This study examines the response of the exhaled nitric oxide (NO) concentration (CNO) and the exhaled NO output (VNO) during incremental exercise and during recovery in six sedentary women, seven sedentary men, and eight trained men. The protocol consisted of increasing the exercise intensity by 30 W every 3 min until exhaustion, followed by 5 min of recovery. Minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production, heart rate, CNO, and VNO were measured continuously. The CNO in exhaled air decreased significantly provided that the exercise intensity exceeded 65% of the peak VO2. It reached similar values, at exhaustion, in all three groups. The VNO increased proportionally with exercise intensity up to exhaustion and decreased rapidly during recovery. At exhaustion, the mean values were significantly higher for trained men than for sedentary men and sedentary women. During exercise, VNO correlates well with VO2, carbon dioxide production, VE, and heart rate. For the same submaximal intensity, and thus a given VO2 and probably a similar cardiac output, VNO appeared to be similar in all three groups, even if the VE was different. These results suggest that, during exercise, VNO is mainly related to the magnitude of aerobic metabolism and that this relationship is not affected by gender differences or by noticeable differences in the level of physical training.

aaMuscular exercise in a cold environment requires both the warming and the humidification of large amounts of inspired air, resulting in a loss of heat and water from the respiratory tract. While these losses are known to induce airway obstruction in subjects with bronchial hyperresponsiveness, their effects are not well defined in normal nonatopic subjects. According to some authors, normal subjects do not develop measurable obstruction in response to airway cooling [1][2][3], whereas other authors claim that they respond by developing measurable obstruction when the stimulus is sufficiently great [4,5]. Under these conditions, the origin and mechanisms involved in the development of bronchial obstruction are still under debate [6][7][8].Endogenous NO is produced in the lung by a family of NO synthases [9][10][11]. This NO is thought to be an important modulator of vascular tone and airway function in normal airways. Therefore, NO may be involved in several physiological mechanisms during airway cooling. Thus, in normal pulmonary circulation, NO mediates the vasodilation response to physical and chemical factors [9]. Moreover, NO mediates the nonadrenergic, noncholinergic neural inhibitory responses which represent the only neural bronchodilator mechanism in human airways [12,13]. In addition, NO may contribute to acute inflammation and host defence in the lung [14].NO may be detected in the air exhaled by humans and the amount of NO exhaled over time (V 'NO) may be measured accurately and continuously [15][16][17][18]. Although the NO detected at the mouth is the difference between what is produced in the respiratory system and what is transformed or eliminated continuously by other endogenous pathways, V 'NO is generally assumed to reflect the NO produced by cells within the respiratory tract. Therefore, if endogenous NO-production takes a part in the mechanisms involved during airway cooling, a change in exhaled [NO] may be expected during inhalation of cold air. The aim of the present study was: 1) to confirm that extensive airway cooling can induce detectable airway obstruction in nonatopic subjects, 2) to determine whether this cooling induces changes in the V 'NO response, and 3) to determine whether a relationship may be established between both of these observations. Methods SubjectsEight well-trained male subjects, engaged in various endurance activities (cross-country skiing, triathlon or running) for >8 h·week -1 , were studied. These subjects were selected because they were able to produce a high ventilatory response during exercise and, would therefore, need to warm up a large amount of air when they exercised in Thus, eight well-trained males performed two incremental exercise tests until exhaustion, followed by 5 min of recovery in temperate (22°C) and cold (-10°C) environments, at random. At -10°C, they were dressed in warm clothes. Ventilation (V'E), oxygen consumption (V'O 2 ), carbon dioxide production, cardiac frequency (fC), and [NO] and V'NO were measured continuously. Before and after...

This study was designed to clarify the effects of cold air exposure on metabolic and hormonal responses during progressive incremental exercise. Eight healthy males volunteered for the study. Informed consent was obtained from every participant. The following protocol was administered to each subject on three occasions in a climatic chamber in which the temperature was 20 degrees, 0 degree or -20 degrees C with relative humidity at 60% +/- 1%. Exercise tests were conducted on an electrically braked ergocycle, and consisted of a progressive incremental maximal exercise. Respiratory parameters were continuously monitored by an automated open-circuit sampling system. Exercise blood lactate (LA), free fatty acids (FFA), glucose levels, bicarbonate concentration (HCO-3), acid-base balance, plasma epinephrine (E) and norepinephrine (NE) were determined from venous blood samples obtained through an indwelling brachial catheter. Maximal oxygen uptake was significantly different between conditions: 72.0 +/- 5.4 ml kg-1 min-1 at 20 degrees C; 68.9 +/- 5.1 ml kg-1 min-1 at 0 degree C and 68.5 +/- 4.6 ml kg-1 min-1 at -20 degrees C. Workload, time to exhaustion, glucose levels and rectal temperature decreased significantly at -20 degrees C. Catecholamines and lactate values were not significantly altered by thermal conditions after maximal exercise but the catecholamines were decreased during rest. Bicarbonate, respiratory quotient, lactate and ventilatory thresholds increased significantly at -20 degrees C. The data support the contention that metabolic and hormonal responses following progressive incremental exercise are altered by cold exposure and they indicate a marked decrease in maximal oxygen uptake, time to exhaustion and workload.

This study examined the effect of acute exposure of the whole body to cold on blood lactate response during incremental exercise. Eight subjects were tested with a cycle ergometer in a climatic chamber, room temperature being controlled either at 24 degrees C (MT) or at -2 degrees C (CT). The protocol consisted of a step increment in exercise intensity of 30 W every 2 min until exhaustion. Oxygen consumption (VO2) was measured at rest and during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for estimations of plasma norepinephrine (NE), epinephrine (E), free fatty acid (FFA) and glucose concentrations, during the last 15 s of each exercise step and also during the 1st, 4th, 7th, and the 10th min following exercise for the determination of blood lactate (LA) concentration. The VO2 was higher during CT than during MT at rest and during nearly every exercise intensity. At CT, lactate anaerobic threshold (LAT), determined from a marked increase of LA above resting level, increased significantly by 49% expressed as absolute VO2, and 27% expressed as exercise intensity as compared with MT. The LA tended to be higher for light exercise intensities and lower for heavy exercise intensities during CT than during MT. The E and NE concentrations increased during exercise, regardless of ambient temperature. Furthermore, at rest and at exhaustion E concentrations did not differ between both conditions, while NE concentrations were greater during CT than during MT. Moreover, an increase off FFA was found only during CT.(ABSTRACT TRUNCATED AT 250 WORDS)