Effect of exercise duration on pro-oxidants and pH in exhaled breath condensate in humans.

Exercise promotes pulmonary oxidative imbalance. In this regard, some evidence has been obtained from the study of exhaled breath condensate (EBC) during urban races, in which the factors involved in the occurrence of this process are still not characterized. In this paper, under laboratory conditions, both the role of time of exercise on the generation of pro-oxidants (H2O2, NO2 (-)) and pH have been assessed in EBC of 16 under-trained subjects who completed three tests of cycloergometric exercise at low intensity (30 % of VO2 max) with a duration of 10, 30, and 90 min. Samples were obtained as follows: immediately before and at 80 min post exertion in each test. In the 90-min test, an increase in H2O2, NO2 (-) concentration in EBC at 80 min post exertion with no changes in the pH was observed. Total O2 consumption and total ventilation weakly correlated with the changes in H2O2 and NO2 (-). In conclusion, the concentration of pro-oxidants in the EBC depends on the duration of the exercise when it is performed at low intensity under laboratory conditions.

Update on the Mechanisms of Pulmonary Inflammation and Oxidative Imbalance Induced by Exercise.

The mechanisms involved in the generation of oxidative damage and lung inflammation induced by physical exercise are described. Changes in lung function induced by exercise involve cooling of the airways, fluid evaporation of the epithelial surface, increased contact with polluting substances, and activation of the local and systemic inflammatory response. The present work includes evidence obtained from the different types of exercise in terms of duration and intensity, the effect of both acute performance and chronic performance, and the influence of special conditions such as cold weather, high altitude, and polluted environments. Levels of prooxidants, antioxidants, oxidative damage to biomolecules, and cellularity, as well as levels of soluble mediators of the inflammatory response and its effects on tissues, are described in samples of lung origin. These samples include tissue homogenates, induced sputum, bronchoalveolar lavage fluid, biopsies, and exhaled breath condensate obtained in experimental protocols conducted on animal and human models. Finally, the need to simultaneously explore the oxidative/inflammatory parameters to establish the interrelation between them is highlighted.

Concordance of the location of the innervation zone of the tibialis anterior muscle using voluntary and imposed contractions by electrostimulation.

BACKGROUND: The innervation zone (IZ) corresponds to the location of the neuromuscular junctions. Its location can be determined by using arranged surface linear electrode arrays. Typically, voluntary muscle contractions (VC) are used in this method. However, it also may be necessary to locate the IZ under clinical conditions such as spasticity, in which this type of contraction is difficult to perform. Therefore, contractions imposed by electrostimulation (ES) can be an alternative. There is little background comparing the locations of IZ obtained by two different types of contractions. OBJECTIVE: Evaluate the concordance between using voluntary and imposed contractions from electrostimulation in order to determine the location of the innervation zone of the tibialis anterior muscle in healthy volunteers. METHODS: The tibialis anterior (TA) muscle of sixteen volunteers (men: 8; women: 8; age: 22.1±1.4years, weight: 61.6±7.5kg, height: 167.1±7.5cm) were evaluated using a linear electrode array. The IZ of the TA muscle was located using two types of muscle contractions, voluntary (10% MVC) and imposed contractions by ES. The concordance between both conditions was evaluated using the Bland-Altman method and the concordance correlation coefficient (CCC). The analyses were applied to the absolute and relative positions to the length of an anatomical landmark frame. RESULTS: CCC for absolute position was 0.98 (p<0.0001, 95% CI [0.98-1.00], and CCC for relative positions also was 0.98 (p<0.0001, 95% CI [0.97-1.00]). The Bland-Altman analysis for absolute data showed an average difference of -0.63mm (SD: 4.1). Whereas, for adjusted data, the average difference was -0.20% (SD: 1.2). The power of the results, based on absolute data, was 98%, whereas for relative data, 82%. CONCLUSION: In healthy volunteers, there was a substantially concordance between the location of the IZ of the TA muscle derived from using contractions imposed by ES and the location derived from using VC.

Electromyographic adjustments during continuous and intermittent incremental fatiguing cycling.

We studied the sensitivity of electromyographic (EMG) variables to load and muscle fatigue during continuous and intermittent incremental cycling. Fifteen men attended three laboratory sessions. Visit 1: lactate threshold, peak power output, and VO2max . Visits 2 and 3: Continuous (more fatiguing) and intermittent (less fatiguing) incremental cycling protocols [20%, 40%, 60%, 80% and 100% of peak power output (PPO)]. During both protocols, multichannel EMG signals were recorded from vastus lateralis: muscle fiber conduction velocity (MFCV), instantaneous mean frequency (iMNF), and absolute and normalized root mean square (RMS) were analyzed. MFCV differed between protocols (P < 0.001), and only increased consistently with power output during intermittent cycling. RMS parameters were similar between protocols, and increased linearly with power output. However, only normalized RMS was higher during the more fatiguing 100% PPO stage of the continuous protocol [continuous-intermittent mean difference (95% CI): 45.1 (8.5% to 81.7%)]. On the contrary, iMNF was insensitive to load changes and muscle fatigue (P = 0.14). Despite similar power outputs, continuous and intermittent cycling influenced MFCV and normalized RMS differently. Only normalized RMS was sensitive to both increases in power output (in both protocols) and muscle fatigue, and thus is the most suitable EMG parameter to monitor changes in muscle activation during cycling.

Increase of pro-oxidants with no evidence of lipid peroxidation in exhaled breath condensate after a 10-km race in non-athletes.

It is a well-established fact that exercise increases pro-oxidants and favors oxidative stress; however, this phenomenon has been poorly studied in human lungs. Pro-oxidative generation (H(2)O(2), NO(2) (-)), lipid peroxidation markers (MDA), and inflammation (pH) in exhaled breath condensate (EBC) have been determined through data from 10 active subjects who ran 10 km; samples were obtained immediately before, at 20, and at 80 min post-exertion. In EBC, the concentration of H(2)O(2) at 80 min post-exertion was increased. NO(2) (-) concentration showed a tendency to increase at 80 min post-exertion, with no variations in MDA and pH. No variations of NO(2) (-) were found in plasma, while there was an increase of NO(2) (-) at 80 min post-exertion in the relation between EBC and plasma. NO(2) (-) in EBC did not correlate to plasmatic NO(2) (-), while it did correlate directly with H(2)O(2) in EBC, suggesting a localized origin for the exercise-related NO(2) (-) increase in EBC. MDA in plasma did not increase nor correlate with MDA in EBC. In conclusion, high-intensity exercise increases lung-originated pro-oxidants in non-athlete subjects with no evidence of early lipid peroxidation and changes in the pH value in EBC.

Lung oxidative damage by hypoxia.

One of the most important functions of lungs is to maintain an adequate oxygenation in the organism. This organ can be affected by hypoxia facing both physiological and pathological situations. Exposure to this condition favors the increase of reactive oxygen species from mitochondria, as from NADPH oxidase, xanthine oxidase/reductase, and nitric oxide synthase enzymes, as well as establishing an inflammatory process. In lungs, hypoxia also modifies the levels of antioxidant substances causing pulmonary oxidative damage. Imbalance of redox state in lungs induced by hypoxia has been suggested as a participant in the changes observed in lung function in the hypoxic context, such as hypoxic vasoconstriction and pulmonary edema, in addition to vascular remodeling and chronic pulmonary hypertension. In this work, experimental evidence that shows the implied mechanisms in pulmonary redox state by hypoxia is reviewed. Herein, studies of cultures of different lung cells and complete isolated lung and tests conducted in vivo in the different forms of hypoxia, conducted in both animal models and humans, are described.

Exhaled breath condensate analysis after long distance races.

The impact of an endurance race on pulmonary pro-oxidative formation and lipoperoxidation was evaluated using exhaled breath condensate (EBC). 3 groups of 12, 12 and 17 healthy recreational runners of both sexes ran 10, 21.1 and 42.2 km, respectively. EBC samples were obtained before the run and at 20 and 80 min post run. Concentrations of H2O2, NO2 - , malondialdehyde and pH were determined. The 10 km group showed no post-run variations for H2O2 and NO2 - concentrations. The 21.1 km group showed significant increments for NO2 - , and H2O2 concentrations in 20 min and 80 min samples. The 42.2 km group, showed increased NO2 - concentration in 20 min and 80 min samples, while H2O2 concentration increased only in the 20 min sample. In the 10 and 42.2 km groups neither malondialdehyde concentration nor pH showed differences. The 42.2 km group exhibited ΔH2O2 and ΔNO2 - medians higher than the 10 km group. ΔpH median decreased in 21.1 and 42.2 km groups, exhibiting values significantly lower than the 10 km group. ΔH2O2 y ΔNO2 - correlated directly with race time, while ΔpH, correlated inversely. In conclusion, intense prolonged exercise favors the increase in pulmonary pro-oxidative levels, with no modifications on lipoperoxidation. Running time relates to the magnitude of acute post exercise pro-oxidative formation.

Lung oxidative stress as related to exercise and altitude. Lipid peroxidation evidence in exhaled breath condensate: a possible predictor of acute mountain sickness.

Lung oxidative stress (OS) was explored in resting and in exercising subjects exposed to moderate and high altitude. Exhaled breath condensate (EBC) was collected under field conditions in male high-competition mountain bikers performing a maximal cycloergometric exercise at 670 m and at 2,160 m, as well as, in male soldiers climbing up to 6,125 m in Northern Chile. Malondialdehyde concentration [MDA] was measured by high-performance liquid chromatography in EBC and in serum samples. Hydrogen peroxide concentration [H(2)O(2)] was analysed in EBC according to the spectrophotometric FOX(2) assay. [MDA] in EBC of bikers did not change while exercising at 670 m, but increased from 30.0+/-8.0 to 50.0+/-11.0 nmol l(-1) (P<0.05) at 2,160 m. Concomitantly, [MDA] in serum and [H(2)O(2)] in EBC remained constant. On the other hand, in mountaineering soldiers, [H(2)O(2)] in EBC under resting conditions increased from 0.30+/-0.12 mumol l(-1) at 670 m to 1.14+/-0.29 mumol l(-1) immediately on return from the mountain. Three days later, [H(2)O(2)] in EBC (0.93 +/-0.23 mumol l(-1)) continued to be elevated (P<0.05). [MDA] in EBC increased from 71+/-16 nmol l(-1) at 670 m to 128+/-26 nmol l(-1) at 3,000 m (P<0.05). Changes of [H(2)O(2)] in EBC while ascending from 670 m up to 3,000 m inversely correlated with concomitant variations in HbO2 saturation (r=-0.48, P<0.05). AMS score evaluated at 5,000 m directly correlated with changes of [MDA] in EBC occurring while the subjects moved from 670 to 3,000 m (r=0.51, P<0.05). Lung OS may constitute a pathogenic factor in AMS.