Influence of inhaled nitric oxide on gas exchange during normoxic and hypoxic exercise in highly trained cyclists

2001 ◽  
Vol 90 (3) ◽  
pp. 926-932 ◽  
Author(s):  
A. William Sheel ◽  
Michael R. Edwards ◽  
Garth S. Hunte ◽  
Donald C. McKenzie
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Gas Exchange ◽  
Inhaled Nitric Oxide ◽  
Metabolic Parameters ◽  
Oxyhemoglobin Saturation ◽  
Arterial Blood ◽  
Hypoxic Fraction ◽  
Exercise Induced ◽  
Hypoxic Exercise

This study tested the effects of inhaled nitric oxide [NO; 20 parts per million (ppm)] during normoxic and hypoxic (fraction of inspired O2 = 14%) exercise on gas exchange in athletes with exercise-induced hypoxemia. Trained male cyclists ( n = 7) performed two cycle tests to exhaustion to determine maximal O2 consumption (V˙o 2 max) and arterial oxyhemoglobin saturation (SaO2 , Ohmeda Biox ear oximeter) under normoxic (V˙o 2 max = 4.88 ± 0.43 l/min and SaO2 = 90.2 ± 0.9, means ± SD) and hypoxic (V˙o 2 max = 4.24 ± 0.49 l/min and SaO2 = 75.5 ± 4.5) conditions. On a third occasion, subjects performed four 5-min cycle tests, each separated by 1 h at their respectiveV˙o 2 max, under randomly assigned conditions: normoxia (N), normoxia + NO (N/NO), hypoxia (H), and hypoxia + NO (H/NO). Gas exchange, heart rate, and metabolic parameters were determined during each condition. Arterial blood was drawn at rest and at each minute of the 5-min test. Arterial Po 2 (PaO2 ), arterial Pco 2, and SaO2 were determined, and the alveolar-arterial difference for Po 2 (A-aDo 2) was calculated. Measurements of PaO2 and SaO2 were significantly lower and A-aDo 2 was widened during exercise compared with rest for all conditions ( P < 0.05). No significant differences were detected between N and N/NO or between H and H/NO for PaO2 , SaO2 and A-aDo 2 ( P > 0.05). We conclude that inhalation of 20 ppm NO during normoxic and hypoxic exercise has no effect on gas exchange in highly trained cyclists.

scholarly journals Coca chewing for exercise: hormonal and metabolic responses of nonhabitual chewers

1996 ◽  
Vol 81 (5) ◽  
pp. 1901-1907 ◽  
Author(s):  
Roland Favier ◽  
Esperanza Caceres ◽  
Laurent Guillon ◽  
Brigitte Sempore ◽  
Michel Sauvain ◽  
...  
Keyword(s):  
Heart Rate ◽  
Gas Exchange ◽  
Oxygen Uptake ◽  
Metabolic Responses ◽  
Physiological Data ◽  
Respiratory Gas Exchange ◽  
Gum Chewing ◽  
Arterial Blood ◽  
Before And After ◽  
Exercise Induced

Favier, Roland, Esperanza Caceres, Laurent Guillon, Brigitte Sempore, Michel Sauvain, Harry Koubi, and Hilde Spielvogel. Coca chewing for exercise: hormonal and metabolic responses of nonhabitual chewers. J. Appl. Physiol. 81(5): 1901–1907, 1996.—To determine the effects of acute coca use on the hormonal and metabolic responses to exercise, 12 healthy nonhabitual coca users were submitted twice to steady-state exercise (∼75% maximal O2 uptake). On one occasion, they were asked to chew 15 g of coca leaves 1 h before exercise, whereas on the other occasion, exercise was performed after 1 h of chewing a sugar-free chewing gum. Plasma epinephrine, norepinephrine, insulin, glucagon, and metabolites (glucose, lactate, glycerol, and free fatty acids) were determined at rest before and after coca chewing and during the 5th, 15th, 30th, and 60th min of exercise. Simultaneously to these determinations, cardiorespiratory variables (heart rate, mean arterial blood pressure, oxygen uptake, and respiratory gas exchange ratio) were also measured. At rest, coca chewing had no effect on plasma hormonal and metabolic levels except for a significantly reduced insulin concentration. During exercise, the oxygen uptake, heart rate, and respiratory gas exchange ratio were significantly increased in the coca-chewing trial compared with the control (gum-chewing) test. The exercise-induced drop in plasma glucose and insulin was prevented by prior coca chewing. These results contrast with previous data obtained in chronic coca users who display during prolonged submaximal exercise an exaggerated plasma sympathetic response, an enhanced availability and utilization of fat (R. Favier, E. Caceres, H. Koubi, B. Sempore, M. Sauvain, and H. Spielvogel. J. Appl. Physiol. 80: 650–655, 1996). We conclude that, whereas coca chewing might affect glucose homeostasis during exercise, none of the physiological data provided by this study would suggest that acute coca chewing in nonhabitual users could enhance tolerance to exercise.

scholarly journals Nitric oxide synthase inhibition does not affect the exercise-induced arterial hypoxemia in Thoroughbred horses

2001 ◽  
Vol 91 (3) ◽  
pp. 1105-1112 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Hemoglobin Concentration ◽  
No Synthase ◽  
Systemic Hypertension ◽  
Maximal Heart Rate ◽  
Arterial Hypoxemia ◽  
Arterial Blood ◽  
Thoroughbred Horses ◽  
Exercise Induced

Because sensitivity of equine pulmonary vasculature to endogenous as well as exogenous nitric oxide (NO) has been demonstrated, we examined whether endogenous NO production plays a role in exercise-induced arterial hypoxemia. We hypothesized that inhibition of NO synthase may alter the distribution of ventilation-perfusion mismatching, which may affect the exercise-induced arterial hypoxemia. Arterial blood-gas variables were examined in seven healthy, sound Thoroughbred horses at rest and during incremental exercise protocol leading to galloping at maximal heart rate without (control; placebo = saline) and with N ω-nitro-l-arginine methyl ester (l-NAME) administration (20 mg/kg iv). The experiments were carried out in random order, 7 days apart. At rest, l-NAME administration caused systemic hypertension, pulmonary hypertension, and bradycardia. During 120 s of galloping at maximal heart rate, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, hyperthermia, and acidosis occurred in the control as well as in NO synthase inhibition experiments. However, statistically significant differences between the treatments were not found. In both treatments, exercise caused a significant rise in hemoglobin concentration, but the increment was significantly attenuated in the NO synthase inhibition experiments, and, therefore, arterial O2 content (CaO2 ) increased to significantly lower values. These data suggest that, whereasl-NAME administration does not affect pulmonary gas exchange in exercising horses, it may affect splenic contraction, which via an attenuation of the rise in hemoglobin concentration and CaO2 may limit performance at higher workloads.

Hypoxia potentiates exercise-induced sympathetic neural activation in humans

1991 ◽  
Vol 71 (3) ◽  
pp. 1032-1040 ◽  
Author(s):  
D. R. Seals ◽  
D. G. Johnson ◽  
R. F. Fregosi
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Muscle Sympathetic Nerve Activity ◽  
Circulatory Arrest ◽  
Plasma Norepinephrine ◽  
Neural Activation ◽  
Arterial Blood ◽  
Systemic Hypoxia ◽  
Exercise Induced ◽  
Hypoxic Exercise

Our purpose was to test the hypothesis that hypoxia potentiates exercise-induced sympathetic neural activation in humans. In 15 young (20–30 yr) healthy subjects, lower leg muscle sympathetic nerve activity (MSNA, peroneal nerve; microneurography), venous plasma norepinephrine (PNE) concentrations, heart rate, and arterial blood pressure were measured at rest and in response to rhythmic handgrip exercise performed during normoxia or isocapnic hypoxia (inspired O2 concn of 10%). Study I (n = 7): Brief (3–4 min) hypoxia at rest did not alter MSNA, PNE, or arterial pressure but did induce tachycardia [17 +/- 3 (SE) beats/min; P less than 0.05]. During exercise at 50% of maximum, the increases in MSNA (346 +/- 81 vs. 207 +/- 14% of control), PNE (175 +/- 25 vs. 120 +/- 11% of control), and heart rate (36 +/- 2 vs. 20 +/- 2 beats/min) were greater during hypoxia than during normoxia (P less than 0.05), whereas the arterial pressure response was not different (26 +/- 4 vs. 25 +/- 4 mmHg). The increase in MSNA during hypoxic exercise also was greater than the simple sum of the separate responses to hypoxia and normoxic exercise (P less than 0.05). Study II (n = 8): In contrast to study I, during 2 min of exercise (30% max) performed under conditions of circulatory arrest and 2 min of postexercise circulatory arrest (local ischemia), the MSNA and PNE responses were similar during systemic hypoxia and normoxia. Arm ischemia without exercise had no influence on any variable during hypoxia or normoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment

2000 ◽  
Vol 89 (2) ◽  
pp. 721-730 ◽  
Author(s):  
Susan R. Hopkins ◽  
Rebecca C. Barker ◽  
Tom D. Brutsaert ◽  
Timothy P. Gavin ◽  
Pauline Entin ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Blood Gases ◽  
Random Order ◽  
Pulmonary Gas Exchange ◽  
Male Athletes ◽  
Prediction Limit ◽  
Fast Running ◽  
Arterial Blood ◽  
Exercise Induced

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial Po 2 (PaO2 ) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O2 uptake (V˙o 2 max) = 51 ml · kg−1 · min−1]. They were studied in random order (C or R), with a fastV˙o 2 max protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% ofV˙o 2 max (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in V˙o 2 maxbetween R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of V˙o 2 max. At 90% ofV˙o 2 max, PaO2 was lower during R (mean ± SE = 94 ± 2 Torr) than during C (105 ± 2 Torr, P < 0.0001), as was ventilation (85.2 ± 3.8 vs. 98.2 ± 4.4 l/min btps, P < 0.0001) and cardiac output (19.1 ± 0.6 vs. 21.1 ± 1.0 l/min, P < 0.001). Arterial Pco 2 (32.0 ± 0.5 vs. 30.0 ± 0.6 Torr, P < 0.001) and alveolar-arterial O2 difference (A-aDo 2; 22 ± 2 vs. 16 ± 2 Torr, P < 0.0001) were greater during R. PaO2 and A-aDo 2 were similar between slow and fast. Nadir PaO2 was ≤80 Torr in four women (24%) but only during fast-R. In all subjects, PaO2 atV˙o 2 max was greater than the lower 95% prediction limit calculated from available data in men ( n = 72 C and 38 R) for both R and C. These data suggest intrinsic differences in gas exchange between R and C, due to differences in ventilation and also efficiency of gas exchange. The PaO2 responses to R and C exercise in our 17 subjects do not differ significantly from those previously observed in men.

scholarly journals Role of nitric oxide-containing factors in the ventilatory and cardiovascular responses elicited by hypoxic challenge in isoflurane-anesthetized rats

2014 ◽  
Vol 116 (11) ◽  
pp. 1371-1381 ◽  
Author(s):  
James P. Mendoza ◽  
Rachael J. Passafaro ◽  
Santhosh M. Baby ◽  
Alex P. Young ◽  
James N. Bates ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Cardiovascular Responses ◽  
Vital Role ◽  
Initial Increase ◽  
Ventilatory Responses ◽  
Arterial Blood ◽  
Anesthetized Rats ◽  
Before And After

Exposure to hypoxia elicits changes in mean arterial blood pressure (MAP), heart rate, and frequency of breathing (fr). The objective of this study was to determine the role of nitric oxide (NO) in the cardiovascular and ventilatory responses elicited by brief exposures to hypoxia in isoflurane-anesthetized rats. The rats were instrumented to record MAP, heart rate, and fr and then exposed to 90 s episodes of hypoxia (10% O2, 90% N2) before and after injection of vehicle, the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME), or the inactive enantiomer d-NAME (both at 50 μmol/kg iv). Each episode of hypoxia elicited a decrease in MAP, bidirectional changes in heart rate (initial increase and then a decrease), and an increase in fr. These responses were similar before and after injection of vehicle or d-NAME. In contrast, the hypoxia-induced decreases in MAP were attenuated after administration of l-NAME. The initial increases in heart rate during hypoxia were amplified whereas the subsequent decreases in heart rate were attenuated in l-NAME-treated rats. Finally, the hypoxia-induced increases in fr were virtually identical before and after administration of l-NAME. These findings suggest that NO factors play a vital role in the expression of the cardiovascular but not the ventilatory responses elicited by brief episodes of hypoxia in isoflurane-anesthetized rats. Based on existing evidence that NO factors play a vital role in carotid body and central responses to hypoxia in conscious rats, our findings raise the novel possibility that isoflurane blunts this NO-dependent signaling.

scholarly journals Residence at 3,800-m altitude for 5 mo in growing dogs enhances lung diffusing capacity for oxygen that persists at least 2.5 years

2007 ◽  
Vol 102 (4) ◽  
pp. 1448-1455 ◽  
Author(s):  
Connie C. W. Hsia ◽  
Robert L. Johnson ◽  
Paul McDonough ◽  
D. Merrill Dane ◽  
Myresa D. Hurst ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Base Excess ◽  
Lactate Concentration ◽  
Diffusing Capacity ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Peak Lactate ◽  
Pulmonary Arterial ◽  
Hypoxic Exercise

Mammals native to high altitude (HA) exhibit larger lung volumes than their lowland counterparts. To test the hypothesis that adaptation induced by HA residence during somatic maturation improves pulmonary gas exchange in adulthood, male foxhounds born at sea level (SL) were raised at HA (3,800 m) from 2.5 to 7.5 mo of age and then returned to SL prior to somatic maturity while their littermates were simultaneously raised at SL. Following return to SL, all animals were trained to run on a treadmill; gas exchange and hemodynamics were measured 2.5 years later at rest and during exercise while breathing 21% and 13% O2. The multiple inert gas elimination technique was employed to estimate ventilation-perfusion (V̇a/Q̇) distributions and lung diffusing capacity for O2 (DlO2). There were no significant intergroup differences during exercise breathing 21% O2. During exercise breathing 13% O2, peak O2 uptake and V̇a/Q̇ distributions were similar between groups but arterial pH, base excess, and O2 saturation were higher while peak lactate concentration was lower in animals raised at HA than at SL. At a given exercise intensity, alveolar-arterial O2 tension gradient (A-aDo2) attributable to diffusion limitation was lower while Dlo2 was 12–25% higher in HA-raised animals. Mean systemic arterial blood pressure was also lower in HA-raised animals; mean pulmonary arterial pressures were similar. We conclude that 5 mo of HA residence during maturation enhances long-term gas exchange efficiency and DlO2 without impacting V̇a/Q̇ inequality during hypoxic exercise at SL.

Arterial Blood Gases, Acid-Base Balance, and Lactate and Gas Exchange Variables During Hypoxic Exercise

1989 ◽  
Vol 10 (04) ◽  
pp. 279-285 ◽  
Author(s):  
T. Yoshida ◽  
M. Udo ◽  
M. Chida ◽  
K. Makiguchi ◽  
M. Ichioka ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Acid Base Balance ◽  
Acid Base ◽  
Arterial Blood ◽  
Base Balance ◽  
Hypoxic Exercise
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