In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 303, No. 12 ( 2012-12-15), p. H1474-H1480
Abstract:
Nitric oxide (NO) can temporally and spatially match microvascular oxygen (O 2 ) delivery (Q̇o 2mv ) to O 2 uptake (V̇o 2 ) in the skeletal muscle, a crucial adjustment-to-exercise tolerance that is impaired in chronic heart failure (CHF). To investigate the effects of NO bioavailability induced by sildenafil intake on muscle Q̇o 2mv -to-O 2 utilization matching and V̇o 2 kinetics, 10 males with CHF (ejection fraction = 27 ± 6%) undertook constant work-rate exercise (70–80% peak). Breath-by-breath V̇o 2 , fractional O 2 extraction in the vastus lateralis {∼deoxygenated hemoglobin + myoglobin ([deoxy-Hb + Mb]) by near-infrared spectroscopy}, and cardiac output (CO) were evaluated after sildenafil (50 mg) or placebo. Sildenafil increased exercise tolerance compared with placebo by ∼20%, an effect that was related to faster on- and off-exercise V̇o 2 kinetics ( P 〈 0.05). Active treatment, however, failed to accelerate CO dynamics ( P 〉 0.05). On-exercise [deoxy-Hb + Mb] kinetics were slowed by sildenafil (∼25%), and a subsequent response “overshoot” ( n = 8) was significantly lessened or even abolished. In contrast, [deoxy-Hb + Mb] recovery was faster with sildenafil (∼15%). Improvements in muscle oxygenation with sildenafil were related to faster on-exercise V̇o 2 kinetics, blunted oscillations in ventilation ( n = 9), and greater exercise capacity ( P 〈 0.05). Sildenafil intake enhanced intramuscular Q̇o 2mv -to-V̇o 2 matching with beneficial effects on V̇o 2 kinetics and exercise tolerance in CHF. The lack of effect on CO suggests that improvement in blood flow to and within skeletal muscles underlies these effects.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.00435.2012
Language:
English
Publisher:
American Physiological Society
Publication Date:
2012
detail.hit.zdb_id:
1477308-9
SSG:
12
Permalink