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Exercise training and muscle microvascular oxygenation: role of nitric oxide bioavailability
Author(s) -
Hirai Daniel M,
Copp Steven W,
Ferguson Scott K,
Holdsworth Clark T,
Musch Timothy I,
Poole David C
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.860.18
Subject(s) - nitric oxide , chemistry , bioavailability , skeletal muscle , medicine , oxygenation , endocrinology , treadmill , nitric oxide synthase , physical exercise , pharmacology
Exercise training induces multiple adaptations within skeletal muscle that may improve local O 2 delivery‐utilization matching (i.e., microvascular O 2 pressure; PO 2 mv). We tested the hypothesis that increased nitric oxide (NO) bioavailability partly underlies improved muscle PO 2 mv kinetics from rest to contractions after exercise training. Rats were assigned to sedentary (S; n=18) or treadmill exercise trained (ET; n=10; 60 min/d, 5 d/wk, ~8 wks, 35 m/min; ‐14% grade) groups. PO 2 mv was measured via phosphorescence quenching in the spinotrapezius muscle at rest and during 1 Hz twitch contractions under control (CON, Krebs‐ Henseleit), SNP (NO donor; 300 μM) and L‐NAME (NO synthase blockade; 1.5 mM) superfusion. ET rats had greater VO 2 peak than S rats (S: 72 ± 2; ET: 81 ± 1 ml/kg/min; p <0.05). The rate of PO 2 mv fall during contractions was defined as ΔPO 2 mv/τ (where τ = time constant) and expressed in mmHg/s. Exercise training slowed ΔPO 2 mv/τ during CON (S: 1.46 ± 0.14; ET: 0.96 ± 0.14; p <0.05). Compared to CON, SNP slowed ΔPO 2 mv/τ only in S rats (S: 0.34 ± 0.06; ET: 0.65 ± 0.17; p <0.05) whereas L‐NAME speeded ΔPO 2 mv/τ only in ET rats (S: −12%; ET: 34%; p <0.05). Exercise training leads to greater microvascular oxygenation at the onset of contractions partly via increased NO bioavailability which likely constitutes an important mechanism for training‐induced metabolic adaptations. (AHA Midwest Affiliate, NIH HL‐108328)