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.

Effects of exercise training on responses of peripheral and visceral arteries in swine

1996 ◽  
Vol 80 (1) ◽  
pp. 216-225 ◽  
Author(s):  
R. M. McAllister ◽  
J. K. Kimani ◽  
J. L. Webster ◽  
J. L. Parker ◽  
M. H. Laughlin
Keyword(s):  
Blood Flow ◽  
Exercise Training ◽  
Acute Exercise ◽  
Contractile Response ◽  
Calcium Ionophore ◽  
Time To Exhaustion ◽  
Miniature Swine ◽  
Contractile Responses ◽  
Vasomotor Reactivity

Blood flow to skeletal muscle during exercise is greater in the trained state. We hypothesized that intrinsic vasomotor reactivity of arteries to active muscle during training bouts would be altered to favor a relative vasodilation after training. To test this hypothesis, miniature swine were pen confined (Sed; n = 30) or treadmill trained for 5 days/wk over 16-20 wk (Trn; n = 32). Efficacy of training was indicated by myocardial hypertrophy (4.84 +/- 0.11 and 5.81 +/- 0.12 g/kg body wt for Sed and Trn, respectively, P < 0.0005), training bradycardia at several submaximal running speeds of a maximal exercise test, increased running time to exhaustion (26 +/- 1 and 35 +/- 1 min for Sed and Trn, respectively, P < 0.0005), and increased oxidative capacities of several locomotory skeletal muscles. Segments of femoral, brachial, mesenteric, renal, and hepatic arteries were isolated from Sed and Trn swine. Isometric contractile and relaxation properties of vascular rings cut from these segments were determined in vitro. Contractile responses to KCl and norepinephrine (NE) were determined, as were relaxation responses to sodium nitroprusside and adenosine, agents acting directly on vascular smooth muscle, and the endothelium-dependent agents bradykinin and the calcium ionophore A-23187. Responses to vasocontractile and vasorelaxation agents were not different between Sed and Trn swine for vessels serving active muscles (i.e., femoral, brachial). On the other hand, renal arterial rings from Trn swine exhibited lesser contractile responses than those from Sed swine across a range of NE concentrations (P < 0.05) and approximately 25% less maximal contractile response to NE (32.7 +/- 2.6 and 24.2 +/- 2.1 g for Sed and Trn, respectively, P < 0.01). Responses of other vessels serving viscera (i.e., mesenteric, hepatic) were unchanged with training. These data indicate that vasomotor reactivity of porcine conduit-type arteries generally does not change with exercise training. An exception is the lesser contractile response to NE in renal artery, which could permit better preservation of renal blood flow during acute exercise in trained animals.

scholarly journals Interaction of gender and exercise training: vasomotor reactivity of porcine skeletal muscle arteries

2001 ◽  
Vol 90 (1) ◽  
pp. 216-227 ◽  
Author(s):  
M. Harold Laughlin ◽  
William G. Schrage ◽  
Richard M. McAllister ◽  
H. A. Garverick ◽  
A. W. Jones
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Vascular Reactivity ◽  
Response Curves ◽  
Miniature Swine ◽  
Contractile Responses ◽  
Relaxation Responses ◽  
Gender Influences ◽  
Endothelium Dependent Relaxation

The purpose of the present study was to test the hypothesis that gender influences exercise training-induced adaptations of vascular reactivity of porcine arteries that provide blood flow to skeletal muscle and femoral and brachial arteries. Male and female Yucatan miniature swine were exercise trained on a motor-driven treadmill or cage confined for 16–20 wk. Contractile responses of arterial rings were evaluated in vitro by determining concentration-response curves for endothelin-1 (ET-1; 10−10 to 10−7 M) and norepinephrine (NE; 10−10 to 10−4 M). Relaxation responses of arteries precontracted with 30 μM PGF2αwere examined for endothelium-dependent agents [bradykinin (BK; 10−11 to 10−6 M), ACh (10−10 to 10−4 M), and a Ca2+ ionophore, A-23187 (10−6 M)] and a endothelium-independent agent [sodium nitroprusside (10−10 to 10−4 M)]. Arteries from female pigs developed greater contractile force in response to ET-1 than arteries from male pigs, whereas contractile responses to NE and KCl were similar in arteries from both genders. Femoral arteries from females exhibited greater endothelium-mediated vasorelaxation (BK and ACh) than did those from males. In contrast, brachial arteries of males were more responsive to BK and ACh than brachial arteries of females. Exercise training increased ET-1-induced contractions in arteries from males (without endothelium) but not in arteries from females. Training had no effect on endothelium-dependent relaxation in arteries from males but increased relaxation responses in brachial arteries from females. We conclude that both gender and anatomic origin of the artery influence exercise training-induced adaptations of vascular reactivity of porcine skeletal muscle conduit arteries.

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.

Inhibition of Platelet Aggregation by Ethanol in Vitro Shows Specificity for Aggregating Agent Used and Is Influenced by Platelet Lipid Composition

1982 ◽  
Vol 48 (01) ◽  
pp. 049-053 ◽  
Author(s):  
C G Fenn ◽  
J M Littleton
Keyword(s):  
Platelet Aggregation ◽  
Lipid Composition ◽  
Saturated Fatty Acids ◽  
Calcium Ionophore ◽  
Cholesterol Content ◽  
Membrane Lipid ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Increased Sensitivity

SummaryEthanol at physiologically tolerable concentrations inhibited platelet aggregation in vitro in a relatively specific way, which may be influenced by platelet membrane lipid composition. Aggregation to collagen, calcium ionophore A23187 and thrombin (low doses) were often markedly inhibited by ethanol, adrenaline and ADP responses were little affected, and aggregation to exogenous arachidonic acid was actually potentiated by ethanol. Aggregation to collagen, thrombin and A23187 was inhibited more by ethanol in platelets enriched with saturated fatty acids than in those enriched with unsaturated fats. Platelets enriched with cholesterol showed increased sensitivity to ADP, arachidonate and adrenaline but this increase in cholesterol content did not appear to influence the inhibition by ethanol of platelet responses. The results suggest that ethanol may inhibit aggregation by an effect on membrane fluidity and/or calcium mobilization resulting in decreased activity of a membrane-bound phospholipase.

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.

Endothelial and vascular smooth muscle responses are altered after left lung autotransplantation

1994 ◽  
Vol 266 (5) ◽  
pp. H2026-H2032 ◽  
Author(s):  
N. A. Flavahan ◽  
T. D. Aleskowitch ◽  
P. A. Murray
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Left Lung ◽  
Calcium Ionophore ◽  
Selective Reduction ◽  
Isometric Tension ◽  
Maximal Response ◽  
No Donor ◽  
Significant Difference ◽  
Increased Sensitivity

Left lung autotransplantation (LLA) increased the pulmonary vasoconstriction evoked by phenylephrine and attenuated the vasodilatation caused by acetylcholine or bradykinin in conscious dogs. To study the mechanisms responsible for these changes, pulmonary arterial rings were isolated from right (control) and left (LLA) lower lobes of dogs 1-26 mo after LLA and were suspended for isometric tension recording. Compared with control rings from the same anatomic location, contractions to phenylephrine were increased after LLA in rings with or without endothelium. In arterial rings contracted to 50% of their maximal response to phenylephrine, acetylcholine, bradykinin, and calcium ionophore caused endothelium-dependent relaxations that were reduced in LLA compared with control rings. In arterial rings from control and LLA lungs, relaxations to acetylcholine were not altered by inhibition of cyclooxygenase (indomethacin) but were reduced after inhibition of NO synthase [N omega-nitro-L-arginine methyl ester (L-NAME)]. After L-NAME, there was no longer any significant difference in acetylcholine-induced relaxation between arterial rings from control and LLA lungs. Relaxation to SIN-1, a NO donor, was similar in arterial rings (without endothelium) from control and LLA lungs. The results suggest that LLA causes an increased sensitivity of vascular smooth muscle to alpha 1-adrenergic activation and endothelial dysfunction that is mediated by a selective reduction in the activity of endothelium-derived relaxing factor/NO.

Calcium-independent stimulation of glycogenolysis by arginine vasotocin and catecholamines in liver of the axolotl (Ambystoma mexicanum) in vitro

1986 ◽  
Vol 109 (1) ◽  
pp. 75-84 ◽  
Author(s):  
P. A. Janssens ◽  
J. Kleineke ◽  
A. G. Caine
Keyword(s):  
Organ Culture ◽  
Calcium Ionophore ◽  
Phosphodiesterase Inhibitors ◽  
Calcium Ionophore A23187 ◽  
Ambystoma Mexicanum ◽  
Arginine Vasotocin ◽  
Maximal Response ◽  
Ionophore A23187 ◽  
Glucose Release

ABSTRACT Arginine vasotocin (AVT) caused a concentrationdependent increase of glycogen phosphorylase a activity, breakdown of glycogen and release of glucose, when added to pieces of axolotl liver in organ culture. The concentration causing half-maximal response (EC50) was about 1 nmol/l. These actions of AVT were unaffected by the adrenergic antagonists propranolol, yohimbine and prazosin, but were blocked by equimolar amounts of d(CH2)5Tyr(Me)AVT, a synthetic antagonist of vasopressin. Arginine vasotocin similarly caused glycogenolysis in isolated perfused axolotl liver where the EC50 was about 0·1 nmol/l. The glycogenolytic action of AVT (10 nmol/l) was sustained for at least 3 h in Ca2+ -free perfusion and longer in organ culture. No increase in Ca2+ concentration in the effluent perfusion medium was apparent during AVT-induced glucose release. Omission of Ca2+ from the medium, together with addition of EGTA (2·5 mmol/l) to the organ culture, had only a slight inhibitory effect upon the rate of glycogenolysis brought about by AVT and did not inhibit the glycogenolytic action of catecholamines. Addition of the calcium ionophore A23187 (5 μmol/l) neither caused glucose release nor abolished the glycogenolytic action of AVT added subsequently. Nevertheless, A23187 caused increased loss of 45Ca from Ca2+-loaded liver pieces whereas AVT was without effect. There was a slight accumulation of cyclic AMP (cAMP), but not cGMP, in axolotl liver pieces cultured in the presence of 0·1 μmol AVT/l and this was accentuated in the presence of phosphodiesterase inhibitors. We conclude that, in contrast to the position in mammals, Ca2+ is not involved in the glycogenolytic actions of AVT or catecholamines in axolotl liver. Preliminary experiments suggest that the same is true in the carp and we suggest that the involvement of Ca2+ in regulation of hepatic glucose release may not have evolved until after the amphibians separated from the ancestors of the mammals. J. Endocr. (1986) 109, 75–84

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.

Effects of hyperthyroidism on vascular contractile and relaxation responses

1998 ◽  
Vol 274 (5) ◽  
pp. E946-E953 ◽  
Author(s):  
Richard M. McAllister ◽  
Vance D. Grossenburg ◽  
Michael D. Delp ◽  
M. Harold Laughlin
Keyword(s):  
Muscle Blood Flow ◽  
Left Ventricular ◽  
Male Rats ◽  
Contractile Responses ◽  
Vascular Rings ◽  
Hyperthyroid State ◽  
Prostaglandin F ◽  
Relaxation Responses ◽  
Endothelium Dependent Relaxation

Previous research has shown that skeletal muscle blood flow, at rest and during muscular contractions, is elevated in the hyperthyroid state. We hypothesized that reduced vascular contractile and enhanced endothelium-dependent relaxation responses contribute to these observations. To test these hypotheses, male rats were administered triiodothyronine (Hyper, n = 27; 300 μg/kg) for 6–12 wk. Compared with euthyroid control rats (Eut, n = 27), Hyper exhibited left ventricular hypertrophy (Eut, 2.01 ± 0.04 mg/g body wt; Hyper, 2.70 ± 0.06; P < 0.0005) and greater oxidative enzyme activity in several skeletal muscles (all P < 0.0005). Vascular rings, 2–3 mm in axial length, were prepared from abdominal aortas, and responses to vasoactive agents were determined in vitro. Compared with Eut, vascular rings with intact endothelium from Hyper exhibited reductions in contractile responses to norepinephrine (NE) across a range of NE concentrations ( P < 0.05). Maximal tension developed in response to NE was reduced ∼30% in hyperthyroidism (Eut, 3.8 ± 0.2 g; Hyper, 2.6 ± 0.4; P < 0.01). Contractile responses to NE were not different between Eut and Hyper in rings denuded of endothelium. Maximal vasorelaxation responses to acetylcholine (ACh), after precontraction with NE (10−7 M), were enhanced in the hyperthyroid state (Eut, 65.1 ± 4.8%; Hyper, 84.0 ± 7.1; P < 0.05). Enhanced vasorelaxation to ACh was also observed when precontraction was induced by prostaglandin F2α. These findings indicate that vascular contractile and relaxation responses are altered in male hyperthyroid rats.

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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