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Biomedical subjects

C M Tipton

Publications and source records attributed to C M Tipton.

At least 55 records · Page 3Linked to original sources

Influence of single hindlimb support during simulated weightlessness in the rat.

Mature male rats (n = 16) were assigned to either 14 days of head-down suspension with one hindlimb supported (HDS) or to control cages (C) of similar dimensions. Hindlimb support during HDS preserved the muscle mass-to-body mass ratio (mg/100g) compared with C conditions for the soleus (48.3 +/- 1.0 to 41.7 +/- 1.0), plantaris (98.4 +/- 3.4 to 103.3 +/- 4.1), and gastrocnemius (484.7 +/- 18.5 to 507.2 +/- 13.9). However, the muscle mass-to-body mass ratio was significantly lower for the soleus (28.9 +/- 1.5), plantaris (83.9 +/- 3.6), and gastrocnemius (411.9 +/- 24.2) muscles from the freely hanging hindlimbs compared with the contralateral muscles from the supported hindlimbs or muscles from C animals. Citrate synthase activity (mumol.g-1.min-1) was significantly lower in soleus muscles from HDS rats in both the supported (19.4 +/- 2.3) and freely hanging (20.0 +/- 1.6) hindlimbs compared with C (28.5 +/- 3.1), whereas soleus muscle glycogen concentration (mg/g) was significantly higher in the freely hanging limbs from HDS rats (5.90 +/- 0.31) but not in the supported limbs (3.80 +/- 0.61) compared with C (4.34 +/- 0.50). Doppler flow probes were used to determine that iliac blood flow to freely hanging hindlimbs was significantly decreased after 48 (-19 +/- 5%) and 72 (-20 +/- 6%)h of HDS compared with presuspension values. In addition, iliac vascular resistance was significantly elevated at most time points during the 72 h of HDS in the freely hanging limbs but not the supported hindlimbs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Exercise training and incidence of cerebrovascular lesions in stroke-prone spontaneously hypertensive rats.

To assess the effects of moderate exercise [40-70% maximal oxygen uptake (VO2max)] on resting blood pressures, the presence of cerebrovascular lesions, and the life spans of stroke-prone hypertensive rats, nontrained and trained male and female rats were assigned to two experimental groups. The first (n = 48) were exercise trained after 38 days of age, whereas the second (n = 44) initiated exercise training when the animals were 134 days of age. To facilitate cerebrovascular lesions, the sodium concentrations in the rat chow and in the drinking solutions were increased. Symptoms utilized to denote the presence of cerebrovascular lesions were irritability, hyperresponsiveness, ataxia, lethargy, unwillingness to run, and combinations thereof. All brains were removed immediately after death, fixed, and evaluated grossly and microscopically for lesions. In the study with the younger animals, training was associated with a 7-9% increase in VO2max that was statistically significant only in animals with no histological evidence of cerebrovascular lesions. For the older animals, a significant 5-8% increase in VO2max was noted for animals with or without lesions. After 42 days of training for both groups, resting blood pressures for the trained groups with histological lesions were significantly lower. However, this trend did not continue, and the older trained rats appeared to have strokes earlier and to die sooner than their nontrained controls. Although 83% of the older animals had subjective evidence for a stroke before they died, the percentage of animals with lesions ranged from 42 to 58%, with the trained groups having higher percentages.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Thermal adjustments to nonexertional heat stress in mature and senescent Fischer 344 rats.

The purpose of this study was to test the hypothesis that the rise in colonic temperature (Tc) during nonexertional heat stress is exaggerated in senescent (SEN, 24 mo, n = 12) vs. mature (MAT, 12 mo, n = 15) conscious unrestrained Fischer 344 rats. On 2 separate days (48 h apart) each SEN and MAT animal was exposed to an ambient temperature (Ta) of 42 degrees C (relative humidity 20%) until a Tc of 41 degrees C was attained and then cooled at a Ta of 26 degrees C until Tc returned to the initial control level. Control Tc was similar in the two groups for both trials. The rate of Tc change during heating was 63% greater (0.070 +/- 0.005 vs. 0.043 +/- 0.004 degrees C/min, P less than 0.05) and the time to 41 degrees C reduced by 36% (54 +/- 6 vs. 85 +/- 10 min, P less than 0.05) in MAT vs. SEN animals during the first exposure, although the cooling rate was slower in the MAT (0.048 +/- 0.004 degrees C/min) vs. SEN (0.062 +/- 0.006 degrees C/min) animals (P less than 0.05). The heating rate was unchanged in MAT animals between trials 1 and 2. However, SEN animals had a 95% increase in heating rate in trial 2 compared with trial 1 (P less than 0.05), and the corresponding time to 41 degrees C was decreased by 44% (P less than 0.05). As a result, rate of heating and time to 41 degrees C were similar in the two groups during trial 2. The cooling rate was similar between trials within each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

Cardiovascular-sympathetic adjustments to nonexertional heat stress in mature and senescent Fischer 344 rats.

The purpose of this study was to test the hypothesis that the cardiovascular-sympathetic nervous system adjustments during nonexertional heat stress are exaggerated in senescent (S, 24 mo) vs. mature (M, 12 mo) conscious unrestrained Fischer 344 rats. During two separate trials (48 h apart), each animal was exposed to an ambient temperature (Ta) of 42 degrees C until a colonic temperature (Tco) of 41 degrees C was attained and then cooled at a Ta of 26 degrees C until Tco returned to the initial control level. Trial 1: heart rate (HR), mean arterial blood pressure (MAP), and arterial plasma concentrations of norepinephrine (NE), epinephrine (E), and lactate (La) were similar between the S and M groups during the baseline (control) period. The absolute increases in HR, MAP, NE, and E from the control period to the end of heating were of similar magnitudes between groups; however, La increased more in the S than M animals (P less than 0.05). During recovery, the declines toward control levels for all variables were similar or even more rapid in the S vs. M animals (P less than 0.05). Trial 2: the changes in HR and MAP during heating were similar to those observed in trial 1 in both groups. Generally, NE and E control levels were elevated in both groups compared with those in trial 1. The absolute increases in NE during heating were similar to trial 1 in both groups, whereas E increased to a greater extent than in trial 1 in the S animals (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

Arterial baroreceptor reflex modulation of sympathetic-cardiovascular adjustments to heat stress.

The purpose of this study was to determine if the arterial baroreceptor reflexes modulate the sympathocirculatory responses to acute heat stress. To address this, arterial pressure, heart rate, mesenteric and renal blood flow velocity (Doppler flow probes), arterial plasma norepinephrine, and colonic temperature were measured before and during whole body heating (42 degrees C ambient temperature) in groups of conscious, unrestrained rats with (sham) or without (sinoaortic deafferentation) intact arterial baroreceptor reflexes. Heating was stopped when a colonic temperature of 41 degrees C was attained. Baseline levels of arterial pressure were similar in the two groups, whereas heart rate was elevated in deafferented versus sham-operated rats (p less than 0.01). The increases above baseline for both arterial pressure (73 +/- 4 vs. 27 +/- 2 mm Hg) and heart rate (127 +/- 10 vs. 33 +/- 5 beats/min) were threefold to fourfold greater at the end of heating in the deafferented versus the sham group (p less than 0.01). Declines in mesenteric and renal blood flow were similar in the two groups during heating; however, deafferented rats had greater increases in both mesenteric and renal vascular resistance (p less than 0.05). Plasma norepinephrine was elevated at baseline in deafferented versus sham rats and increased in both groups during heating (p less than 0.01). The magnitude of the increase in plasma norepinephrine from baseline to 41 degrees C was fivefold greater in the deafferented versus the sham rats (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of hindlimb suspension on VO2 max and regional blood flow responses to exercise.

Male rodents were studied before and after undergoing one of three treatment conditions for 9 days: 1) cage control (n = 15, CON), 2) horizontal suspension (n = 15, HOZ), and 3) head-down suspension (n = 18, HDT). Testing included measurements of maximal O2 uptake (VO2 max) and select cardiovascular responses to graded treadmill exercise. VO2 max expressed on an absolute basis (ml/min) was significantly decreased after HOZ (-14.1 +/- 2.5%) and HDT (-14.3 +/- 2.0%), while being essentially unchanged in CON (-1.0 +/- 3.3%). Significant reductions in body weight were observed after both HOZ (-10.1 +/- 4.2 g) and HDT (-22.5 +/- 3.3 g), whereas CON animals exhibited a significant increase in weight (10.4 +/- 3.8 g). As a result, when VO2 max was normalized for body weight, all groups exhibited similar significant reductions of 6-7%. Although no differences in heart rate and blood pressure response to graded exercise were observed, the HDT group exhibited greater increases in mesenteric resistance at the same absolute exercise intensity. Furthermore, both suspended groups had higher iliac resistance values during exercise at similar relative exercise conditions, suggesting that muscle blood flow during treadmill running may have been reduced after suspension. In general, the decrements associated with the HOZ and HDT conditions were similar. It was concluded that reduction in exercise capacity and altered cardiovascular responses to exercise observed after 6-9 days of suspension were attributable to a combination of hypokinesia, lack of hindlimb weight bearing, or restraint, rather than to hydrostatic influences associated with HDT.

Animals↗

Influences of exogenous insulin on arterial blood pressure measurements of the rat.

Studies were undertaken with adult male rats to test the hypothesis that euglycemic hyperinsulinemia would alter mean arterial blood pressure (MAP) and heart rate (HR) relationships by activation of the sympathetic nervous system. Conscious rats were infused either with insulin or control vehicle (0, 0.47, 1.5, 4.7, 15.0 mU.kg-1.min-1) for 75 min before injection of hexamethonium. Compared with the control period, insulin infusion significantly increased MAP by 7.1 +/- 0.1, 12.7 +/- 2.0, and 19.7 +/- 0.3 (SE) mmHg and HR by 44 +/- 8.4, 66 +/- 10.3, and 95 +/- 6.3 beats/min, respectively, during the three highest rates of infusion. The dose-dependent increases in MAP and HR were due to increases in the activity of hexamethonium-sensitive pathways. In chemically sympathectomized rats, insulin infusion did not produce a significant increase in either MAP or HR. The influence of exogenous norepinephrine on MAP and HR was also studied after insulin infusion. Compared with the insulin-vehicle infusion, insulin infusion significantly depressed (P less than 0.05) the norepinephrine dose-response increase in MAP. In addition, isolated smooth muscle strips were studied to determine the influence of insulin on their in vitro responses to increasing doses of norepinephrine. Although insulin did not alter contractility, it significantly (P less than 0.05) decreased the sensitivity of the vascular strips to norepinephrine. Collectively, the data from these euglycemic experiments indicated that infusions of insulin caused increases in HR and MAP because of activation of the sympathetic nervous system, even though the responsiveness of the vascular smooth muscle was depressed.

Animals↗

Response of hypertensive rats to acute and chronic conditions of static exercise.

To determine whether chronic static exercise would alter resting caudal artery systolic blood pressure (RSBP) in stroke-prone hypertensive rats (SP-SHR), a 20- to 21-wk experimental study was initiated with 24 male and 16 female rats. In addition, eight rats were cannulated for heart rate and blood pressure measurements and implemented with Doppler flow probes (mesenteric and iliac arteries) for determination of the acute responses. The rats were trained to perform static exercise by forelimb hanging over an electrical grid (3-5 mA) activated with a high-frequency sound (2.5-10kHz) of 60 dB. Acute forelimb hanging by nontrained rats caused a 70-mmHg elevation in mean blood pressure, 115-beat/min increase in heart rate, and 71% decrease in mesenteric blood flow. The procedure for chronic forelimb hanging included increasing the number of sets per session from one to three, maintaining the number of repetitions between 6 and 10 and the hang time within 7-10 s/hang, while increasing the amount of weight supported per set from 0 to 12% of body weights for males and 30% for females. Two performance tests, one for endurance (no weights) and one for "strength" (weights), demonstrated that the hanging animals increased their endurance ability by 103% and their strength by 115%. RSBP was not significantly increased in either the male or female trained populations when evaluated by analysis of variance or trend-analysis procedures. Food and water consumption, sodium and potassium excretion, and blood volume measurements exhibited no group differences that had statistical significance. Five animals had evidence for previous strokes, with four being associated with the nonhanging animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Reductions in blood pressure after acute exercise by hypertensive rats.

Postexercise reductions in blood pressure at rest have been reported for hypertensive subjects. To determine whether post-exercise hypotension would occur in spontaneously hypertensive rats and to test the hypothesis that any reductions would result because of decreases in regional vascular resistances, hypertensive rats (n = 19) were instrumented with indwelling arterial catheters and Doppler probes to measure regional blood flows from the iliac, superior mesenteric, and renal arteries. Data were collected from animals who performed a 20- and a 40-min treadmill test at between 60 and 70% of their maximum O2 uptake. When the animals ran for 20 min, there was a pre- to postexercise drop in mean arterial pressure (MAP) from 158 +/- 3.6 to 150 +/- 3.6 mmHg (P less than 0.05), which was recorded 30 min after the exercise had ceased. The pre- to postexercise reduction in MAP after 40 min of treadmill running was from 154 +/- 3.1 to 138 +/- 3.0 mmHg (P less than 0.05) as recorded 30 min postexercise. Postexercise heart rate was significantly lower after the 40-min exercise bout, from a preexercise mean of 351 +/- 3 beats/min to 324 +/- 5 beats/min 30 min after the treadmill had stopped. Surprisingly, marked pre- to postexercise reductions in regional vascular resistance were not observed in either the iliac, superior mesenteric, or renal vascular beds. These data demonstrated the existence of postexercise hypotension in genetic hypertensive rats and suggested that reductions in cardiac output were the primary hemodynamic mechanism for this finding.

Animals↗

Iowa wrestling study: cross-validation of the Tcheng-Tipton minimal weight prediction formulas for high school wrestlers.

Previous research by Tcheng and Tipton developed two prediction equations appropriate for the estimation of minimal weight for high school wrestlers. The purpose of this investigation was to cross-validate these equations using densitometric estimates of minimal weight. Skeletal dimension measurements and hydrostatic weighing were completed on 220 Iowa high school wrestlers at various times in and out of season. High concurrent validity (r = 0.93) and small residual errors (less than 0.33 kg) were observed when compared to densitometric estimates. Regression weights were of similar magnitude to those from the previous study. Two new prediction models were tested. Model II enhanced the multiple R over previous equations to 0.962 and decreased the SEE by 25% (0.55 kg). The equation was: Minimal Weight (lbs) = 0.49 x Current Weight (lbs) + 1.65 x Height (inches) + 1.81 x Chest Diameter (cm) + 6.70 x Right Wrist Diameter (cm) + 1.35 x Chest Depth (cm) - 156.56. It was concluded that the Tcheng-Tipton equations or the new models could be used as valid indicators of a minimal weight for scholastic wrestlers.

Adolescent↗

Influence of exercise training on resting blood pressures of Dahl rats.

To determine whether female Dahl salt-sensitive (SS) hypertensive rats would adapt to chronic treadmill exercise by exhibiting lower resting systolic blood pressures (RSBP), a 12-wk training program was undertaken. Female Dahl salt-resistant (SR) rats were also trained for the same time period a a similar intensity [40-70% maximal O2 consumption (VO2max)] and duration (55 min). Postexperimental treadmill run times and VO2max values [SR: nontrained (NT) 87 +/- 1, trained (T) 97 +/- 2; SS: NT 82 +/- 2, T 92 +/- 3 ml.min-1 X min-1 X kg-1] indicated that the prescribed program had produced a trained state. However, the training program caused no group differences between the SR or the SS and their nontrained controls in measurements associated with sodium chloride intake, fluid consumption, urine production, 24-h sodium excretion, plasma volumes, plasma insulin, or blood volumes. Chronic exercise did significantly lower RSBP in the SR subgroup after 6 wk (NT 123 +/- 4, T 110 +/- 3 mmHg) and 8 wk (NT 120 +/- 4, T 106 +/- 2 mmHg) and remained lower throughout the remaining weeks of the experiment. On the other hand, the RSBP results of the trained SS rats were significantly higher than the nontrained SS rats after 6 wk (NT 155 +/- 8, T 191 +/- 7 mmHg) and were never significantly different than the controls for the remainder of the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Exercise training and the arterial baroreflex.

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.

Animals↗

Select cardiovascular and metabolic responses of diabetic rats to moderate exercise training.

The combined influence of diabetes and moderate treadmill exercise training on select metabolic and cardiovascular parameters was investigated with mature male Sprague-Dawley rats assigned to either control diabetic or diabetic groups receiving exogenous insulin. Experimental diabetes was induced with streptozotocin (80 mg.kg-1, i.v.) and verified by blood glucose concentrations greater than 16 mmol. The animals were designated as control, insulin-injected (5 U.kg-1, twice daily), or saline-injected (twice daily), and assigned to either non-trained or trained sub-groups. Insulin treatment partially restored the measured physiological functions to within normal limits. All animals were trained at 60 to 70% maximal oxygen consumption for 9 wk and exhibited higher maximal oxygen consumption values and cytochrome oxidase activity of the soleus muscles. Diabetes caused lower (P less than 0.05) reductions in resting heart rate but training-induced bradycardia did not occur in any group. Heart rate response to atropine sulfate (1 mg.kg-1, atrial choline acetyltransferase activity, atrial acetylcholine concentration, and quinuclidinyl benzilate binding was measured to evaluate changes in the parasympathetic nervous system. Atropine-induced cardiac acceleration was most pronounced in control and least effective in diabetic animals. Endurance training had no meaningful influence on this response to cholinergic inhibition. Quinuclidinyl benzilate binding for the diabetic and the diabetic groups receiving insulin revealed no change in receptor number, receptor affinity, or training effects. These findings indicated that 9 wk of exercise training improves the aerobic capability of insulin-deficient rats without changing cardiovascular characteristics associated with the parasympathetic nervous system.

Acetylcholine↗

Experimental studies on the influences of physical activity on ligaments, tendons and joints: a brief review.

The clinical practices of the future depend upon the experimental findings of today. Because of the uniqueness of connective tissue, animal experimentation will be essential for advances in this field. During the last decade, the improvements in technology and the increased interest of basic scientists and research clinicians on the effects of physical activity has markedly enhanced the amount of information available to practicing physicians. Studies spanning the appearances of structure to the changes in the crosslinks of collagen, clearly demonstrate that limb immobilization (inactivity) is deleterious to all structures involved whether evaluated anatomically, physiologically, or biomechanically. Furthermore, when surgical repair is included, there are stages when the deleterious processes become accelerated with or without immobilization. Hence, clinical immobilization must be utilized in a prudent and careful manner. There is sufficient experimental evidence for clinicians to utilize motion and mechanical stimuli as a means to improve the structure and function of tendons, ligaments, and joints. However, the unresolved issues are the mode, time of initiation, or the intensity of application. Even when used with repair, recovery of normal structures and function is protracted. The primary or secondary mechanisms associated with these effects of physical activity are unknown and virtually uninvestigated at the present time.

Animals↗