(a).
Author, year | Aim | Sample's characteristics | Exercise protocols | Samples obtained | Oxidative or inflammatory main results |
---|---|---|---|---|---|
Adachi et al. 1997 [50] | eNO and VNO in patients with CHF during exercise∗ | CHF patients and healthy control subjects (C) | Maximal incremental cycloergometer test in CHF patients (10 W/min) and C (25 W/min) until exhaustion | EB | DE: ↑ VNO during exercise peak in C |
| |||||
Agostoni and Bussotti 2003 [51] | Correlation between eNO and lung mechanics during exercise in CHF∗ | CHF patients and healthy control subjects (C) | 25-W constant workload exercise cycle-ergometry test | EB | DE: ↓ eNO during 3rd and 5th minutes of exercise in C |
| |||||
Araneda et al. 2005 [46] | Lung oxidative damage from exercise at a medium altitude∗ | Highly trained mountain bikers | Three repetitions of cycle-ergometries of 1 min at maximum intensity in 670 and 2160 MASL with breaks of 1 min | EBC and serum | PE: ↑ [MDA] in EBC, with no changes in serum at 2160 MASL |
| |||||
Araneda et al. 2012 [52] | Duration of a long distance exercise on pulmonary oxidative damage | Amateur runners | Urban 10 km (~53 min), 21 km (~101 min), and 42.2 km races (~246 min) | EBC | PE: ↑ [H2O2] and ↑ [NO2 −] in 21 km and 42.2 km races and no changes in [MDA]; there was a tendency to ↓ of pH |
| |||||
Araneda et al. 2014 [53] | Pulmonary oxidative damage in long distance exercise | Healthy active subjects | 10 km race in outdoor athletic track (~50 min) | EBC | PE: ↑ [H2O2], ↑ [NO2 −]EBC/[NO2 −]Plasma with no changes in the [MDA]; there was a tendency to ↑ of pH |
| |||||
Bikov et al. 2010 [54] | Changes in [Cys-LTs] caused by exercise in asthmatic patients | Nonsmoking asthmatic patients (A) and nonsmoking healthy control subjects (C) | Race on treadmill at a speed and slope maintaining 80–90% HRmax (220 − age), which was regulated in 2 min and then maintained during 6 min | EBC | PE: with no changes in [Cys-LTs] in C, but ↑ in A |
| |||||
Bikov et al. 2014 [55] | Changes in EBCpH during EIB in asthmatic patients∗ | Asthmatics, who reported breathlessness following exercise, and healthy control subjects (C) | Exercise challenge test on a treadmill (details were not described by authors) | EBC and EB | PE: no change of pH in EBC in C |
| |||||
Bonsignore et al. 2001 [56] | Endurance exercise on inflammatory cells in AWs and eNO | Amateur runners | Marathon race (~179 min) | IS and EB | PE: ↑ PMN in IS and ↑ eNO in EB |
| |||||
Bonsignore et al. 2003 [57] | Swimming on inflammatory cells and eNO in the AWs | Swimmers (S) and healthy control subjects (C) | Swimming of 5 km only in the swimmers group, an open pool series (~70 min) and other series in the sea (~54 min) | IS and EB | B: >PMN and <MØ in the IS of S versus C PE: ↑ eosinophils, ↑ lymphocytes, and ↓ MØ in the sea versus swimming pool; eNO was > in the sea in comparison to swimming pool |
| |||||
Carbonnelle et al. 2008 [58] | eNO after swimming sessions∗ | Trained healthy young people, not trained with swimming | Swimming in 2 sessions of 45 min (~1300 m), in a disinfected pool with [NaClO] and another sanitized with electrical process | EB | PE: ↑ eNO only in sanitized pool |
| |||||
Chimenti et al. 2009 [40] | Inflammation of the AWs in urban races in different climatic seasons∗ | Amateur runners | 21 km race in autumn (~89.1 min), 12 km race in winter (~46.1 min), and 10 km race in summer (~35.4 min) | IS | B: ↑ PMNs with ↑ [TNF-α] and ↑ [IL-8] PE: PMNs tended to ↑ |
| |||||
Chimenti et al. 2010 [5] | Damage and inflammation of the lung epithelium in a long distance exercise | Amateur runners and healthy control subjects | 20 km outdoor races (~90 min) | IS and serum | PE: ↑ [IL-8] in IS and ↑ CC16 in serum |
| |||||
Chirpaz-Oddou et al. 1997 [59] | eNO and VNO during exercise | Healthy control and trained subjects | Incremental cycloergometry to exhaustion with 5 min of passive recovery in sedentary subjects (♂ ~30 min and ♀ ~20 min) and trained subjects (~14 min) | EB | DE: ↓ eNO progressive with ↑ exercise intensity from 65% VO2max and ↑ VNO with the ↑ of the intensity of exercise > 30 W in all subjects |
| |||||
Clini et al. 2000 [60] | To evaluate eNO during exercise in patients with stable COPD∗ | COPD patients and healthy control subjects (C) | Maximal cycle-ergometry test (cadence: 60 cycles/min and load: 10 W/min) until exhaustion | EB | DE: ↓ eNO at peak exercise and ↑ VNO in C |
| |||||
De Gouw et al. 2001 [61] | Role of eNO in the airway response to exercise by using L-NMMA, L-arginine, or placebo as pretreatment to exercise challenge∗ | Asthmatic patients and healthy control subjects (C) | Cycle-ergometry for 6 min using dry air, while ventilation was kept constant in 40–50% of his or her predicted maximal voluntary ventilation (35 × FEV1) | EB | PE: ↑ eNO 30 min after exercise in C |
| |||||
Denguezli-Bouzgarrou et al. 2006 [62] | Endurance exercise and inflammatory cells of the AWs | Long-distance runners | Races on treadmill at 80% of MAS (~60 min) | IS | PE: ↑ PMNs, ↓ MØ, and ↑ lymphocytes |
| |||||
Denguezli-Bouzgarrou et al. 2007 [63] | Inflammatory mediators, cellular composition in AWs, and acute exercise during a sports season | Long-distance runners | Race at 80% MAS during the basic, precompetitive, and competitive period of a sport season in 1 year (~60 min) | IS | PE: ↑ PMNs in the precompetitive and competitive period. ↑ MØ in the precompetitive period; also, ↑ [histamine], ↑ [IL-8], ↑ [LTB4], and ↑ [LTE4] in the competitive phase |
| |||||
Evjenth et al. 2013 [64] | To investigate the effect on FENO of a standardized exercise challenge test on a treadmill∗ | Nonasthmatic children with and without allergic rhinoconjunctivitis (AR) symptoms | Run on treadmill (6 to 8 min); heart rate target during the last 4 min was 95% of predicted maximum heart rate (220 − age) | EB | PE: ↓ eNO in nonasthmatic children without allergic rhinoconjunctivitis |
| |||||
Font-Ribera et al. 2010 [65] | Inflammation and postexercise pulmonary oxidative stress∗ | Healthy subjects | Swimming in a chlorinated indoor-swimming pool (40 min), whose average speed was 22.5 ± 9.7 m/min | EBC and EB | PE: no changes of eNO in EB; [RANTES], [IL-12p70], [IFN-γ], [IL-4], [IL-8], [IL-10], [IFN-γ-induced protein 10], [TNF], [VEGF], and [8-isoprostane] in the EBC were not modified |
| |||||
García-Río et al. 2006 [66] | FENO before and after exercise challenge in patients with asthma and its relationship with airway obstruction∗ | Nonsmoking, steroid-naïve, atopic patients with mild persistent asthma and nonsmoking, nonatopic, healthy subjects (C) | Performing an exercise challenge on a cycloergometer, with monitored ventilation (exercise parameters were not presented) | EB | PE: with no changes in eNO of healthy subjects |
| |||||
Hopkins et al. 1997 [67] | Pulmonary capillary pressure and function of the alveolar-capillary barrier during intense exercise∗ | Athletes with signs of hemoptysis by exercise and healthy control subjects | 4 km cycling with 12% hill sloping during ~7 min | BALF | PE: >alveolar MØ, >[LTB4], and < lymphocytes in athletes versus control subjects |
| |||||
Kippelen et al. 2002 [68] | eNO level in endurance-trained athletes during and after intense exercise∗ | Nine athletes with exercise-induced hypoxaemia (EIH), 12 athletes without EIH, and 10 untrained subjects | 15 min intense cycling exercise at 90% VO2max | EB | DE: ↓ eNO and ↑ VNO (last 3 minutes) in all groups |
| |||||
Larsson et al. 1998 [32] | Cold air and inflammation in the AWs during rest and exercise∗ | Healthy subjects | Race on treadmill at −23°C and +22°C, each with 4 stages with 15 min at moderate intensity and 15 min of recovery | BALF | PE: at −23°C ↑ granulocytes and ↑ MØ; no changes in [IL-8] |
| |||||
Lovell et al. 2000 [69] | eNO and incremental exercise test in chronic congestive cardiac failure∗ | Chronic congestive cardiac failure patients and healthy control subjects (C) | Performing Bruce protocol modified by inclusion of an initial 3 min stage at 5% incline, later performing a constant workload test (6 min at 2.7 km h−1 and 5% incline) | EB | DE: ↓ eNO and ↑ VNO during Bruce test in C; ↑ VNO during constant workload test |
| |||||
Mantione et al. 2007 [70] | eNO breath levels just before engaging in their respective activity | Healthy control subjects | Going up and down the stairs on a 20-foot staircase for 2 min | EB | PE: ↓ eNO 1 minute after exercise |
| |||||
Matsumoto et al. 1994 [71] | eNO and VNO during exercise | Healthy subjects | Cycle-ergometry at 100 W and maximum intensity with 5 min of recovery (~13 min) | EB | DE: ↑ VNO at 100 W and at maximum pedaling intensity |
| |||||
Marek et al. 2008 [72] | [L-lactate] and [H2O2] during exercise∗ | Healthy subjects | Cycle-ergometer steady-state exercise at 60 W (~7 min) and 120 W (~5 min) | EBC | DE: ↑ [L-lactate] and ↑ [H2O2] in 60 W and 120 W |
| |||||
Marek et al. 2009 [73] | Maximal exercise, H2O2 release rate, and acid-base status | Amateur athletes | Incremental cycloergometry to exhaustion (~13 min) | EBC | PE: ↑ [H2O2] with no changes in pH nor [HCO3 −] |
| |||||
Marek et al. 2013 [74] | Exercising in cold weather and release of H2O2 ∗ | Healthy subjects | Races on treadmill at 75–80% HRmax at ~18°C and ~−15°C (~50 min) | EBC | PE: ↑ [H2O2] and ↑ rate of H2O2 release in both temperatures |
| |||||
Maroun et al. 1995 [75] | Physical condition and release of eNO during exercise | Healthy sedentary subjects (S), active subjects (Ac), and athletes (A) | Cycle-ergometries in steady-state at 1 and 2 L/min of VO2 only performing an additional one at 4 L/min of VO2 | EB | PE: ↓ eNO at >VO2 in S and Ac; ↑ lineal of VNO with ↑ VO2 in A |
| |||||
Mercken et al. 2005 [76] | Exercise-induced oxidative stress in COPD∗ | COPD patients and healthy control subjects (C) | Incremental cycle-ergometry exercise test until exhaustion and submaximal constant work rate exercise test (60% maximal power output) | EBC | PE: ↑ [H2O2] in maximal but not in submaximal exercise in C |
| |||||
Mercken et al. 2009 [77] | Pulmonary oxidative stress by endurance exercise in COPD and healthy subjects∗ | COPD patients and healthy control subjects | Cycle-ergometry on one leg at 40% of maximum power output (20 min) | EBC | PE: ↑ [H2O2] in COPD patients but not in healthy control subjects |
| |||||
Morici et al. 2004 [78] | VE during exercise and inflammation in the AWs | Young rowers | Maximal run of 1000 m on the rower ergometer (~3 min) | IS | DE: ↑ tendency in epithelial cells at a higher VE PE: ↑ MØ with both ↑ VE/kg and ↑ VT/kg |
| |||||
Nowak et al. 2001 [79] | Prooxidants and oxidative damage by moderate exercise | Healthy subjects | Cycle-ergometer exercise test at 120 W during 6 min or until a HR of 120 bpm is reached | EBC | PE: with no changes in [H2O2] and [TBARs] |
| |||||
Nadziakiewicz et al. 2006 [80] | Effects of the physical activity on eNO levels in healthy subjects and in CAD patients∗ | CAD patients and healthy control subjects smokers and nonsmokers | Bruce protocol exercise test | EB | PE: without changes in eNO in healthy control subjects nonsmokers |
| |||||
Pedersen et al. 2009 [81] | Inflammation in the AWs after 1-exercise session | High performance swimmers | Swimming in indoor-swimming pool at moderate intensity (45 min) whose average heart rate was 162 bpm | EBC and IS, EB | PE: no changes in the cellular composition in IS, eNO in EB, nor pH in EBC of swimmers |
| |||||
Pogliaghi et al. 1997 [82] | VNO after modifying pulmonary blood flow with head-out water immersion or increased gravity at rest and during exercise∗ | Nonsmokers and healthy subjects who underwent air with normal conditions, water immersion, or increased gravity (1 Gz or 2 Gz) | Incremental cycle-ergometry test, loading was increased progressively by 50 W every 3 min until voluntary exhaustion | EB | DE: ↓ eNO and ↑ VNO in all groups |
| |||||
Pucsok et al. 2007 [83] | Lung PGE2 and TXB2 and exercise | Judo competitors | Incremental run on treadmill until VO2max is reached (run time was not recorded) | EBC | PE: ↑ [PGE2] and ↑ [TXB2] in ♂, but not in ♀ |
| |||||
Riediker and Danuser 2007 [84] | Low-intensity physical activity and pH | Healthy subjects | Walk on treadmill at 60% HRmax predicted with 1 min pause every 10 min (~30 min) | EBC | PE: ↑ pH |
| |||||
Riley et al. 1997 [85] | NO production in patients with abnormalities of the pulmonary circulation∗ | PPH (primary pulmonary hypertension), PF (pulmonary fibrosis), and normal subjects group | Maximal (20 W/min in the normal subjects and 15 W/min in the PF patients and individual estimated exercise tolerance in PPH patients) and submaximal constant work rate cycle-ergometry exercise test (work rate VO2 midway between each patient's anaerobic threshold and VO2max) | EB | DE: ↓ eNO and ↑ VNO in normal subjects at peak exercise in maximal and constant work rate exercise test |
| |||||
Rolla et al. 2003 [86] | Relationship between eNO and exercise tolerance in patients with moderate MS∗ | Patients with moderate MS and healthy control subjects (C) | Symptom-limited incremental exercise test with an upright cycle-ergometer (25 W every 3 min until exhaustion) | EB | DE: ↓ eNO and ↑ VNO in all groups at the end of exercise |
| |||||
Shin et al. 2003 [87] | Relationship between exercise and NO exchange | Nonsmoking healthy adults | High-intensity exercise treadmill test at 90% of the predicted maximum heart rate (220 − age in years) for 20 min | EB | PE: ↑ VNO |
| |||||
St Croix et al. 1999 [88] | Effect of exercise on endogenous NO formation by measuring eNO at a constant airflow rate | Healthy, nonasthmatic, and nonsmoking subjects | 3 min of constant-load cycle-ergometry exercise test at three different exercise intensities corresponding to 30%, 60%, and 90% VO2max | EB | PE: ↓ eNO and ↑ VNO for all intensities of exercise in healthy subjects |
| |||||
Therminarias et al. 1998 [89] | Exercise in cold air on eNO and VNO∗ | Highly trained subjects (cross-country skiers, triathlon, and running) | Incremental cycloergometry to exhaustion in a climate chamber at +22°C and −10°C (~30 min) | EB | DE: ↓ eNO with the ↑ of the intensity >60 W in +22°C and ↑ VNO with the ↑ of the intensity >30 W in both temperatures |
| |||||
Trolin et al. 1994 [90] | eNO and VNO during exercise | Healthy subjects | Moderately heavy exercise on a cycloergometer (♀: 90 W for women and ♂: 150 W for ♂) | EB | DE: ↓ eNO |
| |||||
Tufvesson et al. 2013 [91] | Relationship between CC16 levels in plasma and urine after exercise with exhaled breath temperature and eNO∗ | Asthmatic and healthy control subjects | During first six minutes speed and slope were adjusted to maintain the heart rate subject to 90% of their theoretical maximum heart rate (220 − age); the next two minutes were adjusted again to reach maximum effort | EB | PE: ↓ eNO in both groups |
| |||||
Verges et al. 2006 [92] | Effect of prolonged exercise on the NO concentration in the lung | Nonsmokers undertaking a moderate to intense training program participated in the study | 100 min exercise test was performed on a cycle-ergometer (5 min of rest, 30 min warm-up at 25% P max, 10 min at 60% P max, 2 min at 25% P max repeated five times (S1 to S5), and 10 min of active recovery at 25% P max) | EB | DE: ↓ eNO for all exercise sessions (WU, S1 to S5, and active recovery) |
| |||||
Wetter et al. 2002 [93] | EIAH and pulmonary inflammation∗ | Endurance athletes with EIAH who used anti-inflammatory or placebo | Maximal incremental run on treadmill to exhaustion (~18 min) | IS | PE: with no PMNs, lymphocytes, nor MØ; ↑ [Histamine] in placebo |
| |||||
Yasuda et al. 1997 [94] | To examine the origin and role of eNO during exercise | Healthy control subjects | Two sets of 10 minutes in a cycle-ergometer (5 min without load and 5 minutes with 60 W and 60 RPM) separated, with 15 minutes between them | EB | DE: with no changes in eNO |
| |||||
Zietkowski et al. 2010 [95] | To assess the possible association of EIB with low-grade systemic inflammation in asthmatic patients∗ | Asthmatics (14 with EIB, 10 without EIB) and healthy volunteers | Cycle-ergometer test for 9 min with a fixed workload adjusted to increase the heart rate to 85% of the maximum predicted for the age of each patient | EBC | PE: with no changes in hs-PCR in healthy volunteers |
AWs: airways; BALF: bronchoalveolar lavage fluid; CAD: coronary artery disease; CC16: Clara cell secretory protein; CHF: chronic heart failure; COPD: chronic obstructive pulmonary disease; Cys-Lts: cysteinyl leukotrienes; EB: exhaled breath; EBC: exhaled breath condensate; EIAH: exercise-induced arterial hypoxemia; EIB: exercise-induced bronchoconstriction; eNO: exhaled nitric oxide; FENO: fractional exhaled nitric oxide; HCO3 −: bicarbonate; H2O2: hydrogen peroxide; HRmax: maximum heart rate; IFN-γ: interferon gamma; IFN-γ-induced protein-10: interferon-gamma-induced protein-10; IL-12p70, IL-4, IL-8, and IL-10: interleukin-12p70, interleukin-4, interleukin-8, and interleukin-10; IS: induced sputum; L-NMMA: N-monomethyl-L-arginine; L-lactate: lactate; LTB4: leukotriene B4; LTE4: leukotriene E4; MØ: macrophages; MAS: maximal aerobic speed; MS: mitral stenosis; MDA: malondialdehyde; MPO: myeloperoxidase; MASL: meters above sea level; NaCLO: sodium hypochlorite; NO2 −: nitrite; NO output: nitric oxide output (eNO × VE); PGE2: prostaglandin E2; P max: maximal power output; RANTES: regulated upon activation, normal T-cell expressed, and secreted; TBARs: thiobarbituric acid reactive species; TNF(-α): tumor necrosis factor (alpha); TXB2: thromboxane B2; Se: selenium; VE: minute ventilation; VEGF: vascular endothelial growth factor; VNO: volume of nitric oxide; VO2max: oxygen uptake (maximal); VT: tidal volume. In “Oxidative or inflammatory main results,” DE: during exercise and PE: postexercise. In “Aim,” ∗the effect of exercise was not the primary aim of the study.