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The influence of chronic exercise was investigated with male rats assigned to normal (N) and sympathectomized (IS) groups. Animals in the latter group were injected daily for 5 days with the antiserum to the nerve growth factor beginning 24 h after birth. Training was introduced when the animals were 35--45 days old and lasted for 12 wk. The exercise program used by both groups was progressive in nature and modified in accordance with the performance capability of the IS animals. When IS and N rats performed a standardized treadmill test, the IS rats had significantly higher rectal temperatures than normal animals. Significant training differences were observed in resting heart rate and in mean blood pressures, but only in the N animals. However, both trained groups exhibited significantly less vasoconstricting ability to conditions of lower body negative pressure than their nontrained controls. Varied doses of epinephrine and norepinephrine were injected into both groups and training per se had no significant influence on the responses recorded. However, both IS group had changes which indicated that a supersensitivity to catecholamines had occurred. Although selective training adaptations can occur without sympathetic nerves, it was concluded that an intact nervous system was essential for maximal training effects to occur.

The influence of exercise training on the resting caudal arterial blood pressures (RBP) of hypertensive rats is unclear despite numerous investigations by different investigators. To determine whether RBP values were influenced by the intensity and the initial age of the animal at the time of training, several studies were undertaken that involved more than 100 rats. When male and female rats were endurance trained for 24 wk at an O2 consumption in excess of 75% of their maximum (Vo2 max), RBP results from nontrained (NT) or trained (T) animals were not significantly different even though at several time periods the T animals had higher resting pressures. However, when exercising rats at an intensity level representing 40-60% of their Vo2 max, the T groups had consistently lower RBP than their NT controls during the majority of the experimental time periods. In addition exercising young (2-3 wk old) hypertensive-prone rats at a moderate intensity was associated with lower RBP within 4-6 wk after the initiation of training; however, exercise training could not normalize RBP. Reduced dosages (85% of normal) of antihypertensive medication, when combined with moderate training, was also associated with lower and "normal" RBP in male but not female rats. We conclude that moderate exercise at an early age when combined with subnormal dosages of antihypertensive medication holds promise for the normalization of RBP in male hypertensive rats of a genetic origin.

Metabolic and cardiovascular changes resulting from acute and chronic exercise were examined in male Sprague-Dawley rats assigned to sham-control or hypophysectomized groups. Two weeks after surgery, the hypophysectomized rats had decreased their maximum oxygen consumption (VO2 max) and heart rate values by 4 ml X min-1 X kg-1 and 142 beats X min-1, respectively. Twenty weeks later, hypophysectomy was associated with a 22 ml X min-1 X kg-1 decrease in VO2 max and a 215 beat X min-1 decline in their maximal heart rates when compared with sham-control means. Endurance training was responsible for the significantly higher O2 consumption values. Additionally, trained animals exhibited longer run times, higher muscle cytochrome oxidase activity, and reduced food consumption. Measurements of right atrial choline acetyltransferase (CAT) activity and [3H]quinuclidinyl benzilate (QNB) binding revealed significantly higher CAT values and fewer muscarinic receptors. However, training had no significant effect on resting blood pressure, blood pressure changes with conditions of lower body negative pressure, muscle glycogen concentrations, CAT levels and QNB binding of the left atrium and ventricular regions, or receptor density. These results indicated that many of the adaptations that are characteristic of normal populations can occur in the absence of the hormones from the pituitary gland.

The reactive hyperemic responses to 10-s coronary occlusions were studied in seven sedentary-control (C) and eight exercise-trained (T) anesthetized dogs, with electromagnetic flowmeters placed on the left anterior descending coronary artery. Radiolabeled microspheres (9 +/- 0.8 micron) were used to measure resting coronary flow per gram and to study the effects of isoproterenol infusion (ISO) (1 mg/kg-min) on total and regional coronary flow. Base-line coronary flow per 100 g was significantly greater in the T dogs (122 +/- 7) than in C dogs (100 +/- 4). During ISO, T and C coronary resistances did not differ significantly, whereas the effects of ISO on total and regional coronary flow were quite different in T dogs as compared to C dogs. C and T hyperemic flow debt repayments did not differ significantly; however, the peak reactive hyperemic flow in T dogs (344 +/- 12%) was significantly greater than the control (306 +/- 10%). Since resting coronary flow per gram was greater in T dogs, the greater peak reactive hyperemic flow implies that T dogs have an increased coronary reserve. Although the mechanisms involved are unclear, the results of this study indicate that chronic exercise training may have beneficial effects on coronary physiology.

The acute cardiorespiratory responses of spontaneously hypertensive rats (SHR) to swimming and running exercise was investigated because SHR populations are hyperresponsive to external stimuli, of the paucity of existing data, and of the uncertainty on the role of exercise stimuli for training adaptations to occur. Male rats were assigned to one of five groups (n = 5-6/group) and designated as controls (C), inexperienced or naive free swimmers (NFS), experienced free swimmers (FS), experienced weighted swimmers (WS) (attached weights equal to 2% of their body weight) or experienced runners (R) who ran at an intensity of 75% of their VO2max. After 75 min in the water, all groups were acidotic and hypercapnic with the WS experiencing the greatest changes. Heart rate (HR) was increased in all swimmers during the initial 10 min, but declined thereafter, and after 75 min, the HR of WS (348 +/- 1 beats/min) was significantly lower than the C group (416 +/- 22 beats/min). At the same time interval, mean arterial blood pressure (MAP) was decreased in all swimming groups to values lower than the C animals. In addition, an exaggerated diving reflex was frequently noted when the rats were submerged. When the magnitudes of the changes were evaluated in the swimming animals they were directly associated with their submergence times, i.e., during 65-75 min of the swim, NFS, FS, and WS were submerged for 43, 46, and 66% of their total swim time, respectively. In sharp contrast to the swimmers, the runners exhibited increases in HR and MAP with their blood gas measurements being indicative of hyperventilation. We concluded that swimming as an exercise mode for hypertensive rats is best served to study the combined effects of excitement, prolonged submergence, and the consequences of the diving reflex.

Traditionally, ligaments and tendons (L and T) have been regarded as metabolically inert structures. However, sufficient biochemical evidence on the metabolism of collagen has indicated that such a concept is no longer tenable. To determine whether L and T respond to increased or decreased levels of chronic exercise, studies were undertaken to measure their aerobic capacities. For comparative purposes, similar measurements were obtained from liver and skeletal muscles secured from normal and hypophysectomized male rats. Oxygen consumption and cytochrome oxidase (CO) activity was recorded from cell suspensions that had been prepared with the inclusion of collagenase and with elastase added to the medium. The O2 results showed that L and T had values that were approximately 10 times lower than liver tissue and 7.5 times less than the means from skeletal muscles. Hypophysectomy caused marked reductions in O2 uptake of liver and muscle tissues; but had no impact on L and T. When CO activity of these connective tissues were evaluated, immobilization and hypophysectomy caused significant reductions that ranged from -36% to -59% respectively. Training, on the other hand, resulted in increases of less than 10% in the activity of this enzyme within L and T while being elevated in muscle tissue by 58%. It was concluded that the metabolic activity of L and T was lowered with decreased levels of physical activity but it was unclear why chronic exercise did not produce the opposite effect.

Head-down tilt is considered an effective experimental model to simulate weightlessness. To determine the acute effects of simulated weightlessness on transcapillary fluid balance, tissue fluid shifts, muscle function, and triceps surae reflex time, eight supine subjects were tilted 5 degrees head down for 8 h. A cephalic fluid shift from the legs was indicated by facial edema, nasal congestion, increased urine flow, decreased creatinine excretion, reduced calf girth, and decreased lower leg volume. As measured by wick catheters inserted under local anesthesia, interstitial fluid pressure in the tibialis anterior muscle (4.6 +/- 0.6 mmHg) and subcutaneous tissue (0.6 +/- 0.5 mmHg) of the lower leg fell significantly to -2.8 +/- 0.5 and -3.8 +/- 0.4 mmHg, respectively. Other transcapillary pressures (capillary and interstitial fluid colloid osmotic pressures) were relatively unchanged. Needle-biopsy specimens, obtained just before and after tilt, indicated that total water content of soleus muscle was unchanged during 8 h of head-down tilt. After head-down tilt, isometric strength and isokinetic strength of the plantar flexors were unchanged. Triceps surae reflex time associated with plantar flexion movement slowed slightly after the tilt maneuver. Collectively these results demonstrated a dehydration effect of head-down tilt on muscle and subcutaneous tissues of the lower leg that may affect muscle function.

The effect of fasciotomy on muscle tension (measured by a force transducer attached to the tendon) and interstitial fluid pressure (measured by Wick catheters in the muscle belly) was studied in the anterolateral compartments of 13 dog hindlimbs. Muscle tension and pressure were monitored in the tibialis cranialis muscle after low- and high-frequency stimulation of the peroneal nerve to produce twitch- and tetanic-type contractions. Fasciotomy decreased muscle force during the low-frequency stimulation by 16% (35.3 +/- 4.9 to 28.4 +/- 3.9 N) and during the high-frequency stimulation by 10% (60.8 %/- 4.9 to 54.8 +/- 3.9 N). Muscle pressure decreased 50% after fasciotomy under both conditions, 15 +/- 2 to 6 +/- 1 mmHg and 84 +/- 17 to 41 +/- 8 mmHg), respectively. Repeated functional evaluations during the testing procedure indicated that muscle fatigue was not a major factor in these results. It was concluded that fascia is important in the development of muscle tension and changes in interstitial pressure. Furthermore, the results raised questions concerning the merits of performing a fasciotomy for athletes with a compartment syndrome.

Male Sprague-Dawley rats were assigned to three groups designated as diabetic, diabetic-plus-insulin, and control and tested for maximum oxygen consumption (VO2max) and maximum heart rate on three different occasions during the 6- to 8-wk experimental period. Compared with the prediabetic values and the means of the other two groups, diabetic animals had significantly higher submaximum and lower maximum VO2 values. These relationships prevailed when the groups were evaluated in terms of ml.kg-1.min-1 or ml.(kg0.79-1).min-1. In addition, the diabetic animals had significantly lower submaximum and maximum heart rates and shorter run times. Daily injections of insulin (2 U.day-1.rat-1) restored VO2max to within the limits of the control animals but did not normalize heart rates or run-time values. The linear relationship between heart rates and VO2 was repeatedly demonstrated with normal animals. However, this relationship progressively declined with the time course of diabetes. These results indicate that, in untreated diabetes, functional capacity is markedly reduced with the progression of the disease and suggest that alterations in the autonomic nervous system, tissue metabolic capacity, and decreases in lean body mass are responsible for the changes noted.

A ten-stage treadmill test was developed and standardized to secure the VO2max of male and female rats assigned to various cross-sectional and longitudinal experimental groups. Repeated measurements indicated that the test procedure was reliable and could be used for research purposes. When the test was used with different strains, the untrained Sprague-Dawley rats had significantly higher VO2max values than animals of the Wistar-Kyoto (WKY) or the Okamoto-Aoki (SHR) strains. Exercise schedules were evaluated that were similar to those previously used by various investigators and it was found that most were exercising their rats at levels exceeding 75% VO2max. After 6--10 wk of chronic exercise, significant increases in VO2max occurred that ranged between 12 and 26%. Longitudinal studies (1 yr) with hypertensive (SHR) rats revealed that it was more desirable to logarithmically evaluate the relationship between VO2max and body mass than by the conventional method of ml . kg-1 . min-1. When this approach was used with SHR animals, the VO2max differences between the sexes were not apparent until the animals were 1 yr of age. On the other hand, training by male SHR rats caused significant increases in VO2max regardless of the method used to express the results. It is recommended that future studies designed to elucidate exercise mechanisms in rats should include a standardized VO2max test.

Previous studies have shown that cardiac glycogen content is replenished to supranormal levels after exercise. To better understand this phenomenon glycogen synthase (GS) %I activity as well as glucose 6-phosphate (G-6-P) and glycogen (G) concentrations were measured in hearts from normal and alloxan diabetic rats killed at various time intervals before or after a treadmill run to exhaustion. In normal animals at exhaustion G was reduced but GS %I and G-6-P were elevated. During 2-8 h of recovery G was elevated, %I depressed, and G-6-P unchanged when compared to their preexercise values. By contrast, diabetic hearts that had elevated G and low %I were characterized by abnormally high G-6-P concentrations. At exhaustion in these hearts %I increased significantly in response to a decrease in G. These findings suggest that glycogen repletion occurs in normal heart as a result of the combined increases in GS %I and G-6-P levels present at the cessation of work. In both normal and diabetic hearts there exists an inverse relationship between G content and GS %I activity.