Decrease of resistance to air flow with nasal strips as measured with the airflow perturbation device

BACKGROUND: Nasal strips are used by athletes, people who snore, and asthmatics to ease the burden of breathing. Although there are some published studies that demonstrate higher flow with nasal strips, none had directly measured the effect of the strips on nasal resistance using the airflow perturbation device (APD). The APD is an inexpensive instrument that can measure respiratory resistance based on changes in mouth pressure and rate of airflow. METHOD: This study tested forty-seven volunteers (14 men and 33 women), ranging in age from 17 to 51. Each volunteer was instructed to breathe normally into the APD using an oronasal mask with and without nasal strips. The APD measured respiratory resistance during inhalation, exhalation, and an average of the two. RESULTS: Results of a paired mean t-test comparing nasal strip against no nasal strip were statistically significant at the p = 0.05 level. The Breathe Right™ nasal dilator strips lowered nasal resistance by an average of 0.5 cm H(2)0/Lps from an average nasal resistance of 5.5 cm H(2)0/Lps. CONCLUSIONS: Nasal strips reduce nasal resistance when measured with the APD. The effect is equal during exhalation and during inhalation

Consensus Statement Immunonutrition and Exercise.

In this consensus statement on immunonutrition and exercise, a panel of knowledgeable contributors from across the globe provides a consensus of updated science, including the background, the aspects for which a consensus actually exists, the controversies and, when possible, suggested directions for future research

Inflammatory responses to acute exercise during pulmonary rehabilitation in patients with COPD

Objective Pulmonary rehabilitation is a cornerstone treatment in the management of chronic obstructive pulmonary disease (COPD). Acute bouts of exercise can lead to short bursts of inflammation in healthy individuals. However, it is unclear how COPD patients respond to acute bouts of exercise. This study assessed inflammatory responses to exercise in COPD patients at the start (phase 1) and end (phase 2) of pulmonary rehabilitation. Methods Blood samples were collected before and after an acute exercise bout at the start (phase 1, n = 40) and end (phase 2, n = 27) of pulmonary rehabilitation. The primary outcome was change in fibrinogen concentrations. Secondary outcomes were changes in CRP concentrations, total/differential leukocyte counts, markers of neutrophil activation (CD11b, CD62L and CD66b), and neutrophil subsets (mature, suppressive, immature, progenitor). Results Acute exercise (phase 1) did not induce significant changes in fibrinogen (p = 0.242) or CRP (p = 0.476). Total leukocyte count [mean difference (MD), 0.5 ± 1.1 (109 L−1); p = 0.004], neutrophil count [MD, 0.4 ± 0.8 (109 L−1); p < 0.001], and immature neutrophils (MD, 0.6 ± 0.8%; p < 0.001) increased post-exercise. Neutrophil activation markers, CD11b (p = 0.470), CD66b (p = 0.334), and CD62L (p = 0.352) were not significantly altered post-exercise. In comparison to the start of pulmonary rehabilitation (phase 2), acute exercise at the end of pulmonary rehabilitation led to a greater fibrinogen response (MD, 84 mg/dL (95% CI − 14, 182); p = 0.045). Conclusion An acute bout of exercise does not appear to induce significant alterations in the concentrations of inflammatory mediators but can increase white blood cell subsets post-exercise. A greater fibrinogen response to acute exercise is seen at the end of pulmonary rehabilitation when compared to the start. Further research is required to understand the clinical context of these acute inflammatory responses to exercise

Severe Exercise and Exercise Training Exert Opposite Effects on Human Neutrophil Apoptosis via Altering the Redox Status

Neutrophil spontaneous apoptosis, a process crucial for immune regulation, is mainly controlled by alterations in reactive oxygen species (ROS) and mitochondria integrity. Exercise has been proposed to be a physiological way to modulate immunity; while acute severe exercise (ASE) usually impedes immunity, chronic moderate exercise (CME) improves it. This study aimed to investigate whether and how ASE and CME oppositely regulate human neutrophil apoptosis. Thirteen sedentary young males underwent an initial ASE and were subsequently divided into exercise and control groups. The exercise group (n = 8) underwent 2 months of CME followed by 2 months of detraining. Additional ASE paradigms were performed at the end of each month. Neutrophils were isolated from blood specimens drawn at rest and immediately after each ASE for assaying neutrophil spontaneous apoptosis (annexin-V binding on the outer surface) along with redox-related parameters and mitochondria-related parameters. Our results showed that i) the initial ASE immediately increased the oxidative stress (cytosolic ROS and glutathione oxidation), and sequentially accelerated the reduction of mitochondrial membrane potential, the surface binding of annexin-V, and the generation of mitochondrial ROS; ii) CME upregulated glutathione level, retarded spontaneous apoptosis and delayed mitochondria deterioration; iii) most effects of CME were unchanged after detraining; and iv) CME blocked ASE effects and this capability remained intact even after detraining. Furthermore, the ASE effects on neutrophil spontaneous apoptosis were mimicked by adding exogenous H2O2, but not by suppressing mitochondrial membrane potential. In conclusion, while ASE induced an oxidative state and resulted in acceleration of human neutrophil apoptosis, CME delayed neutrophil apoptosis by maintaining a reduced state for long periods of time even after detraining

APPLICATION OF A NOVEL COLLECTION OF EXHALED BREATH CONDENSATE TO EXERCISE AND WORK PHYSIOLOGY SETTINGS

J.A. Sol, J.C. Quindry, FACSM University of Montana, Missoula, MT Collection of exhaled breath condensate (EBC) is a non-invasive method to obtain biosamples from the lower respiratory tract, an approach amenable to exercise and work physiology applications. Commercially available EBC collection products exist; however, single-use collection devices can be cost-prohibitive, and volumes limit the number of biomarkers that can be examined. PURPOSE: To develop a cost-effective, reproducible methodology for obtaining larger volume EBC samples before and after exercise. METHODS: Participants (26 ± 8 yrs.) completed a 10-min collection of breathing through a novel EBC collection device (N-EBC) while seated and wearing a nose clip. After the initial sample was obtained, a 45-min bout of cycling at 60% VO2max was performed, followed by an immediate post-exercise N-EBC sample collection. In a subset of individuals (n=5), EBC was obtained using both the novel technique and a commercially available EBC collection device (R-EBC) in a randomized fashion. RESULTS: N-EBC volume pre- and post-exercise (2.3±0.8 and 2.6±0.9 mL, respectively) and pH (7.4±0.5 and 7.4±0.5, respectively) were not significantly different. N-EBC Salivary α-Amylase values were below the normal range for saliva samples and comparable to R-EBC (0.08±0.56 and 0.21±0.35 U/mL, respectively). No gender differences were observed (males=10; females=6) for N-EBC comparisons. When normalized for participant body height, device comparisons indicated N-EBC volumes were larger than R-EBC at pre-exercise (+12%) and post-exercise (+48%). Pre-exercise pH was significantly different between the N-EBC and R-EBC trials (7.4±0.5 and 6.3±0.2, respectively;

METABOLIC AND CARDIOVASCULAR ALTERATIONS DURING CRITICAL TRAINING IN WILDLAND FIREFIGHTERS

S.C. Gurney, K.S. Christison, C.M. Williamson-Reisdorph, K.G.S. Tiemessen, J.A. Sol, T.S. Quindry, M.W. Bundle, C.G. Palmer, J.C. Quindry, FACSM, C.L. Dumke, FACSM University of Montana, Missoula, MT Wildland firefighters (WLFF) are confronted with numerous physical and mental stressors. Pre-fire season includes an intense 2- week critical training (CT) period; a preparatory phase that can result in injury, illness, and rhabdomyolysis. PURPOSE: To identify physiologic changes in metabolic biomarkers that occur during 2 weeks of CT in WLFF. METHODS: Eighteen male (29.4±1.1 yr, 182.1±1.6 cm) and three female (26.7±2.6 yr, 169.5±4.2 cm) participants were recruited from a Type I interagency hotshot fire crew and monitored over their 2-week CT. Fitness was assessed via BLM Fitness Challenge (push-ups, pull- ups, sit-ups, 1.5 mi run). Subjects were asked to fast and abstain from caffeine for blood draws on days 1, 4, 8, and 11. Plasma was analyzed for changes in the metabolic profile and oxidative stress markers 3-Nitrotyrosine (3NT), 8-Isoprostane (8ISO), and Lipid Hydroperoxides (LOOH). A one-way repeated measures ANOVA was used to analyze 8ISO, 3NT, and LOOH. Paired samples t-tests were used to compare metabolic biomarkers. Data presented as mean±SEM. RESULTS: CT elicited decrease in total cholesterol (TC) (173.6±12.1 to 153.4±8.6 mg·dL-1, p=0.01), hemoglobin A1c (5.2±0.1 5.1±0.1 %, p=0.003), hemoglobin (15.5±0.4 to 14.3±0.3 g·dL- 1, p=0.003), and estimated plasma volume to (53.8±0.7 to 50.7±1.4 %, p=0.005) from day 1 to 11. No difference was observed in high- density lipoprotein cholesterol. A main effect for time was observed in 8ISO (p- 1). 3NT was significantly elevated from day 4 to day 8 (d4: 2.4±0.6, d8: 2.9±0.6 mg·mL-1). LOOH showed a significant increase across all days (d1: 2.2±0.4, d4: 2.8±0.5, d8: 3.4±0.5, d11: 4.0±0.6 mM). Fitness was significantly correlated with DTC (r=0.58, p=0.046) and D8ISO (r=0.60, p=0.050). CONCLUSION: These data suggest the exertion required of WLFF during CT results in positive alterations to the metabolic profile. The changes in oxidative stress markers may reflect rapid adaptation to the CT stressors. These data suggest that WLFF are able to adapt quickly to the physical stress of CT, where fitness may be a protector of metabolic perturbations. Funded by the US Forest Service 16-CR-11138200-005

SEASONAL CHANGES IN CARDIOVASCULAR FUNCTION, RISK FACTORS, AND OXIDATIVE STRESS OF WILDLAND FIREFIGHTERS

C.M. Williamson-Reisdorph, K.S. Christison, S.C. Gurney, K.G.S. Tiemessen, J.A. Sol, T.S. Quindry, C.G. Palmer, M.W. Bundle, C.L. Dumke, FACSM, J.C. Quindry, FACSM University of Montana, Missoula, MT Wildland firefighters (WLFF) experience extreme physiological strain throughout a typical season due to intense occupational demands and consistent woodsmoke exposure. There is a rationale to indicate that accumulated physiological strain, and oxidative stress, throughout a WLFF season has the potential to negatively alter cardiovascular function and risk factors. PURPOSE: The purpose of the study was to examine the effects of a season on cardiovascular function, risk factors, and markers of oxidative stress in WLFF. METHODS: Fourteen members of a Type I interagency hotshot crew participated in the study (males: n=13, females: n=1, age: 30.1 years ± 4.8). Pre- and post-seasonal resting measurements (May, October) were obtained for heart rate variability (lnRMSSD, lnHF, lnHF, LF:HF), pulse wave velocity (PWV), blood lipid panels (TC, TG, LDL, HDL), metabolic biomarkers (blood glucose, HbA1c), blood pressure (SBP, DBP) and blood oxidative stress (3-nitrotyrosine, 8-isoprostane, lipid hydroperoxides). Paired samples t-tests were used to identify differences among pre- and post- seasonal values. RESULTS: There were no seasonal effects observed on resting heart rate variability, PWV, 3-nitrotyrosine, 8-isoprostane, TC, TG, LDL, blood glucose, SBP, or DBP (p\u3e0.05). A significant reduction occurred in HDL (Pre: 53 mg/dL ± 14, Post: 45 mg/dL ± 18, p=0.043) and both HbA1c (Pre: 5.2% ± 0.2 , Post: 5.3% ± 0.2, p=0.034) and lipid hydroperoxides (Pre: 2.5 ± 0.5, Post: 4.9 ± 0.6, p = 0.003 ) increased from pre- to post-season. CONCLUSION: These data suggest a WLFF season did not impact resting markers of heart rate variability, pulse wave velocity, 3-nitrotyrosine, and 8-isoprostane. Alterations in metabolic biomarkers of cardiovascular risk factors (HDL and HbA1c) and lipid hydroperoxides demonstrate unfavorable seasonal changes, suggesting that the WLFF season may increase cardiovascular risk. Funded by the USFS 16-CR-11138200-005