Exhaled nitric oxide after high‐intensity exercise at 2800 m altitude

Stang, Julie; Bråten, Veslemøy; Caspersen, Cecilie; Thorsen, Einar; Stensrud, Trine

doi:10.1111/cpf.12131

Cited by 6 publications

(9 citation statements)

References 25 publications

(57 reference statements)

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“…Data suggest that NO content is decreased in the exhaled air from the volunteers after running on a treadmill at altitudes of 2800 and 180 m for several minutes. Partial pressure of NO significantly decreases at both altitudes (Stang et al, 2014 ). What are the factors limiting NO signaling?…”

Section: Introductionmentioning

confidence: 99%

Physical exercise associated with NO production: signaling pathways and significance in health and disease

Dyakova

Капилевич

Shylko

et al. 2015

Front. Cell Dev. Biol.

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Here we review available data on nitric oxide (NO)-mediated signaling in skeletal muscle during physical exercise. Nitric oxide modulates skeletal myocyte function, hormone regulation, and local microcirculation. Nitric oxide underlies the therapeutic effects of physical activity whereas the pharmacological modulators of NO-mediated signaling are the promising therapeutic agents in different diseases. Nitric oxide production increases in skeletal muscle in response to physical activity. This molecule can alter energy supply in skeletal muscle through hormonal modulation. Mitochondria in skeletal muscle tissue are highly abundant and play a pivotal role in metabolism. Considering NO a plausible regulator of mitochondrial biogenesis that directly affects cellular respiration, we discuss the mechanisms of NO-induced mitochondrial biogenesis in the skeletal muscle cells. We also review available data on myokines, the molecules that are expressed and released by the muscle fibers and exert autocrine, paracrine and/or endocrine effects. The article suggests the presence of putative interplay between NO-mediated signaling and myokines in skeletal muscle. Data demonstrate an important role of NO in various diseases and suggest that physical training may improve health of patients with diabetes, chronic heart failure, and even degenerative muscle diseases. We conclude that NO-associated signaling represents a promising target for the treatment of various diseases and for the achievement of better athletic performance.

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Section: Introductionmentioning

confidence: 99%

Physical exercise associated with NO production: signaling pathways and significance in health and disease

Dyakova

Капилевич

Shylko

et al. 2015

Front. Cell Dev. Biol.

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“…This study was part of a larger study aiming to assess the effect of different environments including altitude (Stang et al ., ) upon FE NO .…”

Section: Methodsmentioning

confidence: 98%

Exhaled nitric oxide concentration in the period of 60 min after submaximal exercise in the cold

Stensrud

Stang

Thorsen

et al. 2014

Clin Physio Funct Imaging

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“…Several studies, including clinical trials, have shown that aerobic exercise produces anti-inflammatory and antioxidant effects in different diseases, such as heart disease [ 25 ], diabetes [ 26 ], Alzheimer’s disease [ 27 ], and Parkinson’s disease [ 28 ], as well as in lung diseases, such as COPD [ 29 – 31 ], ARDS [ 32 , 33 ] and asthma [ 34 – 38 ]. Notably, Vieira et al, (2011) showed that aerobic exercise at low and moderate intensities resulted in the immunomodulation of epithelial cells from the airway of animals with long-term allergic lung inflammation, thus decreasing the oxidative stress and lung inflammation [ 36 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, Camiletti-Moirón et al (2013) demonstrated a deteriorated antioxidant response in the brains of rats trained using high-intensity aerobic exercise [ 42 ]. Regarding lung effects, specifically, Stang et al (2014), showed that after high-intensity exercise, there is a significant reduction in exhaled nitric oxide concentration, known by its inflammatory role into the lungs [ 31 ]. These studies highlighted the anti-inflammatory and pro-inflammatory response, as well as the changes in redox balance, induced by high-intensity aerobic exercise [ 40 – 43 ].…”

Section: Introductionmentioning

confidence: 99%

“…Due to its dual feature and influence on redox balance, we hypothesized that high-intensity swimming could decrease inflammatory markers by decreasing oxidative stress and increasing antioxidants defenses into lungs [ 30 , 31 ]. Thus, in this study a short period high-intensity exercise (swimming) maintained blood lactate at elevated levels between the 10 th and 30 th minute of exercise.…”

Section: Introductionmentioning

confidence: 99%

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Effects of High-Intensity Swimming on Lung Inflammation and Oxidative Stress in a Murine Model of DEP-Induced Injury

et al. 2015

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Studies have reported that exposure to diesel exhaust particles (DEPs) induces lung inflammation and increases oxidative stress, and both effects are susceptible to changes via regular aerobic exercise in rehabilitation programs. However, the effects of exercise on lungs exposed to DEP after the cessation of exercise are not clear. Therefore, the aim of this study was to evaluate the effects of high-intensity swimming on lung inflammation and oxidative stress in mice exposed to DEP concomitantly and after exercise cessation. Male Swiss mice were divided into 4 groups: Control (n = 12), Swimming (30 min/day) (n = 8), DEP (3 mg/mL—10 μL/mouse) (n = 9) and DEP+Swimming (n = 8). The high-intensity swimming was characterized by an increase in blood lactate levels greater than 1 mmoL/L between 10th and 30th minutes of exercise. Twenty-four hours after the final exposure to DEP, the anesthetized mice were euthanized, and we counted the number of total and differential inflammatory cells in the bronchoalveolar fluid (BALF), measured the lung homogenate levels of IL-1β, TNF-α, IL-6, INF-ϫ, IL-10, and IL-1ra using ELISA, and measured the levels of glutathione, non-protein thiols (GSH-t and NPSH) and the antioxidant enzymes catalase and glutathione peroxidase (GPx) in the lung. Swimming sessions decreased the number of total cells (p<0.001), neutrophils and lymphocytes (p<0.001; p<0.05) in the BALF, as well as lung levels of IL-1β (p = 0.002), TNF-α (p = 0.003), IL-6 (p = 0.0001) and IFN-ϫ (p = 0.0001). However, the levels of IL-10 (p = 0.01) and IL-1ra (p = 0.0002) increased in the swimming groups compared with the control groups, as did the CAT lung levels (p = 0.0001). Simultaneously, swimming resulted in an increase in the GSH-t and NPSH lung levels in the DEP group (p = 0.0001 and p<0.002). We concluded that in this experimental model, the high-intensity swimming sessions decreased the lung inflammation and oxidative stress status during DEP-induced lung inflammation in mice.

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Exhaled nitric oxide after high‐intensity exercise at 2800 m altitude

Cited by 6 publications

References 25 publications

Physical exercise associated with NO production: signaling pathways and significance in health and disease

Physical exercise associated with NO production: signaling pathways and significance in health and disease

Exhaled nitric oxide concentration in the period of 60 min after submaximal exercise in the cold

Effects of High-Intensity Swimming on Lung Inflammation and Oxidative Stress in a Murine Model of DEP-Induced Injury

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