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Biomedical subjects

C V Gisolfi

Publications and source records attributed to C V Gisolfi.

At least 73 records · Page 4Linked to original sources
PubMed1986

Effects of ingesting carbohydrate beverages during exercise in the heat.

Ingesting carbohydrate beverages during exercise in cool temperatures can improve endurance performance. However, because hyperosmotic solutions leave the stomach more slowly than water, carbohydrate beverages could be less effective in minimizing the dehydration and hyperthermia that accompany exercise in the heat. To determine the effect of osmotically different beverages on prolonged (2 h) treadmill exercise (65% VO2max) in the heat (T db = 35 degrees C), five male runners (age 24 to 41 yr) performed three separate runs drinking 200 ml every 20 min of either 10% glucose polymer (GP), 10% glucose (G), or saccharin-sweetened water (WH). A fourth run was performed in a cool (T db = 25 degrees C) room and included drinking saccharin-sweetened water (WC). Drink osmolalities (Osm) for runs GP, G, WH, and WC were 194, 586, 94, and 71 mmol . kg-1, respectively. No significant differences were observed between runs in the heat (GP, G, and WH) for heart rate, rectal and mean skin temperatures, sweat rate, percent change in plasma volume, and gastric residue volume. When compared to the WC run, both the GP and G runs yielded greater (P less than 0.05) declines in percent change in plasma volume, but only the G run had a greater (P less than 0.05) gastric residue volume. Neither plasma osmolality, total protein, nor [Na+] varied between runs. Plasma glucose, insulin, and respiratory exchange ratios were similar between the GP and G runs. However, the GP run yielded the lowest (P less than 0.05) plasma glycerol values. Although gastric residue volume (r = 0.68) and final percent change in plasma volume (r = 0.69) were significantly correlated with drink osmolality, thermoregulation was similar between runs in the heat despite the beverage consumed.

Adult↗
PubMed1985

Heat acclimation: role of norepinephrine in the anterior hypothalamus.

The hypothesis that anterior hypothalamic (AH) sensitivity to norepinephrine (NE) is altered by chronic exercise in the heat was tested in male Sprague-Dawley rats. Treadmill exercise 6 days/wk for 3 wk at 21 m/min was performed at 23 degrees C (control; C) or at 35 degrees C (heat acclimated; HA), progressing from 20 to 50 min/day in 2 wk. Time for core temperature (Tco) to rise from 39.5 to 40.5 degrees C during a heat-tolerance test after conditioning increased (P less than 0.05) in the HA group. To test for a change in AH sensitivity, the change in Tco to 2-, 5-, 10-, 20-, and 40-micrograms doses of NE injected bilaterally into the AH was determined after conditioning. Dose-response regression lines showed that exercise in the heat increased the slope and shifted the Tco-NE dose relation to the left. In a separate series of experiments on 6 sedentary(s), 10 C, and 10 HA animals, the amounts of NE, dopamine, and 3,4-dihydroxyphenylglycol (DOPEG) were determined by high-pressure liquid chromatography in the AH, median preoptic area (PO), cortex, and cerebellum after 9 wk of conditioning. Results showed that in the PO there was a significant increase in NE and DOPEG in the HA vs. C group and a trend of increasing NE from the S to C to HA groups. The data indicate that exercise in the heat increases NE-induced peripheral heat-dissipating capacity and increases catecholamine storage in the PO.

Acclimatization↗
PubMed1984

Temperature regulation during exercise: old concepts, new ideas.

In Figure 13 we have tried to summarize the interactions of thermal and nonthermal control of effector responses, the effects these responses have on the body during exercise, and the ways the changing state of the body feeds back on the central control systems. These systems were depicted in Figure 3 and are included in condensed form in Figure 13. Exercise affects thermoregulatory responses not only by increasing heat production, but also through a number of other mechanisms. For example, the thermoregulatory responses tend to reduce central venous pressure, and sweating without fluid replacement will increase plasma osmolality. The secondary effects of these changes on the control of the thermoregulatory responses may themselves have an important effect on the rise in Tc during prolonged exercise or exercise in the heat. In concluding, it is appropriate to briefly answer the questions raised in the introduction. In our view, the concept of shifting the set point is not different from the concept of resetting the "thermostat," and the temperature regulatory system is governed by only one set point, which does not change during exercise. Tsk does not change the set point as we have defined it. Rather it combines with thermal information from the core and other deep body thermo-detectors to produce a thermoregulatory command signal Tws distributed to all effector responses. To demonstrate a set point shift, one must show that the Tws thresholds for initiating all heat-dissipating responses shift in the same direction. Although this does not occur with exercise, it does occur with time of day, heat acclimation, endurance training, and fever. A hyperosmolar state also can raise the threshold for sweating and vasodilation uniformly, and therefore may also raise the set point. However, a change in posture, for example, which alters the threshold for vasodilation but not for sweating, does not alter the set point. We believe that a shift in threshold for a given effector may be produced by either a central or a peripheral mechanism. For example, an ion-osmotic influence on the sweating: Tc threshold may be at the level of the central nervous system or the sweat gland itself. However, a set point shift must be a central event, since it influences all effector responses uniformly. Is the set point governed by the ratio of sodium to calcium ions in the posterior hypothalamus? This is unlikely. Shifts in ion concentration can influence effector responses, but they do not appear to shift all effectors uniformly.

Blood Volume↗
PubMed1983

Thermoregulatory responses to central injections of excess calcium in monkeys.

In unanesthetized monkeys (4-8 kg), artificial cerebrospinal fluid (ACSF) containing excess (greater than 1.3 mM) amounts of Ca2+ was infused at 20 microliters/min for 5 min into the cerebral ventricles. Core and skin temperatures, respiratory gas exchange, heart rate, and sweat rate were monitored. At 22 degrees C, intracerebroventricular infusions of 13-39 mM Ca2+ produced a dose-related hypothermia associated with a dose-related fall in metabolic rate and heart rate and a rise in average skin temperature. General body sweating was not initiated, and respiratory water loss was unaffected; however, exercise activated sweating and elevated it from 0.05 to 0.22 mg X (cm2 X min)-1. At 35 or 40 degrees C, infusion of 26 mM Ca2+ failed to influence ongoing general body sweating; however, subsequent exercise increased sweat rate by 63%. Heart rate was unaffected. At 15 degrees C metabolic rate increased 50%. After infusing 26 mM Ca2+, metabolism decreased 6% and core temperature declined 0.8 +/- 0.24 degrees C. Skin temperatures continued to fall, heart rate fell, and sweating was not initiated. In contrast, infusing ACSF increased metabolism 11% and core temperature fell only 0.18 +/- 0.14 degrees C. The inability of exogenous Ca2+ to 1) initiate sweating at 22 degrees C, 2) elicit vasodilation at 15 degrees C, 3) initiate or stimulate sweating at 35 or 40 degrees C, or 4) lower core temperature at 35 or 40 degrees C argues against a set-point function for this cation.

Animals↗
PubMed1983

Work-heat tolerance in endurance-trained rats.

The purpose of this study was to determine if training in a cool (23 degrees C) environment would alter the potential for mortality or for tissue damage (as indicated by serum transaminase concentrations) during a work-heat tolerance test (WHTT) to exhaustion. Twenty-nine male Sprague-Dawley rats were trained (T) on a motorized treadmill for 6 wk, while 34 control animals of similar weight remained sedentary (S). Tissue damage among survivors 24 h following the WHTT and percent mortality were the same in both groups; however, T survivors 1) continued the test 44% longer (P less than 0.05), 2) performed significantly more work (P less than 0.05), and 3) sustained a 120% larger (P less than 0.05) thermal load [product of time and colonic temperature (Tc) above 40 degrees C] than S survivors. Mortality first occurred at a range in Tc of 40.6-41.0 degrees C in the S group compared with a range of 41.6-42.0 degrees C in the T group. Thus endurance T rats can run longer in the heat, sustain greater thermal loads, and are less susceptible to work-induced thermal fatality than S rats.

Animals↗
PubMed1983

Temperature regulation during exercise: directions--1983.

During exercise, internal body (core) temperature (Tc) rises to new plateau levels with increasing intensities of steady-state exercise independent of ambient temperature over a wide range (prescriptive zone). This rise in Tc is proportional to relative rather than absolute work load and provides the central stimulus to sweating and cutaneous vasodilation. The system seems to function in the same way during rest and exercise since the rise in Tc during exercise can be explained in fundamental terms of heat production and heat dissipation. Changes in sweating and skin blood flow (SBF) are largely explained by changes in core and skin temperatures; however, there is strong evidence for non-thermal input into the control of these responses. The control of SBF is more complex than the control of sweating because SBF is influenced by cardiovascular as well as temperature regulations. Moreover, hydration state can markedly alter these effectors, indicating that fluid volume and/or fluid composition also contribute to these control mechanisms. Major advances in the future will come from the further development of animal models that allow for studies designed to elucidate the interaction between regulatory systems and the neurochemistry underlying central effector mechanisms.

Body Temperature Regulation↗
PubMed1982

Temperature regulation and dopaminergic systems in the brain: does the substantia nigra play a role?

Male Sprague-Dawley rats (250-300 g) were stereotaxically implanted above the substantia nigra (SN) and preoptic/anterior hypothalamus (PO/AH) with 23 gauge stainless-steel guide tubes. Microinjections of apomorphine (APO), pimozide, or 0.9% saline were made bilaterally in 0.5 or 1.0 microliter vols. using a Harvard infusion pump. Oxygen consumption, and colonic (Tc), tail-skin, and ambient temperatures were monitored each minute. Microinjections of APO into the SN produced a dose dependent hypothermia that was antagonized by the central (1.0 microgram) or systemic (0.5mg/kg i.p.) injection of pimozide. This hypothermia was associated with increased heat loss and decreased heat production and occurred at ambient temperatures of 15, 23 and 25 degree C indicating that APO did not produce a poikilothermic state. Injecting 20 microgram APO into the PO/AH or SN produced similar hypothermic responses; Tc fell 0.87 /+- 0.10 degree C and 1.02 /+- 0.08 degree C, respectively. Pimozide injected into the SN failed to alter thermoregulation during exercise or exogenous heating. Moreover, systemic injections of APO before and after electrolytic lesioning of the SN produced similar hypothermic responses. However, when the SN was lesioned, (a) resting Tc was significantly reduced, and (b) during exposure to a 35 degree C environment for 55 min, Tc rose to 39.5 /+- 0.68 degree C before the lesion compared with a rise to only 38.5 /+- 0.13 degree C after the lesion. We conclude that the pharmacological data implicate a thermoregulatory role for dopamine receptors in the rat, but the functional significance of this central location in temperature regulation remains to be elucidated.

Animals↗
PubMed1982

In vivo and in vitro characteristics of eccrine sweating in patas and rhesus monkeys.

Biopsy specimens from the chest, palm, back, and lateral calf were obtained from three patas (4-6 kg) and two rhesus monkeys (6 and 8 kg) tranquilized with ketamine hydrochloride (10 mg/kg). The eccrine sweat glands of the specimens were subsequently isolated under a stereomicroscope and prepared for analysis. In both palmar and hairy skin (chest, lateral calf) patas eccrine glands were larger than those isolated from corresponding sites obtained from the rhesus specimens. In vitro stimulation of the patas' glands with methacholine (MCH) chloride produced a dose-dependent increase in sweating rate that was blocked by atropine. Maximal palmar sweating was comparable between the two species of monkey. Mean maximal in vitro sweating rates on the chest and lateral calf of the three patas monkeys were 3.79 and 4.6 nl. gl-1.min-1, respectively. In contrast, the in vitro sweating rate of the rhesus chest glands was negligibly small, i.e., 0.05 nl.gl-1. min-1. Maximal in vivo sweating rates measured by resistance hygrometry during exercise in a hot (40 degrees C) environment were usually synchronous, cyclic, and only slightly below maximal in vitro rates. When the monkey (patas) was already sweating, the onset and cessation of exercise produced an immediate rise and decline in sweating, respectively. At any given rectal or mean skin temperature, sweating was two- to sixfold higher in the patas compared with that of the rhesus monkey. These results indicate that the patas monkey is an excellent model for studying the physiology of sweating in humans.

Animals↗
PubMed1981

Effects on breathing of putative neurotransmitters in the rostral hypothalamus of the rat.

The putative neurotransmitters norepinephrine (NE) and thyrotropin releasing hormone (TRH) are normally present in the rostral hypothalamic region (RHT) of the rat, and our aim was to evaluate possible effects of these agents on ventilatory regulations associated with this region. Using haloperidol-tranquilized Sprague-Dawley rats, microinfusions of both NE and TRH into the RHT resulted in an increase in rate, but not depth, of breathing. Control infusions and control infusion sites, mainly in the posterior hypothalamus, yielded no significant effect on breathing rate. Since NE and TRH can inhibit the discharge of some cells in the RHT, it was possible that the observed effects on breathing were due to depression of an inhibitory neural pathway. This idea was further tested by performing microinfusions using lidocaine. Evidence suggests that lidocaine can inhibit discharge in the central nervous system and that inhibitory pathways may be preferentially affected. Lidocaine produced effects on breathing comparable to NE and TRH, thereby supporting the proposition that inhibition of neural pathways in the RHT can stimulate breathing.

Animals↗
PubMed1980

Effects of exercising rats during pregnancy.

To determine the effects of exercise during pregnancy on the cardiovascular system of their progeny, female Sprague-Dawley rats were assigned to one of four groups: 1) trained-nontrained (T-NT) animals who ran for 7 wk at 35 m/min before but not during pregnancy; 2) T-T animals who ran at 35 m/min before and at 32 m/min during pregnancy; 3) control (C) animals who did not exercise; and 4) NT-T animals who only ran (16 m/min) during pregnancy. Significant increases in skeletal muscle cytochrome found between exercised (NT-T, T-T) and nonexercised (C, T-NT) mothers; C animals had significantly lower maximal oxygen consumption (VO2max) values than T-T animals at the end of pregnancy. Offspring mortality was greater (P less than 0.05) in the T-T compared with the C group during the 28 days following birth. Maternal exercise had no significant influence on VO2max in the offspring or on myocardial blood flow when these animals were ventilated with either hypoxic (10% O2) or normoxic (21% O2) gases. Right ventricular fiber areas were smaller (P less than 0.05) in T-T and NT-T animals compared with the T-NT group; no significant changes were observed in the left ventricle. Capillary density and fiber-to-capillary ratios were not different in either the right or left ventricle. These results indicate that mild or heavy exercise does not influence VO2max, coronary blood flow in response to stress, or myocardial structure in the male offspring of rats trained during pregnancy.

Animals↗
PubMed1980

Effects of apomorphine and pimozide on temperature regulation during exercise in the rat.

The purpose of this study was to determine the effects of a specific dopamine receptor agonist (apomorphine) and antagonist (pimozide) on thermoregulation when the heat loss pathway was activated by the stress of exercise. Apomorphine or its control vehicle (0.9% wt/vol saline) was injected systemically (0.5, 1.0, 1.5 mg/kg ip) or within the preoptic-anterior hypothalamus (5, 10, 20 micrograms) immediately before the start of treadmill exercise at 21.5 m/min. Colonic, tailskin, and ambient temperatures were recorded each minute. Oxygen consumption was calculated from on-line measurements of percent O2 and CO2. Pimozide injected systemically (0.5 mg/kg ip) had no effect on resting colonic temperature, but caused a significant (P less than 0.05) hyperthermia during treadmill exercise compared to saline controls. Central and systemic injections of apomorphine caused a dose-dependent hypothermia that was blocked by pretreatment with pimozide. Oxygen uptake values during exercise following the central injection of apomorphine were virtually identical to those following the injection of saline, but colonic temperature was significantly (P less than 0.05) lower than saline controls, indicating that the hypothermia observed was not due to a reduction in metabolic rate. These data indicate that dopamine receptors in the preoptic-anterior hypothalamus of the rat participate in the mediation of heat dissipation when the animal is challenged with a heat stress.

Animals↗
PubMed1980

Thermal effects of injecting norepinephrine into hypothalamus of the rat during rest and exercise.

Norepinephrine (NE) was injected bilaterally through implanted guide cannulas into the anterior hypothalamus (AH) of conscious male Sprague-Dawley rats (300-360 g) at rest and just before treadmill exercise (21.5 m/min for 30 min). Colonic (Tc), tail-skin (Ts), and ambient (Ta) temperatures were monitored each minute by use of a telethermometer. At rest (Ta = 23 degrees C), intrahypothalamic injections of 0.5-40.0 micrograms of NE, in a total of 1.0 microliter delivered within 30 s, produced a dose-dependent hypothermia with a 3-5 degrees C rise in Ts. NE (10 micrograms) injected 2 min before exercise (Ta = 23 degrees C) caused an immediate rise in Ts and a mean decline in Tc of 0.9 +/- 0.1 degree C (SE) below resting levels during exercise. This decline in Tc was statistically the same as that observed after the injections of 10 micrograms of NE at rest. Under control exercise conditions, Tc rose approximately 1 degree C and was associated with an initial decline (0.5 degrees C) followed by a rise (4.0 degrees C) in Ts. When the alpha-adrenergic receptor blocker phentolamine was injected 5-15 min before exercise, it caused a significant (P < 0.01) elevation in Tc during the ensuing exercise compared with controls. These results indicate that 1) over a dose range 0.5-40.0 micrograms, NE microinjected into the AH of the rt produces only hypothermia; 2) alpha-adrenergic receptors in the AH participate in the mediation of heat dissipation when the thermoregulatory system is challenged by the endogenous heat stress of exercise; and 3) exercise per se provides a nonthermal input to the temperature regulatory system that enhances heat dissipation.

Animals↗
PubMed1980

Effects of repeated heat exposure on hypothalamic sensitivity to norepinephrine.

Bilateral stainless steel guide tubes were stereotaxically implanted above the anterior hypothalamus (AH) of 12 male Sprague-Dawley rats (300-360 g). Beginning 3 days postsurgery, norepinephrine (NE) was injected into the AH each day at increasing depths below the guide tube until colonic temperature fell at least 0.8 degrees C. Subsequently, the effects of treadmill exercise at 21.5 m/min for 3 wk at 22 degrees C (n = 6) or 35 degrees C (n = 6) on the magnitude of the NE-induced hypothermia were investigated. Training duration ranged from 12 to 50 min/day, depending on the time required for colonic temperature of the heated rats to rise to a predetermined level: 40.4 degrees C on day 1, increasing 0.1 degree C/day to 41.5 degrees C on day 12 and thereafter. Before and after training, bilateral injections of NE (10 micrograms) at 22 degrees C at rest and just before exercise (21.5 m/min) caused the following mean +/- SE reductions in colonic temperature (degree C). (Formula: See Text). These reductions in colonic temperature were associated with sharp elevations in tail-skin temperature, but there were no significant differences in the response between the two groups. We conclude that repeated heat exposure increased the sensitivity of the AH to exogenous NE.

Acclimatization↗
PubMed1979

Maximum oxygen consumption of rats and its changes with various experimental procedures.

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.

Age Factors↗
PubMed1979

Relationships among training, heat acclimation, and heat tolerance in men and women: the controversy revisited.

For more than a decade there has been a controversy over the beneficial effects of physical training in a cool environment on exercise-heat tolerance. The issues include (a) inadequate controls regarding the physical characteristics of subjects, (b) marked variability in the conditions of the standard heat tolerance tests and (c) differences in the intensity and duration of the training programs employed. Intense training in a cool environment cannot serve as a substitute for exercise in the heat if acclimation is desired within a 2 week period. However, a substantial improvement (50%) in heat tolerance can be derived from 8-11 weeks of training under temperate conditions (21 degrees C) and thermal equilibrium can be maintained for at least 4 hours during mild work (200 W/m2) in dry or wet heat by endurance runners. These adjustments occur in both men and women and appear to be independent of aerobic capacity. The key to improved thermal tolerance with training in a cool environment is maintenance of an elevated core temperature for a sufficient duration of time to produce an adaptive response.

Acclimatization↗