Biomedical subjects

M H Laughlin

Publications and source records attributed to M H Laughlin.

At least 73 records · Page 4Linked to original sources

PubMed1996

Restenosis is associated with decreased coronary artery nitric oxide synthase.

The purpose of the present study was to test the hypothesis that restenosis is associated with decreased constitutive nitric oxide synthase activity. Male miniswine with moderately elevated serum cholesterol levels underwent cardiac catheterization and oversized balloon injury to the right and left circumflex coronary arteries, followed 2 weeks later by repeat injury on the same coronary segments. After 4 weeks, the coronary arteries were either immediately frozen in liquid nitrogen or pressure-perfusion fixed and prepared for histologic examination. Constitutive nitric oxide synthase activity was quantified using a fibroblast reporter cell method, while constitutive nitric oxide synthase protein was compared between balloon-injured and non-balloon-injured arteries using Western blot analysis. Immunohistochemical studies were performed using a specific antibody against constitutive nitric oxide synthase protein. Following balloon injury, there was decreased constitutive nitric oxide synthase activity in balloon-injured coronary arteries, compared to distal non-balloon-injured segments from the same artery. Histological examination demonstrated an intact endothelium. Specific antibody staining revealed that there was less constitutive nitric oxide synthase protein reactivity by immunohistochemical analysis. Western analysis confirmed less constitutive nitric oxide synthase protein. The data are consistent with the hypothesis that restenosis is associated with decreased endothelial cell nitric oxide production. The data suggest this is secondary to a decreased amount of constitutive nitric oxide synthase enzyme in the endothelium. A deficiency in constitutive nitric oxide synthase enzyme may contribute to the impaired second messenger and paracrine functions of the endothelium observed during restenosis following balloon injury, including abnormal vasomotion, extracellular matrix formation, and platelet aggregation.

Angioplasty, Balloon, Coronary↗

PubMed1996

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

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.

Animals↗

PubMed1996

Regional changes in capillary supply in skeletal muscle of high-intensity endurance-trained rats.

The objective of this study was to test the hypothesis that an endurance training program designed to produce recruitment of all extensor muscle fiber types during each exercise bout would stimulate capillary angiogenesis throughout rat gastrocnemius and soleus muscles. Male Sprague-Dawley rats were exercise trained 5 days/wk for 12-14 wk with exercise bouts consisting of a combination of high intensity (32 m/min on a 15% incline) and long duration (90 min/day). On completion of high-intensity endurance training (HIET) or cage activity [sedentary (Sed)], rat hindquarters were vascularly isolated and perfusion fixed with a modified Karnovsky's fixative. Capillary supply was measured in soleus and gastrocnemius muscles by using Olympus Cue 2 image-analyzer software. Capillary supply was reflected in measurements of capillary-to-fiber ratio, capillary numerical density, capillary surface area density, and capillary volume density on transversely cut tissue sections. HIET increased citrate synthase activity by 20 and 42% in the medial and long heads of the triceps brachii, respectively. Sarcomere lengths were similar in gastrocnemius and soleus muscles of Sed and HIET rats after fixation. All four indexes of capillary supply were significantly greater throughout the gastrocnemius muscle of HIET rats compared with Sed values. The relative increase in capillarity was greater in white than in red gastrocnemius muscle of HIET rats. HIET also increased capillary supply of soleus muscle. However, only capillary numerical density was statistically greater (19%) in HIET soleus compared with Sed. These results support the hypothesis that this training program would produce an increase in capillary supply in all extensor muscles.

Animals↗

PubMed1996

Endothelium-medicated control of the coronary circulation. Exercise training-induced vascular adaptations.

This review discusses the role of the endothelium in the regulation of coronary vascular function. The role of endothelium-mediated mechanisms at rest, during exercise, in exercise training-induced adaptations of coronary function and in the presence of coronary heart disease (CHD) are examined. Mechanisms of control of coronary blood flow are briefly discussed with emphasis on endothelium-mediated control of vascular resistance. The concept that the relative importance of vascular control mechanisms differs as a function of position along the coronary arterial tree is developed and discussed. Metabolic, myogenic and endothelium-mediated control systems contribute in parallel to regulating coronary blood flow. The relative importance of these mechanisms varies throughout the coronary arterial tree. Endothelium-dependent vasodilation contributes to maintenance of resting coronary blood flow but the endothelium's role in dilation of small resistance arteries, thereby increasing coronary blood flow during exercise, remains in question. In contrast, the endothelium plays an essential role in dilation of the conduit coronary arteries during exercise. Atherosclerosis and CHD convert this exercise-induced dilation to a vasoconstriction, apparently due to endothelium dysfunction. Long term increases in physical activity and exercise training alter the control of coronary blood flow. Adaptations in endothelium-mediated control play a role in these changes. However, the effects of the mode, frequency, and intensity of exercise training bouts and duration of training on adaptive changes in endothelial function have not been established. The role of the endothelium in control of the permeability characteristics of the exchange vessels in the coronary circulation is discussed. Current evidence indicates that vascular permeability is a dynamic characteristic of the vessel wall that is controlled, at least in part, by endothelium-dependent phenomena. Also, preliminary results indicate that exercise training alters microvessel permeability and the control of permeability in the coronary circulation. Further research is needed to provide clarification of the effects of exercise training on coronary endothelial control of vascular resistance and vascular permeability in atherosclerosis and CHD.

Adaptation, Physiological↗

PubMed1996

Total and regional cerebral blood flow during recovery from G-LOC.

INTRODUCTION: This study measured total and regional cerebral blood flow (BF) in baboons during +Gz-induced loss of consciousness (G-LOC) and during recovery from G-LOC. METHODS: Flowprobes (Transonic Inc., T201, Ithaca, NY) were placed on the common carotid and internal carotid arteries of five male baboons for continuous measurement of total cephalic and cerebral BF, respectively. Radiolabeled microspheres were used to measure regional central nervous system BF at discrete timepoints. G-LOC was determined from visual observations of the animals and from EEG recordings. RESULTS: Cerebral blood flow was maintained and animals remained conscious during 60 s exposure to +4 Gz. In contrast, G-LOC was observed during the first 16-25 s (mean = 20.3 +/- 3.7 s) of exposure to +8 Gz in all five animals. Internal and common carotid artery BF decreased rapidly to zero during the first few seconds of +8 Gz. BF always appeared to cease prior to the occurrence of G-LOC. During early recovery from G-LOC there was no hyperemic response recorded with flowprobes, whereas a hyperemic response was recorded following 60 s exposures to +4 Gz in which the animals did not experience G-LOC. Microsphere measurements of the regional distribution of BF are consistent with the hypothesis of a +Gz-induced differential perfusion deficit throughout the brain and central nervous system during G-LOC. CONCLUSIONS: We conclude that G-LOC is preceded by cessation of cerebral BF. The fact that the hyperemic response following +Gz exposure is less when G-LOC occurs than when G-LOC does not occur suggests CNS energy conservation during G-LOC.

Acceleration↗

PubMed1995

Effects of hyperthyroidism on muscle blood flow during exercise in rats.

Hyperthyroidism is associated with exercise intolerance. Previous research, however, has shown that cardiac output is either normal or enhanced during exercise in the hyperthyroid state. We therefore hypothesized that blood flow to working skeletal muscle is augmented in hyperthyroid animals during in vivo submaximal exercise and, consequently, that noncardiovascular factors are responsible for intolerance to exercise. To test this hypothesis, rats were made hyperthyroid (Hyper) over 6-12 wk with injections of triiodothyronine (300 micrograms/kg). Hyperthyroidism was evidenced by left ventricular hypertrophy [euthyroid (Eut), 2.12 +/- 0.05 mg/g body wt; Hyper, 2.78 +/- 0.06; P < 0.005], 25-60% increases in citrate synthase activities in Hyper hindlimb muscles over those of Eut rats, and higher preexercise heart rates (Eut, 415 +/- 18 beats/min; Hyper, 479 +/- 19; P < 0.025). Regional blood flows were determined by the radiolabeled microsphere method, preexercise, and at 1-2 min of treadmill running at 15 m/min (0% grade). Total hindlimb muscle blood flow preexercise was unaffected (Eut, 31 +/- 4 ml.min-1.(100) g-1, n = 11; Hyper, 40 +/- 6, n = 9; not significant) but was higher (P < 0.025) in Hyper (127 +/- 17, n = 9) compared with Eut (72 +/- 11, n = 9) during treadmill running. During exercise, flows to individual muscles and muscle sections were approximately 50-150% higher in Hyper compared with Eut rats. Visceral blood flows were largely similar between groups. These findings indicate that hyperthyroidism is associated with augmented blood flow to skeletal muscle during submaximal exercise. Thus hypoperfusion of skeletal muscle does not account for the poor exercise tolerance characteristic of hyperthyroidism.

Animals↗

PubMed1995

Exercise training alters aortic vascular reactivity in hypothyroid rats.

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)

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1995

Muscle blood flow during exercise in sedentary and trained hypothyroid rats.

Hypothyroidism is characterized by exercise intolerance. We hypothesized that active muscle blood flow during in vivo exercise is inadequate in the hypothyroid state. Additionally, we hypothesized that endurance exercise training would restore normal blood flow during acute exercise. To test these hypotheses, rats were made hypothyroid (Hypo) over 3-4 mo with propylthiouracil. A subset of Hypo rats was trained (THypo) on a treadmill at 30 m/min (15% grade) for 60 min/day 5 days/wk over 10-15 wk. Hypothyroidism was evidenced by approximately 80% reductions in plasma triiodothyronine levels in Hypo and THypo and by 40-50% reductions in citrate synthase activities in high oxidative muscles in Hypo compared with euthyroid (Eut) rats. Training efficacy was indicated by increased (25-100%) citrate synthase activities in muscles of THypo vs. Hypo. Regional blood flows were determined by the radiolabeled microsphere method before exercise and at 1-2 min of treadmill running at 15 m/min (0% grade). Preexercise muscle blood flows were generally similar among groups. During exercise, however, flows were lower in Hypo than in Eut for high oxidative muscles such as the red section of vastus lateralis [277 +/- 24 and 153 +/- 13 (SE) ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01] and vastus intermedius (317 +/- 32 and 187 +/- 20 ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01) muscles. Training (THypo) did not normalize these flows (168 +/- 24 and 181 +/- 24 ml.min-1.100 g-1 for red section of vastus lateralis and vastus intermedius muscles, respectively). Blood flows to low oxidative muscle, such as the white section of vastus lateralis muscle, were similar among groups (21 +/- 5, 25 +/- 4, and 34 +/- 7 ml.min-1.100 g-1 for Eut, Hypo, and THypo, respectively; P = NS). These findings indicate that hypothyroidism is associated with reduced blood flow to skeletal muscle during exercise, suggesting that impaired delivery of nutrients to and/or removal of metabolites from skeletal muscle contributes to the poor exercise tolerance characteristic of hypothyroidism.

Animals↗

PubMed1995

Exercise training alters the Ca2+ and contractile responses of coronary arteries to endothelin.

We tested the hypothesis that alterations in myoplasmic free Ca2+ (Ca(m)) regulation in coronary smooth muscle after exercise training (Ex) underlie changes in vasomotor function. Yucatan miniature pigs were endurance trained by treadmill running for 16-20 wk. Simultaneous determination of Ca(m) (fura-2 microfluorometry) and contraction during endothelin exposure in coronary arteries were then performed. Endothelin (10(-9) to 10(-7) M) was administered either cumulatively or as a single concentration. Ex significantly attenuated the Ca(m) response to 10(-9) and 10(-8) M endothelin. Developed tension was significantly diminished at 10(-8) M endothelin in Ex pigs, producing a rightward shift in the concentration-developed tension response. Attenuated Ca(m) and contractile response to 10(-8) M endothelin were present after Ex whether endothelin was applied cumulatively or as a single concentration. The developed tension-Ca(m) relationship showed an increased Ca(m) sensitivity of contraction with Ex. Endothelin (10(-8) M)-induced Ca2+ influx, estimated by Ba2+ influx in low-Na+ solution, was increased threefold in coronary arteries from Ex pigs. The decreased Ca(m) in the presence of increased divalent cation (i.e., Ca2+) influx during 10(-8) M endothelin suggests a greatly enhanced sarcolemmal Ca2+ cycling in coronary arteries from Ex pigs.

Animals↗

PubMed1995

Rat aortic vasoreactivity is altered by old age and hindlimb unloading.

Prolonged bed rest in young adults leads to a number of cardiovascular alterations, including orthostatic intolerance and decreased exercise capacity. Similar changes occur with advanced age. These modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Using rat hindlimb unloading as an animal model of physical inactivity, this study was designed to determine whether prolonged decreases in weight-bearing activity induce changes in vascular reactivity that are similar to those occurring in senescent rats and whether the imposition of inactivity on old rats further modifies any age-related alterations in vasomotor responsiveness. Responses to vasoactive compounds were examined in vitro by using isolated abdominal aortic rings. Maximal isometric contractile force evoked by the vasoconstrictors KCl, norepinephrine (NE), and arginine vasopressin was lower in aortic segments from young hindlimb-unloaded (YHU), old control (OC), and old hindlimb-unloaded (OHU) rats compared with that from young control (YC) rats. Sensitivity [mean effective concentration (EC50)] to KCl was enhanced in segments from both old and unloaded animals compared with YC rats, but EC50 values for the other constrictors were not different among groups. Vasorelaxation responses induced by acetylcholine (10(-7) M NE preconstriction) were lower in vessel rings from OC (1 x 10(-7) to 3 x 10(-6) M), YHU (10(-7) to 10(-5) M), and OHU (10(-7) to 10(-5) M) rats than those from YC animals. In addition, vessel rings from OC, YHU, and OHU rats were less sensitive to sodium nitroprusside-induced relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1995

Endothelium-dependent vasodilation of proximal coronary arteries from exercise-trained pigs.

We recently reported that alpha-adrenergic vasoconstriction is blunted and adenosine-induced vasodilation is enhanced in proximal coronary arteries of exercise-trained miniature swine [C. L. Oltman, J. L. Parker, H. R. Adams, and M. H. Laughlin. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H372-H382, 1992]. The purpose of the present study was to determine whether this model of exercise training also alters endothelium-dependent vasodilator responses of proximal coronary arteries. Female Yucatan miniature swine were exercise trained (ET) on a motor-driven treadmill or were cage confined (Sed) for 13-20 wk. Exercise tolerance, heart weight-to-body weight ratios, and skeletal muscle oxidative capacity were all significantly greater in ET than in Sed animals. Vasodilator responses were evaluated in vitro by determining concentration-response curves by using vascular rings (3.5-4 mm in axial length) isolated from right and left coronary arteries. Vasorelaxation responses were determined, after tone had been produced with either 30 microM prostaglandin F2 alpha, 30 mM KCl, or 30 nM endothelin. Concentration-response curves were obtained to endothelium-dependent vasodilators including bradykinin (10(-9)-10(-6) M), substance P (10(-12)-10(-6) M), clonidine (10(-9)-10(-6) M), serotonin (10(-10)-10(-5) M), and the Ca2+ ionophore A-23187 (10(-10)-10(-6) M). Endothelium-independent vasodilator responses to sodium nitroprusside (10(-9)-10(-4) M) were not different between arteries from Sed and ET. Bradykinin, substance P, and A-23187 were potent vasodilators in arteries from both groups, whereas serotonin and clonidine did not consistently produce vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Thyroid status and exercise tolerance. Cardiovascular and metabolic considerations.

Both hypo- and hyperthyroidism are characterised by exercise intolerance. In hypothyroidism, inadequate cardiovascular support appears to be the principal factor involved. Insufficient skeletal muscle blood flow compromises exercise capacity via reduced oxygen delivery, and endurance through decreased delivery of blood-borne substrates. The latter effect results in increased dependence on intramuscular glycogen. Additionally, decreased mobilisation of free fatty acids from adipose tissue and, consequently, lower plasma free fatty acid levels compound the problem of reduced lipid delivery to active skeletal muscle in the hypothyroid state. In contrast, cardiovascular support is enhanced in hyperthyroidism, implicating other factors in exercise tolerance. Greater reliance on muscle glycogen appears to be the primary reason for decreased endurance. Biochemical changes with hyperthyroidism that would favour enhanced flux through glycolysis may account for this dependence on glycogen. Deviations from normal thyroid function, and the ensuing exercise tolerance, require appropriate medical therapy to attain euthyroid status.

Cardiovascular Physiological Phenomena↗

PubMed1995

The effects of intravascular stents on vasomotion in porcine coronary arteries.

Intravascular stents are being increasingly utilized in the treatment of atherosclerotic coronary artery disease, however little is known about the effects of stents on coronary vasomotion. The purpose of the present study was to compare the effects of a heparin treated tantalum stent and balloon injury on coronary artery vasorelaxation and vasoconstriction. Male miniswine underwent cardiac catheterization and oversized balloon injury to the right and left circumflex coronary arteries. After two weeks, one artery was either balloon-injured again, or underwent implantation of a stent. Four weeks later, the coronary arteries were prepared for in vitro isometric ring studies. Vasodilator responses to bradykinin and A23187 calcium ionophore were significantly impaired in balloon-injured vessels. The bradykinin and A23187 responses in stented vessels showed significantly less vasorelaxation, compared to both balloon-injured and normal vessels. There were no significant differences between any of the groups in their vasodilator response to nitroprusside. Vasoconstrictor responses to acetylcholine were significantly greater in balloon-injured vessels, compared to normal vessels. Stented vessels, however, showed markedly less vasoconstriction to acetylcholine compared to both balloon-injured and normal vessels. The maximal KCI vasoconstrictor responses in balloon injured vessels and normal controls were not significantly different. However, the maximal KCI responses in stented vessels showed significantly less constriction compared to both balloon injured and normal vessels. In conclusion, the data demonstrated that coronary arteries implanted with a heparin treated tantalum stent were capable of vasomotor activity. Both conventional balloon angioplasty and stents resulted in impaired endothelium-dependent vasorelaxation. Endothelium-independent vasorelaxation, however, was not impaired.(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗

PubMed1995

Endothelium-mediated control of coronary vascular tone after chronic exercise training.

The purpose of this paper is to examine the role of endothelium-derived relaxing factors in the control of coronary vascular resistance in conditioned subjects (i.e., after exercise training for a period of time sufficient to complete adaptation processes). Results from studies with exercise trained (EX) dogs, miniature swine, and rats are summarized. Since the relative importance of vascular control mechanisms differ in various segments of the coronary arterial tree, the effects of EX on conduit arteries and the coronary arterial microcirculation are discussed separately. Results indicate that endothelium-mediated vasodilator responses are normal in conduit coronary arteries of EX dogs, miniature swine, and rats. It is proposed that endothelium-mediated vasodilation of conduit coronary arteries is enhanced early in the exercise-adaptive process but returns to normal as adaptation to EX is complete, when structural adaptations produce a relative decrease in coronary shear during exercise. EX miniature swine manifest enhanced endothelium-mediated vasodilation stimulated by bradykinin and flow in isolated coronary resistance arteries and appear to have increased expression of NO synthase (ecNOS). Brief training also appears to increase the expression of ecNOS. The role of endothelium-mediated vasodilation in regulation of coronary blood flow in EX animals remains uncertain.

Animals↗

PubMed1994

Influence of endurance exercise training on distribution of vascular adaptations in rat skeletal muscle.

We hypothesized that an exercise training program consisting of treadmill running at 32 m/min up a 15% incline, 90 min/day, 5 days/wk for 12-14 wk, would elicit vascular adaptation in skeletal muscle of all fiber types in rats. This hypothesis was based on previous reports that this intensity and duration of training caused increases in oxidative capacity in rat skeletal muscle of all fiber types. Skeletal muscle vascular transport capacity was examined with measurements of total and regional (radiolabeled microspheres) flow capacity, capillary filtration coefficient (CFC), and permeability-surface area product (PS) for 51Cr-EDTA in maximally vasodilated (papaverine) hindquarters of control (C; n = 25) and exercise-trained (ET; n = 26) rats. CFC was increased in ET (0.038 +/- 0.001 vs. 0.030 +/- 0.001 ml.min-1 x mmHg-1 x 100 g-1; P < or = 0.001). PS was greater in ET than C (7.80 +/- 0.33 vs. 6.39 +/- 0.37 ml.min-1 x 100 g-1; P < or = 0.01). Citrate synthase activity was increased in the soleus (25%; P < or = 0.05), the medial head (35%; P < or = 0.05), and the red portion of the long head (45%; P < or = 0.005) but not in the white portion of the long head of triceps brachii (P = 0.14) of ET rats. Pressure-flow relationships indicate that total flow was greater (P < or = 0.05) in ET hindquarters at all perfusion pressures. Regional flow data revealed that increases in flow capacity were not evident in muscles composed of all fiber types as predicted.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1994

Vasodilator responses of coronary resistance arteries of exercise-trained pigs.

BACKGROUND: The purpose of this study was to test the hypothesis that vasodilator responses of porcine coronary resistance arteries are increased by exercise training. METHODS AND RESULTS: Yucatan miniature swine were randomly divided into groups of exercise-trained (ET) and sedentary (SED) control pigs. ET pigs were placed on a progressive treadmill training program lasting 16 to 20 weeks, and SED pigs remained inactive during the same time period. Coronary resistance arteries 64 to 157 microns in diameter were isolated for in vitro evaluation of relaxation responses to the endothelium-independent dilators sodium nitroprusside (1 x 10(-10) to 1 x 10(-4) mol/L) and adenosine (1 x 10(-10) to 1 x 10(-5) mol/L) and to bradykinin (1 x 10(-13) to 3 x 10(-7) mol/L), an endothelium-dependent agent. Relaxation responses to adenosine and sodium nitroprusside were not altered by exercise training. Endothelium-dependent relaxation to bradykinin was enhanced in coronary resistance arteries from ET pigs (IC50: ET, 0.07 +/- 0.02 nmol/L; SED, 1.59 +/- 0.09 nmol/L). To determine whether prostanoids and/or the nitric oxide synthase pathway were involved in the ET-induced changes in bradykinin-induced vasodilation, responses to bradykinin were examined in coronary resistance arteries from both ET and SED pigs in the presence of indomethacin and in the presence of nitro-monomethyl L-arginine (L-NMMA). Both indomethacin and L-NMMA produced significant inhibition of the bradykinin-induced relaxation in vessels from both groups. Despite decreased bradykinin-induced relaxation after indomethacin, bradykinin-induced vasodilation was still enhanced in vessels from the ET group. L-NMMA caused greater inhibition of the bradykinin-induced relaxation in coronary resistance arteries from ET pigs relative to arteries from SED pigs and eliminated the training-induced enhancement of the bradykinin responses. CONCLUSIONS: These results suggest that exercise training enhances bradykinin-induced vasodilation through increased endothelium-derived relaxing factor/nitric oxide production by the L-arginine/nitric oxide synthase pathway.

Adenosine↗

PubMed1994

Capillary blood transit time in muscles in relation to body size and aerobic capacity.

The mean minimal transit time for blood in muscle capillaries (tc) was estimated in six species, spanning two orders of magnitude in body mass and aerobic capacity: horse, steer, dog, goat, fox and agouti. Arterial (CaO2) and mixed venous (CvO2) blood O2 concentrations, blood hemoglobin concentrations ([Hb]) and oxygen uptake rates were measured while the animals ran on a treadmill at a speed that elicited the maximal oxygen consumption rate (VO2max) from each animal. Blood flow to the muscles (Qm) was assumed to be 85% of cardiac output, which was calculated using the Fick relationship. Total muscle capillary blood volume (Vc) and total muscle mitochondrial volume were estimated by morphometry, using a whole-body muscle sampling scheme. The tc was computed as Vc/Qm. The tc was 0.3-0.5 s in the 4 kg foxes and agoutis, 0.7-0.8 s in the 25 kg dogs and goats, and 0.8-1.0 s in the 400 kg horses and steers. The tc was positively correlated with body mass and negatively correlated with transcapillary O2 release rate per unit capillary length. Mitochondrial content was positively correlated with VO2max and with the product of Qm and [Hb]. These data suggested that Qm, Vc, maximal hemoglobin flux, and consequently tc, are co-adjusted to result in muscle O2 supply conditions that are matched to the O2 demands of the muscles at VO2max.

Aerobiosis↗

PubMed1994

Effects of exercise training on coronary circulation: introduction.

The purpose of this symposium was to evaluate the hypothesis that the beneficial effects of training are the result of training-induced adaptations in the coronary circulation. The approach is to review, summarize, and evaluate data concerning the effects of exercise training on the coronary circulation. Results indicate that aerobic exercise training induces an increase in both blood flow capacity and capillary exchange capacity. These functional changes are the result of two major types of adaptive responses: structural vascular adaptation and altered control of vascular resistance. Structural vascular adaptation occurs in response to exercise training in at least two forms: increases in the cross-sectional area of the proximal coronary arteries, and angiogenesis. Training-induced changes in coronary vascular control have been shown to include altered responses of the coronary circulation and isolated coronary arteries to vasoactive substances, changes in endothelium-mediated vasoregulation, and alterations in the cellular-molecular control of intracellular free Ca2+ in both endothelial and vascular smooth muscle cells isolated from coronary arteries of exercise trained animals. The potential impact of these training-induced adaptations on the coronary collateral circulation and atherosclerotic coronary disease are discussed.

Adaptation, Physiological↗