Sedentary Dogs Research Articles

Cardiac electrophysiological remodeling associated with enhanced arrhythmia susceptibility in a canine model of elite exercise.

The health benefits of regular physical exercise are well known. Even so, there is increasing evidence that the exercise regimes of elite athletes can evoke cardiac arrhythmias including ventricular fibrillation and even sudden cardiac death (SCD). The mechanism of exercise-induced arrhythmia and SCD is poorly understood. Here, we show that chronic training in a canine model (12 sedentary and 12 trained dogs) that mimics the regime of elite athletes induces electrophysiological remodeling (measured by ECG, patch-clamp, and immunocytochemical techniques) resulting in increases of both the trigger and the substrate for ventricular arrhythmias. Thus, 4 months sustained training lengthened ventricular repolarization (QTc: 237.1±3.4 ms vs. 213.6±2.8 ms, n=12; APD90: 472.8±29.6 ms vs. 370.1±32.7 ms, n=29 vs. 25), decreased transient outward potassium current (6.4±0.5 pA/pF vs. 8.8±0.9 pA/pF at 50 mV, n=54 vs. 42), and increased the short-term variability of repolarization (29.5±3.8 ms vs. 17.5±4.0 ms, n=27 vs. 18). Left ventricular fibrosis and HCN4 protein expression were also enhanced. These changes were associated with enhanced ectopic activity (number of escape beats from 0/hr to 29.7±20.3/hr) in vivo and arrhythmia susceptibility (elicited ventricular fibrillation: 3 of 10 sedentary dogs vs. 6 of 10 trained dogs). Our findings provide in vivo, cellular electrophysiological and molecular biological evidence for the enhanced susceptibility to ventricular arrhythmia in an experimental large animal model of endurance training.

Effects of a structured exercise programme in sedentary dogs with chronic diarrhoea

The aim of this investigation was to evaluate the effects of a structured exercise programme in sedentary dogs with chronic diarrhoea. Twenty-two dogs were enrolled in the study. All dogs...

Conditioning causes an increase in glucose transporter-4 levels in mononuclear cells in sled dogs

This study was designed to investigate the effects of physical conditioning on the expression of the insulin sensitive glucose transporter-4 protein (GLUT4) on mononuclear cells and HOMA-IR levels in dogs and compared to results reported in human skeletal muscle and the skeletal muscle of rodent models. Blood was sampled from conditioned dogs (n=8) and sedentary dogs (n=8). The conditioned dogs were exercised four months prior the experiment and were following a uniform training protocol, whereas the sedentary dogs were not. GLUT4 expression in mononuclear cells and plasma insulin levels were measured using commercially available enzyme-linked immunosorbent assay (ELISA). Blood glucose levels were determined using blood plasma. HOMA-IR was calculated using plasma insulin and blood glucose levels using the linear approximation formula. Our results indicate that the state of conditioning had a significant effect on the GLUT4 expression at the surface of mononuclear cells. HOMA-IR was also affected by conditioning in dogs. GLUT4 levels in mononuclear cells of sled dogs were inversely correlated with the homeostasis model assessment of insulin sensitivity. This study demonstrates that conditioning increases GLUT4 levels in mononuclear cells of sled dogs as it has been previously reported in skeletal muscle. Our results support the potential of white blood cells as a proxy tissue for studying insulin signaling and may lead to development of a minimally invasive and direct marker of insulin resistance. This may be the first report of GLUT4 in mononuclear cells in response to exercise and measured with ELISA.

Protecting effect of vitamin E supplementation on submaximal exercise-induced oxidative stress in sedentary dogs as assessed by erythrocyte membrane fluidity and paraoxonase-1 activity

The aim of this placebo-controlled study was to investigate the effects of oral vitamin E supplementation for 10 weeks on exercise-induced oxidative damage in untrained dogs. Eight dogs were randomly assigned to a supplementation ( n = 4) or control ( n = 4) group and underwent two isolated submaximal exercise sessions, 10 weeks apart. Blood was collected during each session to measure erythrocyte membrane fluidity (EMF), paraoxonase-1 (PON1) activity, plasma malondialdehyde (MDA) and vitamin E concentrations. These biomarkers were measured in venous blood samples collected before ( t 0), just after ( t, EMF only) and 1 d ( t + 1 d) and 7 d ( t + 7 d) after the dogs ran on a treadmill. Prior to vitamin E supplementation, exercise induced a significant decrease in PON1 activity, EMF, vitamin E concentration and a significant increase in MDA concentration at t + 1 d. After a 10 week vitamin E supplementation period, these exercise-induced changes in PON1 activity, EMF and MDA concentration were still significant in the control group, but not in the supplemented group. These results suggested that vitamin E supplementation had a protective effect on submaximal exercise-induced oxidative damage in sedentary dogs.

Endurance exercise training attenuates cardiac β2-adrenoceptor responsiveness and prevents ventricular fibrillation in animals susceptible to sudden death

Enhanced cardiac beta(2)-adrenoceptor (beta(2)-AR) responsiveness can increase susceptibility to ventricular fibrillation (VF). Exercise training can decrease cardiac sympathetic activity and could, thereby, reduce beta(2)-AR responsiveness and decrease the risk for VF. Therefore, dogs with healed myocardial infarctions were subjected to 2 min of coronary occlusion during the last minute of a submaximal exercise test; VF was observed in 20 susceptible, but not in 13 resistant, dogs. The dogs were then subjected to a 10-wk exercise-training program (n = 9 susceptible and 8 resistant) or an equivalent sedentary period (n = 11 susceptible and 5 resistant). Before training, the beta(2)-AR antagonist ICI-118551 (0.2 mg/kg) significantly reduced the peak contractile (by echocardiography) response to isoproterenol more in the susceptible than in the resistant dogs: -45.5 +/- 6.5 vs. -19.2 +/- 6.3%. After training, the susceptible and resistant dogs exhibited similar responses to the beta(2)-AR antagonist: -12.1 +/- 5.7 and -16.2 +/- 6.4%, respectively. In contrast, ICI-118551 provoked even greater reductions in the isoproterenol response in the sedentary susceptible dogs: -62.3 +/- 4.6%. The beta(2)-AR agonist zinterol (1 microM) elicited significantly smaller increases in isotonic shortening in ventricular myocytes from susceptible dogs after training (n = 8, +7.2 +/- 4.8%) than in those from sedentary dogs (n = 7, +42.8 +/- 5.8%), a response similar to that of the resistant dogs: +3.0 +/- 1.4% (n = 6) and +3.2 +/- 1.8% (n = 5) for trained and sedentary, respectively. After training, VF could no longer be induced in the susceptible dogs, whereas four sedentary susceptible dogs died during the 10-wk control period and VF could still be induced in the remaining seven animals. Thus exercise training can restore cardiac beta-AR balance (by reducing beta(2)-AR responsiveness) and could, thereby, prevent VF.

Recovery of Muscle Glycogen Concentrations in Sled Dogs during Prolonged Exercise

To determine the depletion of muscle glycogen during five consecutive days of endurance exercise in Alaskan sled dogs consuming a high-fat, low-carbohydrate diet. Forty-two fit Alaskan sled dogs were used in the study, of which six dogs served as nonexercising control animals. The remaining 36 dogs ran 160 km x d(-1) for up to 5 d while consuming a diet providing approximately 50% of calories as fat and 15% as carbohydrate. Muscle biopsies were performed on six randomly selected dogs before feeding and within 4 h after each 160-km run was completed. Muscle samples were prepared for analysis of glycogen content and myosin ATPase staining. Serum creatine kinase (CK) activity was measured once before exercise and after each 160-km run. Thirty-three of 36 dogs completed the runs. Muscle glycogen concentration was highest in sedentary dogs (340 +/- 102 mmol x kg(-1) dry weight), declined to 73 +/- 16 after 160 km and subsequently increased to similar levels between 320 and 800 km (320 km: 177 +/- 34; 800 km: 213 +/- 44). Postexercise serum CK activity was significantly elevated throughout the study. Skeletal muscle in Alaskan sled dogs has remarkable glyconeogenic ability as demonstrated by repletion to greater than 50% of resting muscle glycogen concentrations after the second of five consecutive 160-km runs even when fed a low-carbohydrate, high-fat diet. Whether this finding is attributable to rapid repletion of muscle glycogen during brief recovery periods versus progressive utilization of alternative substrates remains to be investigated.

Exercise-Induced Changes in Insulin and Glucagon Are Not Required for Enhanced Hepatic Glucose Uptake After Exercise but Influence the Fate of Glucose Within the Liver

To test whether pancreatic hormonal changes that occur during exercise are necessary for the postexercise enhancement of insulin-stimulated net hepatic glucose uptake, chronically catheterized dogs were exercised on a treadmill or rested for 150 min. At the onset of exercise, somatostatin was infused into a peripheral vein, and insulin and glucagon were infused in the portal vein to maintain basal levels (EX-Basal) or simulate the response to exercise (EX-Sim). Glucose was infused as needed to maintain euglycemia during exercise. After exercise or rest, somatostatin infusion was continued in exercised dogs and initiated in dogs that had remained sedentary. In addition, basal glucagon, glucose, and insulin were infused in the portal vein for 150 min to create a hyperinsulinemic-hyperglycemic clamp in EX-Basal, EX-Sim, and sedentary dogs. Steady-state measurements were made during the final 50 min of the clamp. During exercise, net hepatic glucose output (mg x kg(-1) x min(-1)) rose in EX-Sim (7.6 +/- 2.8) but not EX-Basal (1.9 +/- 0.3) dogs. During the hyperinsulinemic-hyperglycemic clamp that followed either exercise or rest, net hepatic glucose uptake (mg x kg(-1) x min(-1)) was elevated in both EX-Basal (4.0 +/- 0.7) and EX-Sim (4.6 +/- 0.5) dogs compared with sedentary dogs (2.0 +/- 0.3). Despite this elevation in net hepatic glucose uptake after exercise, glucose incorporation into hepatic glycogen, determined using [3-3H]glucose, was not different in EX-Basal and sedentary dogs, but was 50 +/- 30% greater in EX-Sim dogs. Exercise-induced changes in insulin and glucagon, and consequent glycogen depletion, are not required for the increase in net hepatic glucose uptake after exercise but result in a greater fraction of the glucose consumed by the liver being directed to glycogen.

Exercise does not induce major changes in plasma muscle enzymes, creatinine, glucose and total proteins concentrations in untrained beagle dogs.

Changes in plasma creatinine (Pl-Creat), glucose, total proteins (Pl-TP), creatine kinase (Pl-CK), lactate dehydrogenase, aspartate aminotransferase and packed cell volume were evaluated in untrained Beagle dogs before, during and after a 60 min race at an average speed of 9 km/h. There was no major effect of exercise on those parameters except, when phases are compared, a slight increase of Pl-TP during exercise (max. + 6.4%), a moderate but after exercise (delayed increase of Pl-CK max. + 245%) and a slight decrease of Pl-Creat after exercise (max. -9.6%). It was therefore concluded that strenuous exercise in sedentary dogs did not induce major variations in any of routine plasma variables measured and would not lead to clinically relevant misinterpretation. However, for Pl-CK, the interpretation of repeated measures may be misleading if two samples are collected in the same animal before and after exercise.

Prior exercise increases net hepatic glucose uptake during a glucose load.

The aim of these studies was to determine whether prior exercise enhances net hepatic glucose uptake (NHGU) during a glucose load. Sampling catheters (carotid artery, portal, hepatic, and iliac veins), infusion catheters (portal vein and vena cava), and Doppler flow probes (portal vein, hepatic and iliac arteries) were implanted. Exercise (150 min; n = 6) or rest (n = 6) was followed by a 30-min control period and a 100-min experimental period (3.5 mg. kg-1. min-1 of glucose in portal vein and as needed in vena cava to clamp arterial blood glucose at approximately 130 mg/dl). Somatostatin was infused, and insulin and glucagon were replaced intraportally at fourfold basal and basal rates, respectively. During experimental period the arterial-portal venous (a-pv) glucose gradient (mg/dl) was -18 +/- 1 in sedentary and -19 +/- 1 in exercised dogs. Arterial insulin and glucagon were similar in the two groups. Net hepatic glucose balance (mg. kg-1. min-1) shifted from 1.9 +/- 0.2 in control period to -1.8 +/- 0.2 (negative rates represent net uptake) during experimental period in sedentary dogs (Delta3.7 +/- 0.5); with prior exercise it shifted from 4.1 +/- 0.3 (P < 0.01 vs. sedentary) in control period to -3.2 +/- 0.4 (P < 0.05 vs. sedentary) during experimental period (Delta7.3 +/- 0.7, P < 0.01 vs. sedentary). Net hindlimb glucose uptake (mg/min) was 4 +/- 1 in sedentary animals in control period and 13 +/- 2 during experimental period; in exercised animals it was 7 +/- 1 in control period (P < 0. 01 vs. sedentary) and 32 +/- 4 (P < 0.01 vs. sedentary) during experimental period. As the total glucose infusion rate (mg. kg-1. min-1) was 7 +/- 1 in sedentary and 11 +/- 1 in exercised dogs, approximately 30% of the added glucose infusion due to prior exercise could be accounted for by the greater NHGU. In conclusion, when determinants of hepatic glucose uptake (insulin, glucagon, a-pv glucose gradient, glycemia) are controlled, prior exercise increases NHGU during a glucose load due to an effect that is intrinsic to the liver. Increased glucose disposal in the postexercise state is therefore due to an improved ability of both liver and muscle to take up glucose.

Do more highly organized collagen fibrils increase bone mechanical strength in loss of mineral density after one-year running training?

The aim of this study was to evaluate the effects of long-term running training on the structural properties of bone. Ten beagle dogs ran according to a strenuous progressive program (up to 40 km/day) for 1 year. At the end of the training program, there was a significant reduction in bone mineral density (up to 9.7%) in the vertebrae of the runner dogs as compared with 10 sedentary control dogs. Polarized light microscopy of the vertebral trabecular bone, however, displayed proportionally higher retardation values of the collagen network of the runner dogs than of the sedentary dogs, suggesting a reorganization in a more parallel manner in the collagen fibrils. The concentration and cross-linking of collagen in the bones remained similar in both groups. No differences were observed in the force to failure of bones of the two groups nor in the histomorphometric analysis of the bones. We suggest that the collagen network in the bones accounted for the maintenance of the strength properties in the bones of the runner dogs despite the loss of mineral density.

The movement, roaming behaviour and home range of free-roaming domestic dogs, Canis lupus familiaris, in coastal New South Wales

In this study 10 free-roaming domestic dogs from an Aboriginal community were radio-collared to determine the sizes of their home ranges and to observe their wandering behaviour. Half of the radio-tagged dogs went on wandering forays, while the other five roamed only within the vicinity of the community. Home-range size was highly variable within the study group: the mean for the wandering dogs was 927 ha whereas that of the sedentary dogs was 2.6 ha. Dogs travelled 8–30 km on forays. All forays were initiated at night and those that were recorded had an average duration of 26 h. Foray destinations were usually riparian habitats where macropod quarry were abundant.

Enhanced muscle glucose uptake facilitates nitrogen efflux from exercised muscle.

The hypothesis that glucose ingestion in the postexercise state enhances the synthesis of glutamine and alanine in the skeletal muscle was tested. Glucose was infused intraduodenally for 150 min (44.5 micromol . kg-1 . min-1) beginning 30 min after a 150-min period of exercise (n = 7) or an equivalent duration sedentary period (n = 10) in 18-h-fasted dogs. Prior exercise caused a twofold greater increase in limb glucose uptake during the intraduodenal glucose infusion compared with uptake in sedentary dogs. Arterial glutamine levels fell gradually with the glucose load in both groups. Net hindlimb glutamine efflux increased in response to intraduodenal glucose in exercised but not sedentary dogs (P < 0. 05-0.01). Arterial alanine levels, depleted by 50% with exercise, rose with intraduodenal glucose in exercised but not sedentary dogs (P < 0.05-0.01). Net hindlimb alanine efflux also rose in exercised dogs in response to intraduodenal glucose (P < 0.05-0.01), whereas it was not different from baseline in sedentary controls for the first 90 min of glucose infusion. Beyond this point, it, too, rose significantly. We conclude that oral glucose may facilitate recovery of muscle from prolonged exercise by enhancing the removal of nitrogen in the form of glutamine and alanine.

Effect of prolonged heavy exercise on passive biomechanics of splanchnic and cranial blood vessels in dogs

Abstract Biomechanical changes of large arteries and veins of the splanchnic and cranial regions were studied in dogs subjected to heavy treadmill exercise during a 55 week period. Passive stress-strain properties of the vessels were determined using an in-vitro large-deformation mechanical test. External, internal radii, and consequently lumen capacity per unit length of splenic veins were significantly larger in trained versus sedentary dogs at each intraluminal pressure (IP) level studied (e.g. lumen volume at IP of 8 mmHg: 0.276 ± 0.044 cm 3 /cm vs. 0.132 ± 0.027 cm 3 /cm; p 3 /cm vs. 0.068 ± 0.027 cm 3 /cm, at 8 mmHg; p

EXERCISE TRAINING ENHANCES GLYCOLYTIC AND OXIDATIVE ENZYMES IN CANINE MYOCARDIUM 362

Epidemiological evidence indicates that endurance exercise training renders the myocardium resistant to ischemic injury. However, the mechanisms for exercise-induced cardioprotection are unknown. Exercise training increases activities of glycolytic and oxidative enzymes in skeletal muscle. The goal of this study was to determine whether training can also enhance the metabolic capabilities of cardiac muscle. Mongrel canines were subjected to 9 wk treadmill training; sedentary dogs were cage-rested for 4 wk. Stop-frozen samples of left (LV) and right (RV) ventricular myocardium were obtained from pentobarbital-anesthetized trained (Trn) and sedentary (Sed) dogs. Enzymes(HK: hexokinase; PFK; phosphofructokinase; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; PK: pyruvate kinase; LDH: lactate dehydrogenase; CS: citrate synthase; α-KGDH: α-ketoglutarate dehydrogenase; MDH: malate dehydrogenase) were extracted in phosphate buffer and assayed at 38°C. Thetable reports enzyme activities (U · mg protein-1); data are means ± SE, n = 4 (*: P< 0.05 vs. sedentary). Exercise training increased GAPDH activity in both ventricles. During ischemia, GAPDH is the primary rate controlling glycolytic reaction. Thus, increased GAPDH activity could support enhanced glycolysis in trained myocardium. Citrate synthase, which catalyzes carbon entry into the TCA cycle, was also increased in trained LV; thus, training enhances myocardial oxidative capacity.

Endothelium-dependent relaxation and hyperpolarization evoked by bradykinin in canine coronary arteries: enhancement by exercise-training.

1. Kinins, which are produced locally in arterial walls, stimulate the release of endothelium-derived vasodilator substances. Therefore, they may participate in the metabolic adaptation to chronic exercise that occurs in the coronary circulation. Experiments were designed to compare the reactivity to bradykinin in coronary arteries isolated from sedentary and exercised-trained dogs (for 8-10 weeks). 2. The organ chambers used in this study were designed for measurement of isometric tension and cell membrane potential with glass microelectrodes. Rings of canine isolated coronary arteries with endothelium were suspended in the organ chambers filled with modified Krebs-Ringer bicarbonate solution (37 degrees C, gassed with 5% CO2 in 95 O2), and were all treated with indomethacin to prevent interference from prostaglandins. 3. Bradykinin evoked concentration-dependent relaxations of the coronary arteries. However, the kinin was significantly less potent in relaxing coronary arteries from the sedentary dogs than those from the trained ones. 4. In the presence of NG-nitro-L-arginine (an inhibitor of nitric oxide synthases), concentration-relaxation curves to bradykinin were shifted to the right in both types of preparations. Nonetheless, the peptide was still significantly more potent in arteries from exercise-trained animals. 5. In the electrophysiological experiments, concentration-hyperpolarization curves to bradykinin obtained in arteries from sedentary dogs were also significantly to the right of those in vessels from exercise-trained animals. Thus, in arteries from exercised animals, bradykinin more potently evoked the release of both nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). 7. The angiotensin converting enzyme (ACE)-inhibitor, perindoprilat, shifted to the left the concentration-relaxation curves to bradykinin obtained under control conditions and in the presence of NG-nitro-L-arginine. The concentration-hyperpolarization curves to bradykinin were also shifted to the left by perindoprilat. The shift induced by the ACE-inhibitor in either type of preparation was not significantly different. 8. These findings demonstrate that exercise-training augments the sensitivity of the coronary artery of the dog to the endothelium-dependent effects of bradykinin. This sensitization to bradykinin may reflect an increased role of both NO and EDHF, and is not the consequence of differences in ACE activity in the receptor compartment.

Cardiac adrenergic responses and electrophysiology during ischemia: effect of exercise.

Whether exercise protects the myocardium from arrhythmias during ischemia (ISC) or alters electrophysiology is controversial. We used microelectrode techniques in isolated cardiac fibers from exercise-trained (ET: 8-10 wk daily exercise) and sedentary (SED: 8-10 wk cage-rest) dogs to examine the effect of exercise on cellular electrophysiology during simulated ISC. We superfused fibers first with normal Tyrode's, then "ischemic Tyrode's" ([K+]o = 10 mM, pH = 6.7, pO2 < 25 mm Hg), and then again with normal Tyrode's. In automatic fibers, maximum diastolic potential in normal Tyrode's was -98 +/- 1 mV (ET, N = 22) and -97 +/- 1 mV (SED, N = 23); rates were 20 +/- 2 and 18 +/- 3 bpm for ET and SED, respectively. All fibers depolarized to -61 +/- 2 mV with ISC. Abnormal rhythms (abnormal automaticity with or without delayed afterdepolarizations) during ISC alone were seen in 0% of ET and 33% of SED; during ISC with alpha-adrenergic stimulation with 5 x 10(-8) M phenylephrine the incidence was 25% of ET and 0% of SED; during ISC with isoproterenol it was 75% for ET (P < 0.05 vs control) and 38% for SED. Transmembrane potentials in paced subendocardial fibers were similar for ET and SED during control, ISC, and reperfusion. Exercise did not alter cellular electrophysiology but did influence ectopic rhythms seen with beta-stimulation during ISC.

Effects of exercise on myocardial catecholamine content and ischemic injury in dogs with gradual coronary occlusion

The effects of exercise on catecholamine content and the extent of myocardial damage in dogs with Ameroid constrictor occlusion of the left circumflex coronary artery were determined. Tissue samples from both the anterior and posterior walls of the left ventricle were obtained for determination of catecholamine content, and the rest of the ventricles were processed for histologic examination. When subjected to treadmill exercise for 40 days after surgery, obstructed animals performed significantly less exercise than sham-operated animals and showed significantly higher percentages of ischemia and necrosis in the left ventricle than sedentary, obstructed, sham-operated, or control dogs. Levels of norepinephrine and epinephrine in the posterior wall of the left ventricle were significantly lower than in the other groups. Our data show that exercise in this well-known model of chronic coronary artery stenosis produced deleterious effects on the myocardium and suggest a marked heterogeneity of catecholamine stores in the myocardium that may have important functional and electrophysiologic consequences.

Training in dogs with normal coronary arteries: lack of effect on collateral development

STUDY OBJECTIVE - The aim of the study was to investigate the effect of exercise training on coronary collateral development in a normal heart animal model. DESIGN - Dogs with normal hearts were fitted with balloon occluders around the left circumflex coronary artery. Haemodynamic variables and myocardial blood flow (using radioactive microspheres) were measured during 1 min circumflex occlusions at rest and during exercise, before and after a 12 week exercise programme. Resting measurements were also made after 4 weeks. SUBJECTS - Trained subjects were 10 one year old beagles; eight beagles served as sedentary controls. Although measurements were made in all dogs at 4 weeks, four trained and three control animals died during the experiment because of complications, so the data reported at 12 weeks are derived from six trained and five sedentary animals. Except during the few occasions when the left circumflex artery was transiently occluded to allow measurement of collateral flow, all coronary arteries were patent and without impediment to normal flow. MEASUREMENTS and RESULTS - Measurements of haemodynamic variables and coronary blood flow were made at the start and repeated at 4 weeks (resting measurements only) and 12 weeks of exercise training. Initial resting circumflex collateral flow was 0.26(SEM 0.05) cm3.g-1.min-1 in the training group and 0.23(0.03) in the control group (NS). The ratio of ischaemic to normal blood flow was 0.16(0.02) in both groups. At 4 weeks there were no changes in either group. At 12 weeks the ischaemic to normal blood flow ratio had increased in both trained and sedentary dogs to 0.24(0.05) and 0.26(0.06) respectively, but the trend over the 12 week period was not significant. The decline in cardiac output and dramatic increase in left atrial pressure during combined coronary occlusion and exercise were comparable in both groups at weeks 1 and 12. CONCLUSIONS - Exercise does not accelerate the development of coronary collaterals in dogs with normal coronary arteries.

Lack of effect of prior training on subsequent ischaemic and infarcting myocardium and collateral development in dogs with normal hearts.

To determine whether exercise training in animals with normal coronary arteries has a salutary effect on ischaemic myocardium, 24 dogs were randomly assigned to be either trained or confined to cages for three months. All dogs then underwent left thoracotomy for placement of indwelling right and left atrial and aortic catheters and a loose snare ligature around the proximal left circumflex coronary artery. Three days after operation control scintigrams were recorded after injection of thallous chloride-201 in animals running on a treadmill to achieve exercise heart rates of 220 beats.min-1. Four days later the snares were pulled to occlude the left circumflex artery and infarct size determined by measuring venous activity of creatine phosphokinase. Three days after infarction the first post-ligation scintigram was performed after thallium-201 injection in exercising animals. Exercise scans were repeated at 10 days and 2, 4, and 6 weeks after coronary ligation. During the final exercise study collateral blood flow was measured with radioactive microspheres. There was no difference in mean creatine phosphokinase appearance time, peak creatine phosphokinase activity, or measured infarct size between the trained and sedentary dogs. The ratio of thallium-201 activity in left circumflex artery or ischaemic area to left anterior descending artery or normally perfused myocardium fell from 100% before occlusion to 86.6% in the sedentary animals and 80.6% in the trained dogs three days after coronary ligation. Although these falls were significant (p less than 0.025 and p less than 0.005 respectively), there was no difference between groups. Over the next five and a half weeks the scintigraphic defect shrank as the thallium-201 ratio gradually increased, but changes were again similar in both groups. At six weeks there was little difference in exercise collateral flow to left circumflex artery myocardium and flow to normal myocardial tissue in cage confined and trained dogs. Therefore, no beneficial effect of exercise training in dogs with normal hearts could be seen on ischaemic or infarcting myocardium or coronary collateral development after coronary ligation.

Left ventricular performance characteristics in trained and sedentary dogs.

Training effects on left ventricular (LV) performance were studied in 14 dogs. Nine had chronically implanted LV pressure transducers, five dogs had sham operations. Ventriculographic evaluation of LV function was performed initially in all animals. The sham-operated dogs were killed. The remaining nine dogs were divided into an exercise group (n - 5) and a sedentary group (n = 4). The exercise group ran on a treadmill for 10 wk with a progressively more rigorous routine. The trained dogs had a decreased heart rate response to graded exercise after 10 wk. At similar heart rates, LV end-diastolic volume (pre: 30.3 +/- 3.0, post: 41.8 +/- 2.4 ml) increased significantly after training (P less than 0.05), but ejection fraction was unchanged (pre: 0.68 +/- 0.03, post: 0.67 +/- 0.06). Stroke work (pre: 1848 +/- 199 X 103, post: 4968 +/- 168 X 103 dyn-cm, P less than 0.05) also increased after training. In the presence of a tachycardia, peak dP/dt and peak contractile element shortening velocity showed increases after training. No significant changes in LV volumes, pump performance, or contractility indices were found in the sedentary group. Chronic endurance training alters the size, and appears to improve pump performance of the LV.