Positive effects on the tensile characteristics of swine digital extensors were found following twelve months of exercise training. Compared to sedentary controls, the tendons from the exercised animals became stronger as a material and exhibited hypertrophy. These biomechanical results were supported by biochemical analyses of tendon composition. Exercise increased the concentration of collagen as well as the total weights of the tendons. For determining stress and strain in tendon material, we used specially designed instruments to measure the tendon cross-sectional area, and a video dimensional analyzer system to measure accurately its "non-contact" tensile strain. With these newly developed apparatus, the mechanical properties of the tendons were accurately determined so that the effects of exercise training could be compared.

SUMMARY Intramyocardial hemorrhage often occurs with reperfusion in experimental acute myocardial infarction and is thought to be associated with extension of necrosis. To determine if hemorrhage was associated with extension of necrosis, 20 anesthetized dogs were reperfused after 6 hours of circumflex coronary artery occlusion and 10 others had control occlusion with no reperfusion. Fifteen of the 20 reperfused dogs had gross hemorrhage and none of the control dogs did. In 12 reperfused and 10 control dogs, radioactive microspheres were injected after coronary occlusion to quantitate collateral flow and in the reperfusion group microspheres were injected to quantitate reflow. Complete flow data were available in eight reperfused and 10 control dogs. Twenty-four hours after coronary occlusion, 1-g segments of infarct and control regions were analyzed for hemorrhage, collateral flow and creatine kinase activity. Serial microscopic examination was performed in eight additional dogs reperfused after 6 hours to determine if hemorrhage occurs into otherwise microscopically normal myocardium.Pathologic examination indicated that hemorrhage did not occur into otherwise microscopically normal myocardium. In dogs with hemorrhage, the extent of hemorrhage was inversely related to myocardial creatine kinase concentration and collateral flow. Mean collateral flow in 47 hemorrhagic segments was 4.5 ml/100 g (4.2% of control). Mean creatine kinase in 36 hemorrhagic segments was 233 mIU/g (21% of control). No hemorrhage was found in areas with collateral flow more than 21% of control or creatine kinase more than 37% of control. Mean reflow in hemorrhagic segments was 78.5% of control flow. These studies indicate that hemorrhage on reperfusion is associated with severe myocardial necrosis and markedly depressed flow before reperfusion and thus occurs only into myocardium already markedly compromised at the time of reperfusion. There is no evidence for hemorrhage into areas that had normal or even moderately depressed flows before reperfusion.THE BENEFITS of reperfusion after acute coronary occlusion are controversial. Extent of infarction is an important determinant of prognosis after coronary occlusion,' and restitution of flow would appear to provide an effective means of rectifying ischemia and thus limiting infarct size. Jennings et al.2 demonstrated that reperfusion after 20 minutes of occlusion prevented the development of ischemic injury, while other studies using enzyme analysis, histologic examination and functional assessment have shown limitation of infarct size with reperfusion 3 hours after coronary occlusion.'-" Other studies have not substantiated significant improvement after reperfusion. Bresnahan et al.6 demonstrated an increase in infarct size in seven of 16 dogs reperfused 5 hours after coronary occlusion. Other investigators have reported ventricular dysrhythmias7 accelerated morphologic changes of ischemia8 and exacerbation of functional'0 and metabolic measurements of ischemia.9The deleterious consequence...

We determined the effect of exhaustive exercise on the acid-base balance, O2 consumption, and cardiac output in dogs and pigs to examine which species was comparable with humans in its physiological response to exercise. We ran 11 dogs and 11 pigs on a motor-driven treadmill at steady-state (heart rate 75% maximum) and exhaustive (maximum heart rate) exercise levels. Measuring heart rate, cardiac output, and aortic pressure via implanted probes we obtained arterial and venous blood samples before, during, and after exercise to determine hematocrit, blood gas tensions, pH, and lactic acid levels. Dogs had a twofold greater work capacity than the pigs, but the dogs could not run at maximal heart rate as long as the pigs did. Although O2 consumption correlated well with cardiac output and total work in both species, dogs were capable of a greater range of values. The acid-base studies showed that exhaustive exercise in the pigs resulted in a severe metabolic acidosis, whereas this did not occur in dogs. Respiratory alkalosis was noted in dogs. This suggested that the supply of O2 to the working muscles of the pig was insufficient to maintain aerobic metabolism. The pigs' responses to exercise conformed to those found by others in the human, suggesting that the pig is a more appropriate model for some exercise studies.

We measured changes in organ blood flow (OBF) distribution and systemic hemodynamics in 9 dogs running 5-13 km/h during steady-state (SS) and exhaustive (EE) exercise on a treadmill at 8-15% grade for an average of 35 min. SS was defined when a heart rate (HR) of 80% maximum was attained and when HR was constant for 5-8 min. EE was defined as when the dog collapsed, unable to run longer. We measured heart rate, mean aortic pressure, cardiac output, and stroke volume via implanted probes and catheters. All hemodynamic parameters rose significantly (P less than 0.05) with exercise. Stroke volume and aortic pressure did not rise above SS levels during EE. OBF, determined with microspheres, to the liver, stomach, and intestines declined during SS and returned to control levels during EE. OBF to the kidneys and pancreas was not significantly changed by either SS or EE. OBF to the spleen declined progressively with SS and EE. We concluded that 1) the effect of exercise on OBF depends on the severity of exercise, emphasizing the need to quantify work loads in exercise studies, and 2) the splanchnic organs do not respond homogeneously to exercise and that this response is not adequately described by % of CO assessments.

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To study the effects of exercise on collateral development in myocardial ischemia, we induced coronary arterial stenosis of the left circumflex coronary artery (LCCA) in 18 of 30 pigs. During that surgery, we identified the coronary bed at risk. Nine of these pigs were then subjected to 5 mo of exercise training on a treadmill. After exercise training, we determined regional collateral and myocardial blood flow using radiolabeled microspheres. At autopsy, all animals had complete occlusion of the LCCA. Infarct size in the exercise-trained pigs was significantly less than in the sedentary pigs (5.9 +/- 1.0 vs. 11.7 +/- 1.0% of the left ventricle). The exercise-trained animals had a greater increase in collateral flow, 35.1 +/- 3.0 vs. 28.7 +/- 4.1 ml X min-1 X 100 g-1, in the noninfarcted jeopardized zone of the LCCA bed. The major findings of the study were the following: 1) chronic coronary artery stenosis progressing to occlusion stimulated development of the collateral circulation and salvaged tissue in the jeopardized myocardium of an animal model with sparse collaterals; 2) development of the collateral circulation and tissue salvage is increased by exercise training; 3) collaterals develop primarily in or near the ischemic zone; and 4) all collateral beds develop a circumferential flow gradient following occlusion.