combination treatment compared to pre-treatment, there was no significant difference (p>0.017) 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 (p<0.05) in F(E)NO, exhaled breathe condensate pH and cysteinyl-leukotrienes, while the fish oil and combination treatment significantly reduced (p<0.05) urinary 9α, 11ß-prostaglandin F(2) after EVH compared to the usual diet; however, there was no significant difference (p>0.017) in these biomarkers between treatments. CONCLUSION: 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. TRIAL REGISTRATION: ClinicalTrials.gov NCT00676468.