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

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.

1997 ◽  
Vol 82 (5) ◽  
pp. 1438-1444 ◽  
Author(s):  
Richard M. McAllister ◽  
M. Harold Laughlin

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.


2001 ◽  
Vol 90 (1) ◽  
pp. 216-227 ◽  
Author(s):  
M. Harold Laughlin ◽  
William G. Schrage ◽  
Richard M. McAllister ◽  
H. A. Garverick ◽  
A. W. Jones

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.


2011 ◽  
Vol 110 (3) ◽  
pp. 695-704 ◽  
Author(s):  
Danielle J. McCullough ◽  
Robert T. Davis ◽  
James M. Dominguez ◽  
John N. Stabley ◽  
Christian S. Bruells ◽  
...  

With advancing age, there is a reduction in exercise tolerance, resulting, in part, from a perturbed ability to match O2 delivery to uptake within skeletal muscle. In the spinotrapezius muscle (which is not recruited during incline treadmill running) of aged rats, we tested the hypotheses that exercise training will 1) improve the matching of O2 delivery to O2 uptake, evidenced through improved microvascular Po2 (PmO2), at rest and throughout the contractions transient; and 2) enhance endothelium-dependent vasodilation in first-order arterioles. Young (Y, ∼6 mo) and aged (O, >24 mo) Fischer 344 rats were assigned to control sedentary (YSED; n = 16, and OSED; n = 15) or exercise-trained (YET; n = 14, and OET; n = 13) groups. Spinotrapezius blood flow (via radiolabeled microspheres) was measured at rest and during exercise. Phosphorescence quenching was used to quantify PmO2 in vivo at rest and across the rest-to-twitch contraction (1 Hz, 5 min) transition in the spinotrapezius muscle. In a follow-up study, vasomotor responses to endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) stimuli were investigated in vitro. Blood flow to the spinotrapezius did not increase above resting values during exercise in either young or aged groups. Exercise training increased the precontraction baseline PmO2 (OET 37.5 ± 3.9 vs. OSED 24.7 ± 3.6 Torr, P < 0.05); the end-contracting PmO2 and the time-delay before PmO2 fell in the aged group but did not affect these values in the young. Exercise training improved maximal vasodilation in aged rats to acetylcholine (OET 62 ± 16 vs. OSED 27 ± 16%) and to sodium nitroprusside in both young and aged rats. Endurance training of aged rats enhances the PmO2 in a nonrecruited skeletal muscle and is associated with improved vascular smooth muscle function. These data support the notion that improvements in vascular function with exercise training are not isolated to the recruited muscle.


1986 ◽  
Vol 251 (3) ◽  
pp. H520-H527 ◽  
Author(s):  
V. M. Miller ◽  
L. L. Aarhus ◽  
P. M. Vanhoutte

To determine whether the blood flow and O2 tension to which a blood vessel is chronically exposed could modulate endothelium-dependent responses, these parameters were altered in the dog either by causing partial occlusion of the femoral artery or by creating a fistula between the femoral artery and vein. Blood flow was reduced by 75% in the clamped artery; mean arterial pressure was unchanged. In the vessels proximal to the fistula, blood flow was elevated and O2 tensions were similar in the vein and artery. After 6 wk the femoral arteries and veins were excised, and their endothelium-dependent responses were studied in vitro. The endothelium-dependent relaxations to acetylcholine, adenosine diphosphate, and alpha 2-adrenergic stimulation were augmented in fistula-operated compared with sham-operated arteries. The responses to these agents in the clamp-operated vessels were not different from those of the sham-operated ones. Relaxation to arachidonic acid in the arteries showed an inverse relationship to blood flow. In the veins proximal to the fistula, the endothelium-dependent relaxations to acetylcholine were augmented and an endothelium-dependent relaxation to alpha 2-adrenergic stimulation was present; only a contractile response was observed in veins from the sham-operated limb in response to the latter. These studies suggest a pattern of increased endothelium-dependent relaxation in vessels exposed to chronically elevated blood flow.


1997 ◽  
Vol 272 (3) ◽  
pp. R793-R799 ◽  
Author(s):  
A. Cases ◽  
J. M. Stulak ◽  
Z. Katusic ◽  
E. Villa ◽  
J. C. Romero

It is well known that hemoglobin binds nitric oxide (NO) and produces a pronounced vasoconstriction in isolated arteries. However, it is debatable whether such an effect takes place in whole animals, because hemoglobin also catalyzes the formation of prostaglandins from arachidonic acid. Short-term studies were performed to evaluate the effects induced by intravenous infusion of cross-linked hemoglobin (XL-Hb) on blood pressure (BP) and renal, iliac, and mesenteric flows, and on renal function in six anesthetized dogs. A similar volume-matched expansion with 6% dextran was used as a control (n = 6). Glomerular filtration rate (GFR), urinary flow, and total and fractional sodium excretion were measured before and after XL-Hb or dextran infusion to evaluate possible renal function changes. XL-Hb administration resulted in a 29% elevation in BP and a significant decrease of blood flow (30-37%) to the three vascular beds. XL-Hb did not alter GFR or sodium excretion, despite the increase in BP. In contrast, the administration of dextran did not significantly alter BP but induced a significant increase (6-13%) of blood flow in the three vascular beds. These changes were accompanied by threefold increases in urinary flow and sodium excretion without alterations in GFR. The binding effect of XL-Hb on NO was studied in isolated renal arteries in organ chambers. These in vitro studies showed that XL-Hb blunted the endothelium-mediated vasodilator response to calcium ionophore A-23187 and to acetylcholine. Our results demonstrate that XL-Hb administration is followed by hypertension, vasoconstriction, and blunted natriuresis. All these effects are compatible with the scavenging effect on NO attributed to XL-Hb.


2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Joseph R Libonati ◽  
Kathleen Sturgeon ◽  
Keri Schadler ◽  
Geetha Muthukumaran ◽  
Dennis Ding ◽  
...  

Introduction: Cardiotoxicity often occurs in cancer patients treated with doxorubicin (DOX). DOX induces cardiomyocyte death, due in part to DOX-mediated DNA damage, myofiber degeneration, ischemia-related metabolic alterations, and activation of apoptotic pathways. While exercise is often recommended for cancer patients, it remains unclear whether the metabolic stress of exercise with DOX treatment benefits or impairs cardiac performance. Purpose: To test the hypothesis that acute exercise training performed with DOX therapy offsets cardiotoxicity. Methods: B16F10 melanoma cells (3x10 5 ) were injected into 6-8 week old male C57BL/6 mice (n= 48). A 4 mg/kg cumulative dose of DOX (IP) was administered over 2 weeks and exercise (EX) consisted of treadmill walking (45 min/d, 10 m/min, 5 days/week, 2 weeks). Four groups were tested: 1) Sedentary (SED) +Vehicle, 2) SED +DOX, 3) EX+Vehicle, 4) EX+DOX. Echocardiography [LV systolic (EF, %) and diastolic (E/A ratio) function] and tissue harvest were performed 48 hours after EX. Results: Tumor volume was attenuated in DOX and lowest in EX+DOX (p<0.05). Body weight (BW), heart weight (HT), HT/BW, and HT/Tibia were attenuated in DOX (p<0.05) and were lowest in EX+DOX. LV fibrosis increased with DOX (p<0.05) and was greatest in EX+DOX (SED+Vehicle 2 ± 0.3%, SED+DOX 4 ± 0.5%, EX+Vehicle 3 ± 0.3%, and EX+DOX 6 ± 0.4%; p<0.05). Cardiomyocyte area and β myosin heavy chain gene expression were similar between groups. Diastolic function was reduced with DOX and EX+DOX (both p<0.05), but systolic function was similar between groups. DOX induced significant alterations the expression profiles of genes in the mTOR signaling pathway, with similar expression patterns in SED+DOX and EX+DOX. Insulin improved in vitro cardiomyocyte cell survival (p<0.05) to a greater extent than IGF-1 treatment during DOX. Neither insulin nor IGF-1 impacted cardiomyocyte proliferation during DOX. Conclusion: While the addition of EX to DOX treatment more effectively inhibited tumor growth, EX did not alleviate DOX mediated LV diastolic impairment, and actually increased LV fibrosis. Acute, short term exercise appears to impair LV function in DOX-treated mice. Exercise-induced reductions in insulin secretion may underlie this effect.


1986 ◽  
Vol 240 (3) ◽  
pp. 651-657 ◽  
Author(s):  
T A Davis ◽  
I E Karl

To determine whether the enhanced insulin-sensitivity of glucose metabolism in muscle after acute exercise also extends to protein metabolism, untrained and exercise-trained rats were subjected to an acute bout of exercise, and the responses of protein synthesis and degradation to insulin were measured in epitrochlearis muscles in vitro. Acute exercise of both untrained and trained rats decreased protein synthesis in muscle in the absence or presence of insulin, but protein degradation was not altered. Exercise training alone had no effect on protein synthesis or degradation in muscle in the absence or presence of insulin. Acute exercise or training alone enhanced the sensitivities of both protein synthesis and degradation to insulin, but the enhanced insulin-sensitivities from training alone were not additive to those after acute exercise. These results indicate that: a decrease in protein synthesis is the primary change in muscle protein turnover after acute exercise and is not altered by prior exercise training, and the enhanced insulin-sensitivities of metabolism of both glucose and protein after either acute exercise or training suggest post-binding receptor events.


1993 ◽  
Vol 75 (6) ◽  
pp. 2677-2682 ◽  
Author(s):  
J. M. Muller ◽  
P. R. Myers ◽  
M. H. Laughlin

The purpose of this study was to test the hypothesis that myogenic responsiveness in porcine coronary resistance arteries is attenuated by exercise training. Twenty-four female Yucatan miniature swine were randomly separated into two groups of 12 pigs: exercise trained (ET) and sedentary control (SED). The ET pigs were trained on a motor-driven treadmill for 16–22 wk while the SED pigs remained confined to their pens. After training, heart weight-to-body weight ratio, skeletal muscle oxidative capacity, and exercise tolerance were significantly increased in ET pigs compared with SED pigs. Coronary resistance arteries 75–150 microns diam were isolated for in vitro evaluation of myogenic responses to changes in intraluminal pressure in the absence of intraluminal flow. Coronary resistance arteries from ET and SED pigs developed spontaneous tone at 40 mmHg intraluminal pressure. Active changes in diameter measured in response to intraluminal pressures < 40 mmHg were similar in coronary resistance arteries from ET and SED pigs. When pressure was raised above 40 mmHg, myogenic constriction was greater in coronary resistance arteries from ET pigs, as indicated by significantly greater reductions in diameter. At 60 and 70 mmHg intraluminal pressure, constriction was 8 and 16% greater, respectively, in resistance arteries from ET pigs. After maximal relaxation with sodium nitroprusside (100 microM), passive diameter changes measured in response to changes in intraluminal pressure from 10 to 80 mmHg were not significantly different in coronary resistance arteries from ET and SED pigs. We conclude that, contrary to our hypothesis, exercise training in pigs enhances myogenic constrictor responses in coronary resistance arteries.(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 268 (4) ◽  
pp. H1428-H1435 ◽  
Author(s):  
M. D. Delp ◽  
R. M. McAllister ◽  
M. H. Laughlin

Hypothyroidism induces a number of cardiovascular adaptations in rats, including decreases in blood flow to high-oxidative skeletal muscle and increases in total peripheral resistance. Conversely, exercise training results in elevations in blood flow to high-oxidative skeletal muscle and decreases in vascular resistance. The purpose of this study was to determine whether hypothyroidism induces changes in the vasomotor responses of arterial vessels and whether exercise training modifies these responses. Rats were divided into three groups, sedentary euthyroid (S-Eut), sedentary hypothyroid (S-Hypo), and exercise-trained hypothyroid (ET-Hypo). Responses to vasoactive compounds were examined in vitro using abdominal aortic rings. Maximal isometric contractile tension (g/mm2) evoked by KCl and norepinephrine (NE) were not different among groups. However, sensitivity to KCl [agonist concentration producing 50% of maximal vasoconstrictor response (EC50; in mM): S-Eut, 21.1 +/- 1.1; S-Hypo, 35.7 +/- 2.7; ET-Hypo, 43.8 +/- 2.0] and to NE [EC50 (in M): S-Eut, 4.0 x 10(-8) +/- 2.3 x 10(-8); S-Hypo, 8.3 x 10(-8) +/- 3.4 x 10(-8); ET-Hypo, 3.6 x 10(-7) +/- 1.1 x 10(-7)] was different among groups, and in the order S-Eut > S-Hypo > ET-Hypo. Maximal vasodilator responses induced by acetylcholine (10(-7) M NE preconstriction) were lower in rings from S-Hypo animals than those from S-Eut and ET-Hypo rats. Dilatory responses induced by sodium nitroprusside (SNP) with the same NE preconstriction were not different among groups. However, with a 10(-4) M NE preconstriction, maximal dilatory responses induced by SNP were lower in vessels from hypothyroid animals. Dilatory responses to forskolin (10(-4) M NE preconstriction) were not different among groups.(ABSTRACT TRUNCATED AT 250 WORDS)


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