scholarly journals Vascular nitric oxide: effects of exercise training in animals

2008 ◽  
Vol 33 (1) ◽  
pp. 173-178 ◽  
Author(s):  
Richard M. McAllister ◽  
Sean C. Newcomer ◽  
M. Harold Laughlin
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Maximal Exercise ◽  
Muscle Blood Flow ◽  
Disease Process ◽  
Vascular Health ◽  
Endurance Exercise Training ◽  
Resistance Vessels

Exercise training is known to induce several adaptations in the cardiovascular system, one of which is increased skeletal muscle blood flow at maximal exercise. Improved muscle blood flow, in turn, could in part be accounted for by augmented endothelium-dependent, nitric oxide (NO)-mediated vasodilation. Studies have indeed demonstrated that endothelium-dependent, NO-mediated dilation of conductance-type vessels is augmented after endurance exercise training; recently, this adaptation has been extended into resistance-type vessels within rodent skeletal muscle. With the latter, however, it appears that only resistance vessels supplying muscle active during training sessions exhibit this adaptation. These findings in rats are in contrast to those from human studies, in which increased endothelium-dependent dilation has been observed in vasculatures not associated with elevated blood flow during exercise. Increased expression of endothelial NO synthase (eNOS) appears to underlie enhanced endothelium-dependent, NO-mediated dilation of both conductance and resistance vessels. Greater eNOS expression may also underlie the preventive and (or) rehabilitative effect(s) of exercise training on atherosclerosis, given that NO inhibits several steps of the atherosclerotic disease process. Thus, exercise training may induce adaptations that benefit both vasodilation and vascular health.

scholarly journals Nonuniform effects of endurance exercise training on vasodilation in rat skeletal muscle

2005 ◽  
Vol 98 (2) ◽  
pp. 753-761 ◽  
Author(s):  
R. M. McAllister ◽  
J. L. Jasperse ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Gastrocnemius Muscle ◽  
Muscle Blood Flow ◽  
Second Order ◽  
Skeletal Muscle Blood Flow ◽  
Endurance Exercise Training

Endurance exercise training (Ex) has been shown to increase maximal skeletal muscle blood flow. The purpose of this study was to test the hypothesis that increased endothelium-dependent vasodilation is associated with the Ex-induced increase in muscle blood flow. Furthermore, we hypothesized that enhanced endothelium-dependent dilation is confined to vessels in high-oxidative muscles that are recruited during Ex. To test these hypotheses, sedentary (Sed) and rats that underwent Ex (30 m/min × 10% grade, 60 min/day, 5 days/wk, 8–12 wk) were studied using three experimental approaches. Training effectiveness was evidenced by increased citrate synthase activity in soleus and vastus lateralis (red section) muscles ( P < 0.05). Vasodilatory responses to the endothelium-dependent agent acetylcholine (ACh) in situ tended to be augmented by training in the red section of gastrocnemius muscle (RG; Sed: control, 0.69 ± 0.12; ACh, 1.25 ± 0.15; Ex: control, 0.86 ± 0.17; ACh, 1.76 ± 0.27 ml·min−1·100 g−1·mmHg−1; 0.05 < P < 0.10 for Ex vs. Sed during ACh). Responses to ACh in situ did not differ between Sed and Ex for either the soleus muscle or white section of gastrocnemius muscle (WG). Dilatory responses of second-order arterioles from the RG in vitro to flow (4–8 μl/min) and sodium nitroprusside (SNP; 10−7 through10−4 M), but not ACh, were augmented in Ex (vs. Sed; P < 0.05). Dilatory responses to ACh, flow, and SNP of arterioles from soleus and WG muscles did not differ between Sed and Ex. Content of the endothelial isoform of nitric oxide synthase (eNOS) was increased in second-order, fourth-order, and fifth-order arterioles from the RG of Ex; eNOS content was similar between Sed and Ex in vessels from the soleus and WG muscles. These findings indicate that Ex induces endothelial adaptations in fast-twitch, oxidative, glycolytic skeletal muscle. These adaptations may contribute to enhanced skeletal muscle blood flow in endurance-trained individuals.

scholarly journals Sex differences with aging in nutritive skeletal muscle blood flow: impact of exercise training, nitric oxide, and α-adrenergic-mediated mechanisms

2014 ◽  
Vol 307 (4) ◽  
pp. H524-H532 ◽  
Author(s):  
Justin D. La Favor ◽  
Raymond M. Kraus ◽  
Jonathan A. Carrithers ◽  
Steven L. Roseno ◽  
Timothy P. Gavin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Healthy Aging ◽  
Muscle Blood Flow ◽  
Young Men ◽  
Men And Women ◽  
Skeletal Muscle Blood Flow ◽  
Age Related

The incidence of cardiovascular disease increases progressively with age, but aging may affect men and women differently. Age-associated changes in vascular structure and function may manifest in impaired nutritive blood flow, although the regulation of nutritive blood flow in healthy aging is not well understood. The purpose of this study was to determine if nitric oxide (NO)-mediated or α-adrenergic-mediated regulation of nutritive skeletal muscle blood flow is impaired with advanced age, and if exercise training improves age-related deficiencies. Nutritive blood flow was monitored in the vastus lateralis of healthy young and aged men and women via the microdialysis-ethanol technique prior to and following seven consecutive days of exercise training. NO-mediated and α-adrenergic-mediated regulation of nutritive blood flow was assessed by microdialysis perfusion of acetylcholine, sodium nitroprusside, NG-monomethyl-l-arginine, norepinephrine, or phentolamine. Pretraining nutritive blood flow was attenuated in aged compared with young women (7.39 ± 1.5 vs. 15.5 ± 1.9 ml·100 g−1·min−1, P = 0.018), but not aged men (aged 13.5 ± 3.7 vs. young 9.4 ± 1.3 ml·100 g−1·min−1, P = 0.747). There were no age-associated differences in NO-mediated or α-adrenergic-mediated nutritive blood flow. Exercise training increased resting nutritive blood flow only in young men (9.4 ± 1.3 vs. 19.7 ml·100 g−1·min−1, P = 0.005). The vasodilatory effect of phentolamine was significantly reduced following exercise training only in young men (12.3 ± 6.14 vs. −3.68 ± 3.26 ml·100 g−1·min−1, P = 0.048). In conclusion, the age-associated attenuation of resting nutritive skeletal muscle blood flow was specific to women, while the exercise-induced alleviation of α-adrenergic mediated vasoconstriction that was specific to young men suggests an age-associated modulation of the sympathetic response to exercise training.

Biphasic effect of hydrogen peroxide on skeletal muscle arteriolar tone via activation of endothelial and smooth muscle signaling pathways

2004 ◽  
Vol 97 (3) ◽  
pp. 1130-1137 ◽  
Author(s):  
Csongor Csekő ◽  
Zsolt Bagi ◽  
Akos Koller
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Hydrogen Peroxide ◽  
Blood Flow ◽  
Smooth Muscle ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Local Regulation ◽  
Prostaglandin H ◽  
Arteriolar Tone

We hypothesized that hydrogen peroxide (H2O2) has a role in the local regulation of skeletal muscle blood flow, thus significantly affecting the myogenic tone of arterioles. In our study, we investigated the effects of exogenous H2O2 on the diameter of isolated, pressurized (at 80 mmHg) rat gracilis skeletal muscle arterioles (diameter of ∼150 μm). Lower concentrations of H2O2 (10−6–3 × 10−5 M) elicited constrictions, whereas higher concentrations of H2O2 (6 × 10−5–3 × 10−4 M), after initial constrictions, caused dilations of arterioles (at 10−4 M H2O2, −19 ± 1% constriction and 66 ± 4% dilation). Endothelium removal reduced both constrictions (to −10 ± 1%) and dilations (to 33 ± 3%) due to H2O2. Constrictions due to H2O2 were completely abolished by indomethacin and the prostaglandin H2/thromboxane A2 (PGH2/TxA2) receptor antagonist SQ-29548. Dilations due to H2O2 were significantly reduced by inhibition of nitric oxide synthase (to 38 ± 7%) but were unaffected by clotrimazole or sulfaphenazole (inhibitors of cytochrome P-450 enzymes), indomethacin, or SQ-29548. In endothelium-denuded arterioles, clotrimazole had no effect, whereas H2O2-induced dilations were significantly reduced by charybdotoxin plus apamin, inhibitors of Ca2+-activated K+ channels (to 24 ± 3%), the selective blocker of ATP-sensitive K+ channels glybenclamide (to 14 ± 2%), and the nonselective K+-channel inhibitor tetrabutylammonium (to −1 ± 1%). Thus exogenous administration of H2O2 elicits 1) release of PGH2/TxA2 from both endothelium and smooth muscle, 2) release of nitric oxide from the endothelium, and 3) activation of K+ channels, such as Ca2+-activated and ATP-sensitive K+ channels in the smooth muscle resulting in biphasic changes of arteriolar diameter. Because H2O2 at low micromolar concentrations activates several intrinsic mechanisms, we suggest that H2O2 contributes to the local regulation of skeletal muscle blood flow in various physiological and pathophysiological conditions.

ATP-induced vasodilation and purinergic receptors in the human leg: roles of nitric oxide, prostaglandins, and adenosine

2009 ◽  
Vol 296 (4) ◽  
pp. R1140-R1148 ◽  
Author(s):  
Stefan P. Mortensen ◽  
José González-Alonso ◽  
Laurids T. Bune ◽  
Bengt Saltin ◽  
Henriette Pilegaard ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Purinergic Receptors ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Pcr Analysis ◽  
Receptor Subtypes ◽  
Vastus Lateralis Muscle

Plasma ATP is thought to contribute to the local regulation of skeletal muscle blood flow. Intravascular ATP infusion can induce profound limb muscle vasodilatation, but the purinergic receptors and downstream signals involved in this response remain unclear. This study investigated: 1) the role of nitric oxide (NO), prostaglandins, and adenosine as mediators of ATP-induced limb vasodilation and 2) the expression and distribution of purinergic P2 receptors in human skeletal muscle. Systemic and leg hemodynamics were measured before and during 5–7 min of femoral intra-arterial infusion of ATP [0.45–2.45 μmol/min] in 19 healthy male subjects with and without coinfusion of NG-monomethyl-l-arginine (l-NMMA; NO formation inhibitor; 12.3 ± 0.3 (SE) mg/min), indomethacin (INDO; prostaglandin formation blocker; 613 ± 12 μg/min), and/or theophylline (adenosine receptor blocker; 400 ± 26 mg). During control conditions, ATP infusion increased leg blood flow (LBF) from baseline conditions by 1.82 ± 0.14 l/min. When ATP was coinfused with either l-NMMA, INDO, or l-NMMA + INDO combined, the increase in LBF was reduced by 14 ± 6, 15 ± 9, and 39 ± 8%, respectively (all P < 0.05), and was associated with a parallel lowering in leg vascular conductance and cardiac output and a compensatory increase in leg O2 extraction. Infusion of theophylline did not alter the ATP-induced leg hyperemia or systemic variables. Real-time PCR analysis of the mRNA content from the vastus lateralis muscle of eight subjects showed the highest expression of P2Y2 receptors of the 10 investigated P2 receptor subtypes. Immunohistochemistry showed that P2Y2 receptors were located in the endothelium of microvessels and smooth muscle cells, whereas P2X1 receptors were located in the endothelium and the sacrolemma. Collectively, these results indicate that NO and prostaglandins, but not adenosine, play a role in ATP-induced vasodilation in human skeletal muscle. The expression and localization of the nucleotide selective P2Y2 and P2X1 receptors suggest that these receptors may mediate ATP-induced vasodilation in skeletal muscle.

scholarly journals Effects of neuronal nitric oxide synthase inhibition on microvascular and contractile function in skeletal muscle of aged rats

2012 ◽  
Vol 303 (8) ◽  
pp. H1076-H1084 ◽  
Author(s):  
Daniel M. Hirai ◽  
Steven W. Copp ◽  
Clark T. Holdsworth ◽  
Scott K. Ferguson ◽  
Timothy I. Musch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Contractile Function ◽  
Muscle Blood Flow ◽  
Force Production ◽  
Microvascular Function ◽  
Brown Norway ◽  
Phosphorescence Quenching ◽  
Nnos Inhibition

Advanced age is associated with derangements in skeletal muscle microvascular function during the transition from rest to contractions. We tested the hypothesis that, contrary to what was reported previously in young rats, selective neuronal nitric oxide (NO) synthase (nNOS) inhibition would result in attenuated or absent alterations in skeletal muscle microvascular oxygenation (Po2mv), which reflects the matching between muscle O2 delivery and utilization, following the onset of contractions in old rats. Spinotrapezius muscle blood flow (radiolabeled microspheres), Po2mv (phosphorescence quenching), O2 utilization (V̇o2; Fick calculation), and submaximal force production were measured at rest and following the onset of contractions in anesthetized old male Fischer 344 × Brown Norway rats (27 to 28 mo) pre- and postselective nNOS inhibition (2.1 μmol/kg S-methyl-l-thiocitrulline; SMTC). At rest, SMTC had no effects on muscle blood flow ( P > 0.05) but reduced V̇o2 by ∼23% ( P < 0.05), which elevated basal Po2mv by ∼18% ( P < 0.05). During contractions, steady-state muscle blood flow, V̇o2, Po2mv, and force production were not altered after SMTC ( P > 0.05 for all). The overall Po2mv dynamics following onset of contractions was also unaffected by SMTC (mean response time: pre, 19.7 ± 1.5; and post, 20.0 ± 2.0 s; P > 0.05). These results indicate that the locus of nNOS-derived NO control in skeletal muscle depends on age and metabolic rate (i.e., rest vs. contractions). Alterations in nNOS-mediated regulation of contracting skeletal muscle microvascular function with aging may contribute to poor exercise capacity in this population.

Nitric oxide and muscle blood flow in exercise

2008 ◽  
Vol 33 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Michael E. Tschakovsky ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Integrated Control ◽  
Muscle Blood Flow ◽  
Dynamic Adjustment ◽  
Resistance Vessels ◽  
Sympathetic Vasoconstriction ◽  
Exercise Hyperemia ◽  
Blood Flow Control

Despite being the subject of investigation for well over 100 years, the nature of exercising muscle blood flow control remains, in many respects, poorly understood. In this review we focus on the potential role of nitric oxide in vasodilation of muscle resistance vessels during a bout of exercise. Its contribution is explored in the context of whether it contributes to steady-state exercise hyperemia, the dynamic adjustment of muscle blood flow to exercise, or the modulation of sympathetic vasoconstriction in exercising muscle. It appears that the obligatory role of nitric oxide in all three of these categories is modest at best. The elucidation of the integrated nature of exercise hyperemia control in terms of synergy and redundancy of mechanism interaction remains in its infancy, and much more remains to be learned about the role of nitric oxide in this type of integrated control.

Muscle Blood Flow and Mitochondrial Function: Influence of Aging

2002 ◽  
Vol 12 (3) ◽  
pp. 368-378 ◽  
Author(s):  
Ronald L. Terjung ◽  
Ryszard Zarzeczny ◽  
H.T. Yang
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Muscle Blood Flow ◽  
The Elderly ◽  
Exchange Capacity ◽  
Oxygen Exchange ◽  
Whole Body ◽  
Tissue Blood Flow ◽  
Fiber Types

Skeletal muscle mitochondrial capacity (mito), tissue blood flow (BF) capacity, and oxygen exchange capacity (e.g., DO2) appear to be well matched. The different skeletal muscle fiber types and muscle remodeled, due to inactivity >(e.g., related to aging or disease) or exercise training, exhibit widely differing aerobics capacities (V̇O2max). Yet, there are remarkably coordinated alterations in these 3 parameters in each of these conditions. With such a balance, there is likely shared control among these parameters in limiting (V̇O2max) of muscle, although this is a matter of considerable debate. The reduction in aerobic capacity in elderly can be improved by submaximal aerobic exercise training; this is related to increases in muscle mitochondria concentration and capillarity, but probably not BF capacity, as this is limited by central cardiovascular function. Thus, exercise-induced biochemical adaptations and angiogenesis occur in the elderly. The increase in muscle capillarity likely contributes to the increased oxygen exchange capacity, typical of endurance type training. The increase in [mito] appears essential to realize the increased in muscle V̇O2max with training and amplifies the rate-limiting influence of the muscle’s oxygen exchange capacity. Further, vascular remodeling induced by exercise in the elderly could be effective at improving flow capacity, if limited by peripheral obstruction. Thus, the limits to aerobic function specific to aged muscle appear most influenced by inactivity, whereas central cardiovascular changes impact whole body performance. Some may consider the aged myocyte as a small, inactive, normal myocyte in need of activity!

Effects of high-intensity sprint training on skeletal muscle blood flow in rats

1991 ◽  
Vol 71 (4) ◽  
pp. 1387-1395 ◽  
Author(s):  
T. I. Musch ◽  
J. A. Terrell ◽  
M. R. Hilty
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
High Intensity ◽  
Maximal Exercise ◽  
Regional Blood Flow ◽  
Muscle Blood Flow ◽  
Female Rats ◽  
Sprint Training ◽  
Skeletal Muscle Blood Flow ◽  
Abdominal Region

The regional blood flow response (via radioactive microspheres) was determined for female rats after 6 wk of high-intensity sprint training (HIST) or limited cage activity as the animals exercised at work loads that would elicit maximal O2 uptake. Blood flow to the different organs of the abdominal region was greatly reduced during maximal exercise conditions, and the magnitude of the reduction appeared to be similar for both the HIST group of rats and their sedentary (SED) control counterparts. Of the 20 different hindlimb muscles examined in the present study, blood flow to the soleus, plantaris, gastrocnemius, flexor hallicus longus, vastus lateralis, rectus femoris, biceps femoris, and adductor magnus and brevis muscles was significantly greater (P less than 0.05) in the HIST rats during maximal exercise conditions than in the SED control rats. Correspondingly, blood flow to the total hindlimb during maximal exercise was also significantly greater in the HIST rats than in the SED control rats [240 +/- 18 vs. 192 +/- 15 (SE) ml.min-1.100 g-1]. These results support the contention that the increase in maximal cardiac output that is produced by HIST in the rat is primarily directed toward the working skeletal muscle and not toward the organs found in the abdominal region. We conclude from these experiments that HIST will produce significant adaptations in central cardiac function and skeletal muscle blood flow in the rat.

scholarly journals Combined inhibition of nitric oxide and prostaglandins reduces human skeletal muscle blood flow during exercise

2002 ◽  
Vol 543 (2) ◽  
pp. 691-698 ◽  
Author(s):  
Robert Boushel ◽  
Henning Langberg ◽  
Carsten Gemmer ◽  
Jens Olesen ◽  
Regina Crameri ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Human Skeletal Muscle ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow
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