Short-term training enhances endothelium-dependent dilation of coronary arteries, not arterioles

2003 ◽  
Vol 94 (1) ◽  
pp. 234-244 ◽  
Author(s):  
M. Harold Laughlin ◽  
Leona J. Rubin ◽  
James W. E. Rush ◽  
E. M. Price ◽  
William G. Schrage ◽  
...  
Keyword(s):  
Exercise Training ◽  
Coronary Arteries ◽  
Citrate Synthase ◽  
Immunoblot Analysis ◽  
Intraluminal Pressure ◽  
Mrna Levels ◽  
Short Term ◽  
Miniature Swine ◽  
Aortic Endothelial Cells ◽  
Coronary Arterioles

Our objective was to test the hypothesis that short-term exercise training (STR) of pigs increases endothelium-dependent dilation (EDD) of coronary arteries but not coronary arterioles. Female Yucatan miniature swine ran on a treadmill for 1 h, at 3.5 mph, twice daily for 7 days (STR; n = 28). Skeletal muscle citrate synthase activity was increased in STR compared with sedentary controls (Sed; n = 26). Vasoreactivity was evaluated in isolated segments of conduit arteries (1–2 mm ID, 3–4 mm length) mounted on myographs and in arterioles (50–100 μm ID) isolated and cannulated with micropipettes with intraluminal pressure set at 60 cmH2O. EDD was assessed by examining responses to increasing concentrations of bradykinin (BK) (conduit arteries 10−12–10−6 M and arterioles 10−13–10−6 M). There were no differences in maximal EDD or BK sensitivity of coronary arterioles from Sed and STR hearts. In contrast, sensitivity of conduit arteries (precontracted with PGF2α) to BK was increased significantly ( P < 0.05) in STR (EC50, 2.33 ± 0.62 nM, n = 12) compared with Sed animals (EC50, 3.88 ± 0.62 nM, n = 13). Immunoblot analysis revealed that coronary arteries from STR and Sed animals had similar levels of endothelial nitric oxide synthase (eNOS). In contrast, eNOS protein was increased in STR aortic endothelial cells. Neither protein nor mRNA levels of eNOS were different in coronary arterioles from STR compared with Sed animals. STR did not alter expression of superoxide dismutase (SOD-1) protein in any artery examined. We conclude that pigs exhibit increases in EDD of conduit arteries, but not in coronary arterioles, at the onset of exercise training. These adaptations in pigs do not appear to be mediated by alterations in eNOS or SOD-1 expression.

Short-term exercise training alters responses of porcine femoral and brachial arteries

1997 ◽  
Vol 82 (5) ◽  
pp. 1438-1444 ◽  
Author(s):  
Richard M. McAllister ◽  
M. Harold Laughlin
Keyword(s):  
Exercise Training ◽  
Citrate Synthase ◽  
Calcium Ionophore ◽  
Maximal Response ◽  
Short Term ◽  
Miniature Swine ◽  
Vascular Rings ◽  
Increased Sensitivity ◽  
Relaxation Responses

McAllister, Richard M., and M. Harold Laughlin.Short-term exercise training alters responses of porcine femoral and brachial arteries. J. Appl. Physiol. 82(5): 1438–1444, 1997.—The primary purpose of this study was to test the hypothesis that short-term exercise training enhances endothelium-dependent relaxation of porcine femoral and brachial arteries. Miniature swine ran on a treadmill for 1 h at 3.5 miles/h, twice daily, for 7 consecutive days (Trn; n = 8). Compared with sedentary controls (Sed; n = 7), Trn swine exhibited increased skeletal muscle citrate synthase activity ( P < 0.05). Vascular rings ∼3 mm in axial length were prepared from segments of femoral and brachial arteries, and responses to vasoactive agents were determined in vitro. Sensitivity to bradykinin (BK) was enhanced in brachial vascular rings from Trn swine compared with those from Sed swine, as indicated by lower concentration of vasorelaxing agent eliciting 50% of maximal response values [Sed, 8.63 ± 0.09 (−log M); Trn, 9.07 ± 0.13; P < 0.05]. This difference between groups was preserved in brachial rings in which formation of nitric oxide and vasodilator prostaglandins were inhibited [Sed, 8.57 ± 0.17 (−log M); Trn, 8.97 ± 0.13; P < 0.05]. Sensitivity to BK was not different between Sed and Trn in femoral arterial rings. Relaxation responses to the calcium ionophore A-23187 and sodium nitroprusside were not altered with training. Femoral and brachial arterial rings from Trn swine, compared with those from Sed swine, exhibited augmented vasocontraction across a range of concentrations and increased sensitivity to norepinephrine (all P < 0.05). These findings indicate that responses of porcine femoral and brachial arteries change in response to short-term training. Together with findings from previous studies involving longer term training, our data suggest that vascular adaptations may differ at different time points during long-term endurance exercise training.

Training induces nonuniform increases in eNOS content along the coronary arterial tree

2001 ◽  
Vol 90 (2) ◽  
pp. 501-510 ◽  
Author(s):  
M. H. Laughlin ◽  
J. S. Pollock ◽  
J. F. Amann ◽  
M. L. Hollis ◽  
C. R. Woodman ◽  
...  
Keyword(s):  
Exercise Training ◽  
Coronary Arteries ◽  
Oxidative Capacity ◽  
Heart Weight ◽  
Resistance Arteries ◽  
Miniature Swine ◽  
Arterial Tree ◽  
Small Arteries ◽  
Enos Protein ◽  
Coronary Arterioles

Exercise training produces enhanced nitric oxide (NO)-dependent, endothelium-mediated vasodilator responses of porcine coronary arterioles but not conduit coronary arteries. The purpose of this study was to test the hypothesis that exercise training increases the amount of endothelial NO synthase (eNOS) in the coronary arterial microcirculation but not in the conduit coronary arteries. Miniature swine were either exercise trained or remained sedentary for 16–20 wk. Exercise-trained pigs exhibited increased skeletal muscle oxidative capacity, exercise tolerance, and heart weight-to-body weight ratios. Content of eNOS protein was determined with immunoblot analysis in conduit coronary arteries (2- to 3-mm ID), small arteries (301- to 1,000-μm ID), resistance arteries (151- to 300-μm ID), and three sizes of coronary arterioles [large (101- to 150-μm ID), intermediate (51- to 100-μm ID), and small (<50-μm ID)]. Immunoblots revealed increased eNOS protein in some sizes of coronary arteries and arterioles but not in others. Content of eNOS was increased by 60–80% in small and large arterioles, resistance arteries, and small arteries; was increased by 10–20% in intermediate-sized arterioles; and was not changed or decreased in conduit arteries. Immunohistochemistry revealed that eNOS was located in the endothelial cells in all sizes of coronary artery. We conclude that exercise training increases eNOS protein expression in a nonuniform manner throughout the coronary arterial tree. Regional differences in shear stress and intraluminal pressures during exercise training bouts may be responsible for the distribution of increased eNOS protein content in the coronary arterial tree.

Gender influences coronary L-type Ca2+current and adaptation to exercise training in miniature swine

2001 ◽  
Vol 91 (6) ◽  
pp. 2503-2510 ◽  
Author(s):  
D. K. Bowles
Keyword(s):  
Smooth Muscle ◽  
Exercise Training ◽  
Endurance Training ◽  
Coronary Arteries ◽  
Current Density ◽  
Adaptive Response ◽  
Heart Weight ◽  
Internal Diameter ◽  
Resistance Arteries ◽  
Miniature Swine

Endurance exercise training increases smooth muscle L-type Ca2+current density in both resistance and proximal coronary arteries of female miniature swine. The purpose of the present study was to determine 1) whether gender differences exist in coronary smooth muscle (CSM) L-type Ca2+ current density and 2) whether endurance training in males would demonstrate a similar adaptive response as females. Proximal, conduit (∼1.0 mm), and resistance [∼200 μm (internal diameter)] coronary arteries were obtained from sedentary and treadmill-trained swine of both sexes. CSM were isolated by enzymatic digestion (collagenase plus elastase), and voltage-gated Ca2+-channel current ( I Ca) was determined by using whole cell voltage clamp during superfusion with 75 mM tetraethylammonium chloride and 10 mM BaCl2. Current-voltage relationships were obtained at test potentials from −60 to 70 mV from a holding potential of −80 mV, and I Ca was normalized to cell capacitance (pA/pF). Endurance treadmill training resulted in similar increases in heart weight-to-body weight ratio, endurance time, and skeletal muscle citrate synthase activity in male and female swine. I Ca density was significantly greater in males compared with females in both conduit (−7.57 ± 0.58 vs. −4.14 ± 0.47 pA/pF) and resistance arteries (−11.25 ± 0.74 vs. −6.49 ± 0.87 pA/pF, respectively). In addition, voltage-dependent activation of I Ca in resistance arteries was shifted to more negative membrane potentials in males. Exercise training significantly increased I Ca density in both conduit and resistance arteries in females (−7.01 ± 0.47 and −9.73 ± 1.13 pA/pF, respectively) but had no effect in males (−8.61 ± 0.50 and −12.04 ± 1.07 pA/pF, respectively). Thus gender plays a significant role in determining both the magnitude and voltage dependence of I Ca in CSM and the adaptive response of I Ca to endurance training.

Effect of short-term, high-intensity exercise training on human skeletal muscle citrate synthase maximal activity: single versus multiple bouts per session

2019 ◽  
Vol 44 (12) ◽  
pp. 1391-1394
Author(s):  
Martin J. MacInnis ◽  
Lauren E. Skelly ◽  
F. Elizabeth Godkin ◽  
Brian J. Martin ◽  
Thomas R. Tripp ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Maximal Activity ◽  
High Intensity Exercise ◽  
Short Term ◽  
Significant Difference

The legs of 9 men (age 21 ± 2 years, 45 ± 4 mL/(kg·min)) were randomly assigned to complete 6 sessions of high-intensity exercise training, involving either one or four 5-min bouts of counterweighted, single-leg cycling. Needle biopsies from vastus lateralis revealed that citrate synthase maximal activity increased after training in the 4-bout group (p = 0.035) but not the 1-bout group (p = 0.10), with a significant difference between groups post-training (13%, p = 0.021). Novelty Short-term training using brief intense exercise requires multiple bouts per session to increase mitochondrial content in human skeletal muscle.

scholarly journals Exercise Training-Induced PPARβ Increases PGC-1α Protein Stability and Improves Insulin-Induced Glucose Uptake in Rodent Muscles

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 652 ◽  
Author(s):  
Ju-Sik Park ◽  
John O. Holloszy ◽  
Kijin Kim ◽  
Jin-Ho Koh
Keyword(s):  
Cytochrome C ◽  
Exercise Training ◽  
Protein Stability ◽  
Glucose Uptake ◽  
Citrate Synthase ◽  
Peroxisome Proliferator ◽  
Mitochondrial Enzymes ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Peroxisome Proliferator Activated Receptor

This study aimed to investigate the long-term effects of training intervention and resting on protein expression and stability of peroxisome proliferator-activated receptor β/δ (PPARβ), peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC1α), glucose transporter type 4 (GLUT4), and mitochondrial proteins, and determine whether glucose homeostasis can be regulated through stable expression of these proteins after training. Rats swam daily for 3, 6, 9, 14, or 28 days, and then allowed to rest for 5 days post-training. Protein and mRNA levels were measured in the skeletal muscles of these rats. PPARβ was overexpressed and knocked down in myotubes in the skeletal muscle to investigate the effects of swimming training on various signaling cascades of PGC-1α transcription, insulin signaling, and glucose uptake. Exercise training (Ext) upregulated PPARβ, PGC-1α, GLUT4, and mitochondrial enzymes, including NADH-ubiquinone oxidoreductase (NUO), cytochrome c oxidase subunit I (COX1), citrate synthase (CS), and cytochrome c (Cyto C) in a time-dependent manner and promoted the protein stability of PPARβ, PGC-1α, GLUT4, NUO, CS, and Cyto C, such that they were significantly upregulated 5 days after training cessation. PPARβ overexpression increased the PGC-1α protein levels post-translation and improved insulin-induced signaling responsiveness and glucose uptake. The present results indicate that Ext promotes the protein stability of key mitochondria enzymes GLUT4, PGC-1α, and PPARβ even after Ext cessation.

Exercise training restores adenosine-induced relaxation in coronary arteries distal to chronic occlusion

2000 ◽  
Vol 278 (6) ◽  
pp. H1984-H1992 ◽  
Author(s):  
Cristine L. Heaps ◽  
Michael Sturek ◽  
Julie A. Rapps ◽  
M. Harold Laughlin ◽  
Janet L. Parker
Keyword(s):  
Coronary Artery ◽  
Exercise Training ◽  
Sodium Nitroprusside ◽  
Coronary Arteries ◽  
Coronary Occlusion ◽  
Circumflex Coronary Artery ◽  
Miniature Swine ◽  
Chronic Occlusion ◽  
Chronic Coronary Occlusion ◽  
Camp And Cgmp

We previously reported that canine collateral-dependent coronary arteries exhibit impaired relaxation to adenosine but not sodium nitroprusside. In contrast, exercise training enhances adenosine sensitivity of normal porcine coronary arteries. These results stimulated the hypothesis that chronic coronary occlusion and exercise training produce differential effects on cAMP- versus cGMP-mediated relaxation. To test this hypothesis, Ameroid occluders were surgically placed around the proximal left circumflex coronary artery (LCx) of female Yucatan miniature swine 8 wk before initiating sedentary or exercise training (treadmill run, 16 wk) protocols. Relaxation to the cAMP-dependent vasodilators adenosine (10− 7 to 10− 3 M) and isoproterenol (3 × 10− 8 to 3 × 10− 5 M) were impaired in collateral-dependent LCx versus nonoccluded left anterior descending (LAD) arterial rings isolated from sedentary but not exercise-trained pigs. Furthermore, adenosine-mediated reductions in simultaneous tension and myoplasmic free Ca2+ were impaired in LCx versus LAD arteries isolated from sedentary but not exercise-trained pigs. In contrast, relaxation in response to the cAMP-dependent vasodilator forskolin (10− 9 to 10− 5 M) and the cGMP-dependent vasodilator sodium nitroprusside (10− 9 to 10− 4 M) was not different in LCx versus LAD arteries of sedentary or exercise-trained animals. These data suggest that chronic occlusion impairs receptor-dependent, cAMP-mediated relaxation; receptor-independent cAMP- and cGMP-mediated relaxation were unimpaired. Importantly, exercise training restores cAMP-mediated relaxation of collateral-dependent coronary arteries.

SOD-1 expression in pig coronary arterioles is increased by exercise training

2000 ◽  
Vol 279 (5) ◽  
pp. H2068-H2076 ◽  
Author(s):  
James W. E. Rush ◽  
M. Harold Laughlin ◽  
Christopher R. Woodman ◽  
Elmer M. Price
Keyword(s):  
Exercise Training ◽  
Half Life ◽  
Superoxide Anion ◽  
Aerobic Exercise Training ◽  
Internal Diameter ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Biological Half Life ◽  
Copper Zinc ◽  
Coronary Arterioles

Coronary arterioles of exercise-trained (EX) pigs have enhanced nitric oxide (NO·)-dependent dilation. Evidence suggests that the biological half-life of NO· depends in part on the management of the superoxide anion. The purpose of this study was to test the hypothesis that expression of cytosolic copper/zinc-dependent superoxide dismutase (SOD)-1 is increased in coronary arterioles as a result of exercise training. Male Yucatan pigs either remained sedentary (SED, n = 4) or were EX ( n = 4) on a motorized treadmill for 16–20 wk. Individual coronary arterioles (∼100-μm unpressurized internal diameter) were dissected and frozen. Coronary arteriole SOD-1 protein (via immunoblots) increased as a result of exercise training (2.16 ± 0.35 times SED levels) as did SOD-1 enzyme activity (measured via inhibition of pyrogallol autooxidation; ∼75% increase vs. SED). In addition, SOD-1 mRNA levels (measured via RT-PCR) were higher in EX arterioles (1.68 ± 0.16 times the SED levels). There were no effects of exercise training on the levels of SOD-2 (mitochondrial), catalase, or p67phox proteins. Thus chronic aerobic exercise training selectively increases the levels of SOD-1 mRNA, protein, and enzymatic activity in porcine coronary arterioles. Increased SOD-1 could contribute to the enhanced NO·-dependent dilation previously observed in EX porcine coronary arterioles by improving management of superoxide in the vascular cell environment, thus prolonging the biological half-life of NO·.

scholarly journals Effect of exercise training on nitric oxide and superoxide/H2O2 signaling pathways in collateral-dependent porcine coronary arterioles

2012 ◽  
Vol 112 (9) ◽  
pp. 1546-1555 ◽  
Author(s):  
Wei Xie ◽  
Janet L. Parker ◽  
Cristine L. Heaps
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Exercise Training ◽  
Vascular Function ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Miniature Swine ◽  
Protein Levels ◽  
Endothelial Nitric Oxide ◽  
Coronary Arterioles

Endothelial nitric oxide (NO) synthase (NOS) has been shown to contribute to enhanced vascular function after exercise training. Recent studies have revealed that relatively low concentrations of reactive oxygen species can contribute to endothelium-dependent vasodilation under physiological conditions. We tested the hypothesis that exercise training enhances endothelial function via endothelium-derived vasodilators, NO and superoxide/H2O2, in the underlying setting of chronic coronary artery occlusion. An ameroid constrictor was placed around the proximal left circumflex coronary artery to induce gradual occlusion in Yucatan miniature swine. At 8 wk postoperatively, pigs were randomly assigned to sedentary (pen-confined) or exercise-training (treadmill-run: 5 days/wk for 14 wk) regimens. Exercise training significantly enhanced concentration-dependent, bradykinin-mediated dilation in cannulated collateral-dependent arterioles (∼130 μm diameter) compared with sedentary pigs. NOS inhibition reversed training-enhanced dilation at low bradykinin concentrations in collateral-dependent arterioles, although increased dilation persisted at higher bradykinin concentrations. Total and phosphorylated (Ser1179) endothelial NOS protein levels were significantly increased in arterioles from collateral-dependent compared with the nonoccluded region, independent of exercise. The H2O2 scavenger polyethylene glycol-catalase abolished the training-enhanced bradykinin-mediated dilation in collateral-dependent arterioles; similar results were observed with the SOD inhibitor diethyldithiocarbamate. Fluorescence measures of bradykinin-stimulated H2O2 levels were significantly increased by exercise training, independent of occlusion. The NADPH inhibitor apocynin significantly attenuated bradykinin-mediated dilation in arterioles of exercise-trained, but not sedentary, pigs and was associated with significantly increased protein levels of the NADPH subunit p67phox. These data provide evidence that, in addition to NO, the superoxide/H2O2 signaling pathway significantly contributes to exercise training-enhanced endothelium-mediated dilation in collateral-dependent coronary arterioles.

Effect of short-term exercise training on angiogenic growth factor gene responses in rats

2001 ◽  
Vol 90 (4) ◽  
pp. 1219-1226 ◽  
Author(s):  
Timothy P. Gavin ◽  
Peter D. Wagner
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Exercise Training ◽  
Citrate Synthase ◽  
Short Term ◽  
Vegf Mrna ◽  
Oxidative Potential ◽  
Factor Gene ◽  
Growth Factor Gene ◽  
Exercise Induced

We investigated whether 1) 5 days of exercise training would reduce the acute exercise-induced increase in skeletal muscle growth factor gene expression; and 2) reductions in the increase in growth factor gene expression in response to short-term exercise training would be coincident with increases in skeletal muscle oxidative potential. Female Wistar rats were used. Six groups (rest; exercise for 1–5 consecutive days) were used to measure the growth factor response through the early phases of an exercise training program. Vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1), and basic fibroblast growth factor (bFGF) mRNA were analyzed from the left gastrocnemius by quantitative Northern blot. Citrate synthase activity was analyzed from the right gastrocnemius. VEGF and TGF-β1 mRNA increased after each of 5 days of exercise training, whereas exercise on any day did not increase bFGF mRNA. On day 1, the VEGF mRNA response was significantly greater than on days 2–5. However, the reduced increase in VEGF mRNA observed on days 2–5 was not coincident with increases in citrate synthase activity. These findings suggest that, in skeletal muscle, 1) VEGF and TGF-β1 mRNA are increased through 5 days of exercise training and 2) the reduced exercise-induced increase in VEGF mRNA responses on days 2–5 does not result from increases in oxidative potential.

Biochemical characterization of exercise-trained porcine myocardium

1991 ◽  
Vol 71 (1) ◽  
pp. 229-235 ◽  
Author(s):  
M. H. Laughlin ◽  
C. C. Hale ◽  
L. Novela ◽  
D. Gute ◽  
N. Hamilton ◽  
...  
Keyword(s):  
Exercise Training ◽  
Cardiac Muscle ◽  
Cardiac Tissue ◽  
Biochemical Characterization ◽  
Citrate Synthase ◽  
Oxidative Capacity ◽  
Miniature Swine ◽  
Metabolic System ◽  
Skeletal Muscle Myosin ◽  
Biochemical Systems

The purpose of this study was to determine whether cardiac biochemical adaptations are induced by chronic exercise training (ET) of miniature swine. Female Yucatan miniature swine were trained on a treadmill or were cage confined (C) for 16–22 wk. After training, the ET pigs had increased exercise tolerance, lower heart rates during exercise at submaximal intensities, moderate cardiac hypertrophy, increased coronary blood flow capacity, and increased oxidative capacity of skeletal muscle. Myosin from both the C and ET hearts was 100% of the V3 isozyme, and there were no differences between the myosin adenosine triphosphatase (ATPase) or myofibrillar ATPase activities of C and ET hearts. Also, the sarcoplasmic reticulum Ca(2+)-ATPase activity and Na(+)-Ca2+ exchange activity of sarcolemmal vesicles were the same in cardiac muscle of C and ET hearts. Finally, the glycolytic and oxidative capacity of ET cardiac muscle was not different from control, since phosphofructokinase, citrate synthase, and 3-hydroxyacyl-CoA dehydrogenase activities were the same in cardiac tissue from ET and C pigs. We conclude that endurance exercise training does not provide sufficient stress on the heart of a large mammal to induce changes in any of the three major cardiac biochemical systems of the porcine myocardium: the contractile system, the Ca2+ regulatory systems, or the metabolic system.

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