Exhaled nitric oxide during incremental and constant workload exercise in chronic cardiac failure

• Published in: European journal of clinical investigation Vol. 30; no. 3; pp. 181 - 187
• Main Authors: LOVELL, S. L, STEVENSON, H, YOUNG, I. S, MCDOWELL, G, MCENEANEY, D, RILEY, M. S, NICHOLLS, D. P
• Format: Journal Article
• Language: English
• Published: Oxford BSL Blackwell Science Ltd 01-03-2000; Blackwell
• Subjects: Aged; Biological and medical sciences; Cardiovascular system; exercise; Exercise - physiology; Exercise Test; Female; heart failure; Heart Failure - metabolism; Heart Failure - physiopathology; Heart Rate; Humans; Investigative techniques, diagnostic techniques (general aspects); Male; Medical sciences; Middle Aged; Nitrates - blood; Nitric oxide; Nitric Oxide - biosynthesis; Nitrites - blood; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Respiration; Space life sciences; Physical exercise; Human; Heart failure; Expiration; Parameter variation; Cardiovascular disease; Workload; Gases; Chronic; Heart disease; Nitric oxide; Ventilation; Comparative study; Quantitative analysis
• ISSN: 0014-2972; 1365-2362
• DOI: 10.1046/j.1365-2362.2000.00613.x

Background
Nitric oxide (NO) is present in exhaled breath and produced by the pulmonary vascular endothelium as a potent vasodilator. Exercise is normally associated with pulmonary vasodilatation and a decrease in pulmonary vascular resistance to accommodate the increase in cardiac output. If production of NO is impaired in patients with chronic congestive cardiac failure (CCF), this might contribute to their exercise intolerance.
Patients and methods
We quantified NO production (V˙ NO) in 12 patients with chronic stable CCF and 12 controls, at rest and during incremental cardiopulmonary exercise on a treadmill, and at a later date during constant workload exercise.
Results
Patients had reduced V˙ NO compared with controls during incremental exercise [381 (180) vs. 777 (275) nL min−1; mean (SD); P < 0.0001] but at constant workload V˙ NO was similar between the two groups [353 (124) vs. 389 (189) nL min−1; P = 0.25]. Plasma levels of nitrate, the stable end‐product of NO production, were significantly higher in patients [resting value 46.1 (21.6) vs. 23.0 (10.0) μM; P = 0.004] and were not influenced by exercise.
Conclusion
Impaired NO‐mediated pulmonary vasodilatation does not appear to contribute to exercise limitation in CCF. Alternatively, the lower NO production observed during maximal exercise in the patient group compared with controls may reflect a reduced incremental response of a system that is already abnormally activated in heart failure.