Premium
Nitric oxide bioavailability modulates the dynamics of microvascular oxygen exchange during recovery from contractions
Author(s) -
Hirai D. M.,
Copp S. W.,
Ferreira L. F.,
Musch T. I.,
Poole D. C.
Publication year - 2010
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2010.02137.x
Subject(s) - bioavailability , sodium nitroprusside , nitric oxide , chemistry , kinetics , skeletal muscle , medicine , pharmacology , physics , quantum mechanics , organic chemistry
Aim: Lowered microvascular P O 2 ( P O 2 mv) during the exercise off‐transient likely impairs muscle metabolic recovery and limits the capacity to perform repetitive tasks. The current investigation explored the impact of altered nitric oxide (NO) bioavailability on P O 2 mv during recovery from contractions in healthy skeletal muscle. We hypothesized that increased NO bioavailability (sodium nitroprusside: SNP) would enhance P O 2 mv and speed its recovery kinetics while decreased NO bioavailability ( l ‐nitro arginine methyl ester: l ‐NAME) would reduce P O 2 mv and slow its recovery kinetics. Methods: P O 2 mv was measured by phosphorescence quenching during transitions (rest–1 Hz twitch‐contractions for 3 min–recovery) in the spinotrapezius muscle of Sprague–Dawley rats under SNP (300 μ m ), Krebs‐Henseleit (Control) and l ‐NAME (1.5 m m ) superfusion conditions. Results: Relative to recovery in Control, SNP resulted in greater overall microvascular oxygenation as assessed by the area under the P O 2 mv curve ( P O 2 AREA ; Control: 3471 ± 292 mmHg s; SNP: 4307 ± 282 mmHg s; P < 0.05) and faster off‐kinetics as evidenced by the mean response time (MRToff; Control: 60.2 ± 6.9 s; SNP: 34.8 ± 5.7 s; P < 0.05), whereas l ‐NAME produced lower P O 2 AREA (2339 ± 444 mmHg s; P < 0.05) and slower MRToff (86.6 ± 14.5 s; P < 0.05). Conclusion: NO bioavailability plays a key role in determining the matching of O 2 delivery‐to‐O 2 uptake and thus the upstream O 2 pressure driving capillary‐myocyte O 2 flux (i.e. P O 2 mv) following cessation of contractions in healthy skeletal muscle. Additionally, these data support a mechanistic link between reduced NO bioavailability and prolonged muscle metabolic recovery commonly observed in ageing and diseased populations.