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.
The purpose of this study was to develop a dynamic exercise model in the rat that could be used to study central nervous system control of the cardiovascular system. Rats of both sexes were decerebrated under halothane anesthesia and prepared for induced locomotion on a freely turning wheel. Electrical stimulation of the mesencephalic locomotor region (MLR) elicited locomotion at different speeds and gait patterns and increased heart rate and blood pressure. Two maneuvers were performed to illustrate the potential use of the preparation. The first maneuver consisted of muscular paralysis, which prevents excitation of muscle mechanoreceptors and chemoreceptors resulting from exercise. MLR stimulation still increased blood pressure. The second maneuver was performed to determine whether the blood pressure response obtained during paralysis was an artifact of electrical stimulation of the MLR. After microinjection of gamma-aminobutyric acid into the MLR, electrical current thresholds for blood pressure and locomotion increased in parallel. gamma-Aminobutyric acid injection also reduced the pressor response to suprathreshold electrical stimulation by 76%. The injection results suggest that electrical stimulation of the MLR activates cells rather than fibers of passage. The blood pressure response of the exercise model is probably not an artifact of stimulation. The decerebrate rat locomotor preparation should offer another approach to investigate difficult problems in exercise physiology.
To test the hypothesis that endurance training would attenuate the carotid sinus baroreflex in rats, studies were undertaken with 25 nontrained (NT) and 22 trained (T) male Sprague-Dawley rats that were exercised for 11-14 wk. Maximal O2 consumption was significantly increased 10% after training. The left carotid sinus region was functionally isolated in anesthetized animals. Subsequently, static carotid sinus pressure was raised in 20-Torr increments from 95 Torr until a maximal response in systemic arterial pressure and regional blood flows was recorded. Compared with the NT group, baroreflex control of blood pressure and calculated regional resistance of the T animals was less responsive to changes in carotid sinus pressure. Resting blood pressure, heart rate, and changes in peripheral blood flow velocity were similar for the two groups. Peripheral sensitivity to phenylephrine-HCl and hexamethonium bromide were also similar in the T and NT groups. It was concluded that the arterial baroreflex control of blood pressure was attenuated by exercise training. These findings support the concept that the trained individual is at disadvantage during hypotensive episodes and that endurance training will attenuate the sympathetic component of the arterial baroreflex.
The decerebrate rat locomotor preparation described in a previous study requires extensive brain surgery with the possibility of significant blood loss. The purpose of this study was to improve on the previous model by using lightly anesthetized instead of decerebrated rats. After initial surgery consisting of boring a small hole through the parietal bone, the animals were maintained on low levels of halothane anesthetic. The mesencephalic locomotor region was then located by physiological criteria using stereotaxic coordinates from the previous study. Locomotor speed, blood pressure and heart rate responses were then measured over a wide range of stimulation currents that elicited a maximal running speed. Stimulation currents ranged from 36 microA for walking to 82 microA for fast galloping. Locomotor speeds ranged from 20 m/min for walking to 64 m/min for fast galloping. Some animals easily achieved galloping speeds beyond 100 m/min. Blood pressure and heart rate increased with increasing stimulation currents. Blood pressure also increased during stimulation after muscular paralysis. This was not due to current spread, suggesting that the mesencephalic locomotor region might be involved in central command mechanisms. Heart rate did not increase after paralysis. This supports other multi-joint dynamic studies suggesting that movement per se may be necessary to induce heart rate changes, presumably via joint mechanoreceptors. The range of locomotor patterns and cardiovascular responses were obtained under self-supported conditions. By defining the mesencephalic locomotor region via physiological criteria, and by grouping blood pressure and heart rate measurements by gait rather than by stimulation currents, the potential use of the intact model for cardiovascular control studies was demonstrated. The animals were able to run and gallop at high speeds considering they were anesthetized. The simplified preparation will be useful for more complex cardiovascular experiments requiring intact and self-supported conditions.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.