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C V Gisolfi

Publications and source records attributed to C V Gisolfi.

At least 55 records · Page 3Linked to original sources

Guidelines for optimal replacement beverages for different athletic events.

During exercise, especially endurance exercise in the heat, vital body fluids and essential ions are lost in sweat, and the body may deplete its glycogen stores. Unless essential body fluids are restored, these conditions can produce hypovolemia, hypoglycemia, hyponatremia, hyperthermia, and dehydration. Performance may also be reduced. This paper briefly reviews pertinent aspects of gastric emptying and intestinal absorption and proposes the formulation of beverages for ingestion both pre-event and during exercise. For events lasting less than 1 h, 300-500 ml of a 6-10% CHO beverage is recommended pre-event (0-15 min), and cool (5-15 degrees C) water in a volume approximately half the subjects sweat rate is recommended during exercise. For events between 1-3 h long, 300-500 ml of water is recommended pre-event, and 800-1600 ml.h-1 of a 6-8% CHO solution with 10-20 mEq Na+ is recommended during exercise. For events longer than 3 h, 300-500 ml of water is recommended pre-event, and 500-1000 ml.h-1 of a 6-8% CHO beverage with 20-30 mEq Na+ is recommended during exercise. In recovery, a beverage containing 5-10% CHO with 30-40 mEq Na+ should be ingested to achieve euhydration. A minimum of 50 g.h-1 of CHO should be ingested in the first 2 h to maximize glycogen repletion. Guidelines to follow in formulating these beverages are reviewed and the rationale for each formulation is provided.

Dietary Carbohydrates↗

Consumption of carbonated and noncarbonated sports drinks during prolonged treadmill exercise in the heat.

These studies were done to determine the effect of carbonation and carbohydrate content on either gastric emptying or ad libitum drinking during treadmill exercise in the heat. Four test drinks were used: a 6% carbohydrate, noncarbonated; a 6% carbohydrate, carbonated; a 10% carbohydrate, noncarbonated; and a 10% carbohydrate, carbonated drink. For gastric emptying studies, subjects completed four 1-hr treadmill runs in the heat. They were given 400 mL of test drink at 0 min and 200 mL at 15, 30, and 45 min of exercise. For ad libitum drinking studies, subjects completed four 2-hr treadmill runs in the heat. Gastric residual volumes were similar during the four 1-hr runs. During the 2-hr runs, ad libitum drinking of the four beverages was also similar. Mean values for sweat rate, percentage of body weight lost, and percentage of fluid replaced by ad libitum drinking were similar for the four trials. Similar changes in heart rate, rectal temperature, and ratings of perceived exertion were also observed during the four 2-hr treadmill runs. We conclude that the presence of carbonation in a carbohydrate drink did not have a significant effect on either gastric emptying or ad libitum drinking.

Adult↗

Synthesis of 70K stress protein by human leukocytes: effect of exercise in the heat.

To determine whether reinduction of 70,000-Da (70K) stress protein synthesis could be used as an assay for thermal history and/or cellular levels of 70K stress protein in hyperthermic humans, leukocytes were obtained before and after 2 h of exercise and then incubated at 37 or 41 degrees C. Five healthy males completed 2 h of treadmill exercise consisting of running at 4-6 km/h for 30-45 min followed by 75-90 min of walking up a 2-10% grade. This exercise bout was performed by two subjects in hot (46 degrees C, 15% relative humidity) and by five subjects in cooler (30 degrees C, 40% relative humidity) environmental conditions. Exercise resulting in rectal temperature (Tre) less than 40 degrees C did not alter the amount of 70K stress protein synthesized by leukocytes incubated at 41 degrees C. In contrast, exercise resulting in Tre greater than 40 degrees C reduced the amount of 70K stress protein synthesized by leukocytes incubated at 41 degrees C. A protein immunoblot, probed with an antibody specific for the inducible 72K stress protein, showed that the reduction of 35S-labeled 70K stress protein in these postexercise leukocyte samples occurred without marked elevations of this protein. In vitro incubation of human leukocytes at 40 degrees C for 15-120 min reduced, in a time-dependent manner, the amount of 70K stress protein synthesized during a subsequent 41 degrees C heat stress. This reduction of 70K stress protein synthesis in 41 degrees C-treated leukocytes was abolished when cycloheximide was present during the 40 degrees C preincubation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Splanchnic sympathetic nerve activity and circulating catecholamines in the hyperthermic rat.

The mechanisms responsible for the initial rise in splanchnic vascular resistance with environmental heating are controversial, and those responsible for the subsequent fall in splanchnic resistance in the severely hyperthermic animal are unknown. Thus we examined the effect of environmental heating on plasma catecholamine concentration, splanchnic sympathetic nerve activity (SNA), and select blood chemistries. In one study, 25 male Sprague-Dawley rats (270-300 g) were assigned to one of five groups on the basis of their core temperature (Tc, 37, 39, 41, 43, or 44 degrees C) at death. Heart rate (HR), mean arterial pressure (MAP), and Tc were monitored during heat stress under alpha-chloralose anesthesia (12.5 mg.ml-1.h-1). At each predetermined Tc, an aortic blood sample was drawn and analyzed for mean plasma concentration of norepinephrine (NE), epinephrine (E), Na+, K+, and lactate. From 41 to 43 degrees C, NE and E rose significantly, and the animals became hyperkalemic and lactacidemic. In a separate study, we quantitated SNA from the greater splanchnic nerve during heat exposure of artificially respired animals anesthetized with pentobarbital sodium (50 mg/kg). MAP, splanchnic SNA, and Tc were recorded. Tc was elevated from 37.0 +/- 0.12 to 41.3 +/- 0.18 degrees C in 70 min by increase of ambient temperature to 38 degrees C in an environmental chamber. Splanchnic SNA was 54 +/- 8 spikes/s at a Tc of 37 degrees C and increased significantly as Tc exceeded 39 degrees C (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of cycle exercise on intestinal absorption in humans.

Intestinal absorption was measured in six trained male cyclists during rest, exercise, and recovery periods with the segmental perfusion technique. Each subject passed a multilumen tube into the duodenojejunum. The experiments consisted of 1) a sequence of 1-h bouts of cycling exercise at 30, 50, and 70% maximal O2 uptake (Vo2max) separated by 1-h rest periods or 2) a 90-min bout at 70% VO2max. The cycling was performed on a constant-load Velodyne trainer. Absorption of water and a 6% carbohydrate-electrolyte (2% glucose, 6% sucrose, 20 meq Na+, 2.6 meq K+) solution (both perfused at 15 ml/min) were compared. The effects of perfusing an isotonic electrolyte solution during mild (30% VO2max) exercise were also studied. Fluid was sampled every 10 min from ports 10 and 50 cm distal to the infusion site. Water flux was determined by differences in polyethylene glycol concentration across the 40-cm test segment. Results showed 1) no difference in water or electrolyte absorption rates among rest, exercise, and recovery periods; 2) no difference in absorption rates among the three exercise intensities or different exercise durations; and 3) significantly greater fluid absorption rates from the carbohydrate-electrolyte (CE) solution than from water. Water flux during rest, exercise, and recovery was about sixfold greater from the CE solution than from the isotonic solution without carbohydrate. We conclude that 1) exercise has no effect on water or solute absorption in the duodenojejunum, 2) fluid absorption occurs significantly faster from a CE solution than from water, and 3) fluid absorption is increased sixfold by addition of carbohydrate to an electrolyte solution.

Adult↗

Human intestinal water absorption: direct vs. indirect measurements.

Distilled water, a carbohydrate-electrolyte (CE; 4% sucrose, 2% glucose, 17.2 meq/l NaCl, and 2.8 meq/l KCl) solution, or a 10% glucose solution, all containing the nonabsorbed indicator polyethylene glycol (PEG) and deuterium oxide (D2O, 30 ppm), were infused (15 ml/min) into the duodenojejunum of seven men by using the triple lumen technique. Net water absorption was determined directly from the change in PEG concentration and was calculated from plasma D2O derived from D2O in the perfusion solutions. The protocol included a 45-min equilibration period followed by a 90-min test period. Intestinal samples were drawn at 10-min intervals from 15 to 45 min and at 15-min intervals thereafter. Blood was drawn at 45, 50, 55, 60, 75, 90, 105, 120, and 135 min. Intestinal samples were analyzed for D2O, Na+, K+, osmolality, PEG, and glucose; blood was analyzed for D2O. Results (+/- SE; positive values secretion, negative values absorption) showed net fluid absorption from distilled water (-9.40 +/- 1.28 ml.h-1.cm-1) and the CE (-13.30 +/- 1.22 ml.h-1.cm-1) solution, but net secretion (4.40 +/- 1.25 ml.h-1.cm-1) from the 10% glucose solution. All values were significantly (P less than 0.05) different from each other. Perfusing the CE solution caused net Na+ and K+ absorption, whereas perfusing the 10% dextrose solution caused net electrolyte secretion. Rates of D2O accumulation in the plasma were independent of the solutions perfused.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose↗

Circulatory responses to vasoconstrictor agents during passive heating in the rat.

The purpose of this study was to determine the actions of several pharmacological agents on the circulatory system, and more specifically on the superior mesenteric vascular bed, in response to environmental heat stress in chloralose-anesthetized rats. Animals were instrumented with Doppler flow probes on the mesenteric and renal arteries and exposed to an ambient temperature of 40 degrees C. Heart rate, mean arterial blood pressure (MAP), and core (Tc) and tail skin temperatures were also monitored. As Tc progressively increased from 37 degrees C during heat exposure, MAP rose to a plateau and then fell precipitously as Tc exceeded 41.5 degrees C. Mesenteric resistance increased throughout the early stages of heating before sharply declining prior to the reduction in MAP. The pressor and mesenteric resistance responses to constant infusions of several adrenergic agonists after MAP began falling (Tc = 41.3 degrees C) were significantly (P less than 0.05) attenuated compared with infusions into normothermic animals. In a second set of experiments, injections of both norepinephrine and angiotensin II were made 30 min before and approximately 10, 30, 50, 70, and 90 min after initiation of heating. These injections increased both MAP and mesenteric resistance; however, at TcS greater than 40 degrees C, the responses to both agonists were progressively and significantly attenuated. In a final group of animals, barium chloride infusions produced similar pressor and regional resistance changes during both normothermia and severe hyperthermia (Tc greater than 42 degrees C). These results indicate that, in the chloralose-anesthetized rat, hyperthermia disrupts adrenoceptor function but does not alter the intrinsic ability of vascular smooth muscle to contract.

Angiotensin II↗

Functional and morphological changes in the eccrine sweat gland with heat acclimation.

Three adult male patas monkeys (11-15 kg) were heat acclimated by continuous exposure to an ambient temperature of 33 +/- 1 degree C at 13% relative humidity for 9 mo. During the last month, they were also exposed to 45 degrees C at 10% relative humidity for 4 h/day and 5 days/wk. Before and after 3 wk of acclimation, the animals were given a heat-tolerance test in which rectal (Tre) and mean skin (Tsk) temperatures, heart rate, and sweat rate (msw) were monitored during a 90-min exposure to 45 degrees C heat with 24% relative humidity under lenperone (1.0-1.4 mg/kg im) tranquilization. Maximal in vivo msw was also determined in response to subcutaneous injections (1 and 10% solutions) of methacholine (MCh). Before and after 9 wk and 9 mo of acclimation, sweat glands were dissected from biopsy specimens of the lateral calf, cannulated, and stimulated in vitro with MCh. Morphological measurements of isolated tubules were compared with maximal secretory rates produced by MCh stimulation. Three weeks of acclimation 1) reduced Tre and Tsk and increased msw during the heat tolerance test and 2) significantly increased maximal msw in response to MCh stimulation. Acclimation also increased (P less than 0.05) sweat gland size, as measured by tubular length and tubular volume. Maximal in vitro msw produced by MCh stimulation and msw per unit length of secretory coil also increased significantly. We conclude that heat acclimation increases the size of eccrine sweat glands and that these larger glands produce more sweat. They are also more efficient because they produce more sweat per unit length of secretory coil.

Acclimatization↗

Circulatory responses to heat after celiac ganglionectomy or adrenal demedullation.

Chloraloseanesthetized rats were implanted with Doppler flow probes on the mesenteric, renal, and external caudal arteries and were exposed to an ambient temperature of 40 degrees C. Heart rate, core (Tc) and tail-skin temperatures, and mean arterial blood pressure (MAP) were also monitored. Before heating, the celiac ganglion was removed (ganglionectomy) from one group of animals (n = 11) and a bilateral adrenal demedullation was performed in a second group (n = 14). As Tc progressively increased from 37 degrees C to 43 degrees C, MAP rose to a plateau then fell precipitously as Tc exceeded 41 degrees C. Ganglionectomy eliminated the rise in mesenteric resistance (P less than 0.05) and attenuated the rise in MAP compared with an intact control group (n = 11). Ganglionectomy also increased the heating rate (P less than 0.05) and reduced heat tolerance time (P less than 0.05). Demedullation attenuated the rise in both mesenteric resistance and MAP (P less than 0.05) and increased the rate of heating (P less than 0.05) compared with controls (n = 10). Renal and caudal resistance changes were similar in all groups. These data show the importance of intact adrenal medullas and sympathetic innervation to the splanchnic region in contributing to thermal tolerance in the rat. However, neither factor alone can explain splanchnic vasoconstriction during severe heat stress.

Acclimatization↗

Effect of cerebrospinal fluid hyperosmolality on sweating in the heat-stressed patas monkey.

Dehydration increases the osmolality of body fluids and decreases the rate of sweating during thermal stress. By localizing osmotic stimuli to central nervous system tissues, this study assessed the role of central stimulation on sweating in a heat-stressed nonhuman primate. Lenperone-tranquilized patas monkeys (Erythrocebus patas n = 5), exposed to 41 +/- 2 degrees C, were monitored for calf sweat rate, rectal and mean skin temperatures, oxygen consumption, and heart rate during infusions (255-413 microliters) of hypertonic artificial cerebrospinal fluid (ACSF) into the third cerebral ventricle. ACSF made hypertonic with NaCl to yield osmolalities of 800 and 1,000 mosmol/kgH2O significantly decreased sweat rate compared with control ACSF (285 mosmol/kgH2O), achieving maximal reductions during infusion of 37 and 53%, respectively. Rectal temperature significantly increased during the recovery period, reaching elevations of 0.69 and 0.72 degrees C, respectively, at 20 min postinfusion. In contrast, ACSF made hypertonic with sucrose (800 mosmol/kgH2O) failed to change sweat rate or rectal temperature during infusion in three animals. Thus, intracerebroventricular infusions of hypertonic ACSF mimicked dehydration-induced effects on thermoregulation. The reduction in heat loss during infusion appeared to depend on an elevation in cerebrospinal fluid [Na+] and not osmolality per se.

Animals↗

Effects of CSF ANG II and AVP on sweating in the heat-stressed patas monkey.

Increasing cerebrospinal fluid [Na+] reduces sweat rate (msw) in the heat-stressed patas monkey (Erythrocebus patas). This study determined the potential role of two neuropeptides, angiotensin II (ANG II) and arginine vasopressin (AVP), in mediating this response. Artificial cerebrospinal fluid, containing either ANG II or AVP, was infused into the third cerebral ventricle of lenperone-tranquilized monkeys (n = 4) exposed to 41 +/- 2 degrees C. Solutions were infused at 16.5 microliters/min for 25 min (total vol approximately 413 microliters). ANG II (1.25, 2.5, 5, and 10 ng/microliters) tended to decrease .msw. However, during infusion, only the decline at 10 min associated with the 1.25-ng/microliters dose (26%) was different (P less than 0.004) from control. This dose elevated (P less than 0.004) core rectal temperature by 1.14 degrees C at 20 min postinfusion. In contrast, AVP (0.5 and 1.5 micrograms/microliters artificial cerebrospinal fluid) had no significant effect on .msw compared with control infusions. Both doses of AVP produced a slight but significant increase in rectal temperature of 0.14 and 0.22 degrees C, respectively, at 20 min postinfusion. In conclusion, the magnitude and time course of the change in .msw with central ANG II suggest that it does not act as the sole mediator of the decline in .msw observed with elevated cerebrospinal fluid [Na+]. The minimal effects produced by third ventricular AVP exclude this route as a means by which AVP could modulate .msw during dehydration.

Angiotensin II↗

Gastric emptying during prolonged cycling exercise in the heat.

Eight trained male cyclists (age 20-33 yr) completed four 3-h bouts of cycling at 60% peak VO2 in the heat (33 degrees C) drinking either water (W), 5% glucose (G), 5% glucose polymer (GP), or 3.2% glucose polymer + 1.8% fructose (GP/F) at a rate of 350 ml every 20 min (3.15 l total volume). Similar changes in heart rate, sweat rate, rectal and mean skin temperatures, and plasma [Na+], [K+], and osmolality were observed during all trials. Mean changes in plasma volume, although not significantly different between trials, were lowest for the GP/F drink (-2.6%) and greatest for the G (-8.1%) drink. Plasma volume decreased (P less than 0.05) below pre-exercise control values during the W, G, and GP trails but was maintained at control values during the GP/F trials. In contrast to water ingestion, G, GP, and GP/F ingestion maintained plasma glucose and respiratory exchange ratios throughout the 3-h exercise bouts. Gastric residual volume (GRV) obtained at the end of exercise was similar for the W, GP, and GP/F trials. The G trials yielded greater (P less than 0.05) GRV than W trials. For all drinks ingested, over 90% of the 3.15 l consumed was emptied from the stomach during the 3-h exercise bouts. At a mean sweat rate of 1.2 l.h-1, cyclists replaced 73% of fluid lost and experienced only a 1.6% loss in body weight. This study demonstrates that, during prolonged (3-h) cycling exercise in the heat, large volumes of W and 5% carbohydrate can be emptied from the stomach to help minimize the effects of dehydration.

Adult↗

Fluid replacement during and after exercise in the heat.

This study sought to determine whether ad libitum drinking of a carbohydrate-electrolyte (CE) beverage would minimize the physiological disturbances associated with prolonged (3 h) continuous exercise in the heat (Tdb = 31.5 degrees C, percent RH = 22.3). Seven male subjects performed two bouts of cycle exercise (60% VO2max) drinking either a CE beverage (4.85% polycose, 2.65% fructose) or distilled water. Subjects continued to drink ad libitum for 3 h during recovery in the heat. No significant differences were observed between drinks for rectal temperature, heart rate, or sweat rate during exercise. Subjects tended to drink more (P less than 0.0565) water than the CE beverage during exercise, but plasma volume (percent PV) decreased less (P less than 0.0253) and plasma [( glucose], P less than 0.0001 and [K+], P less than 0.0047) were higher when subjects drank the CE solution. At the end of exercise, plasma osmolality and [Na+] were also higher (P less than 0.05) when subjects drank the CE beverage rather than water. Rating of perceived exertion was higher (P less than 0.0001) when drinking water. In recovery, ingesting the CE beverage, 1) subjects drank more (P less than 0.0012); 2) plasma volume increased to a higher level (P less than 0.0017); 3) plasma osmolality (P less than 0.0001), [Na+] (P less than 0.0001), glucose (P less than 0.0001), and [K+] (P less than 0.0015) were greater; and 4) body weight increased more (P less than 0.0422) than when water was ingested. Thus, in terms of minimizing physiological disturbances, ad libitum drinking of the CE beverage was as effective as drinking water during exercise but was more effective in recovery.

Adult↗

Effects of changing hypothalamic temperature on eccrine sweating in the patas monkey.

Two male (10-13 kg) patas monkeys (Erythrocebus patas) were implanted with bilateral thermodes to control hypothalamic temperature. Animals were restrained in primate chairs and instrumented to yield hypothalamic (THYPO), colonic (Tc), and mean skin (Tsk) temperatures, chest sweat rate (mSW), and heart rate (HR). THYPO was monitored using a thermocouple inserted to the tip of a non-perfused thermode; mSW was measured using resistance hygrometry. After the monkey equilibrated to a selected ambient temperature, four thermodes were perfused with water from a temperature-controlled bath. Increasing THYPO from 37 to 41 degrees C increased mSW from 0.05 to 0.30 mg.cm-2.min-1. Reducing Tsk shifted the THYPO:mSW relationship to the right (p less than 0.05) without significantly altering its slope. Activity-induced changes in HR, when THYPO was constant, caused fluctuations in ongoing sweating that closely tracked HR. We conclude that mSW in the patas monkey is controlled by both peripheral and central thermal inputs and nonthermal factors.

Animals↗

Changes in jejunal myoelectrical activity during exercise in fed untrained dogs.

Seven female dogs (15-20 kg) were instrumented with seven bipolar electrodes sutured at 3-cm intervals to the serosal surface of the proximal jejunum and were exercised at different intensities and durations on a motor-driven treadmill. Slow-wave frequency increased (P less than 0.05) from preexercise control during prolonged (90 min) exercise and during recovery after short-term exercise (30 min) at 70% heart rate reserve (HRR). These changes were associated with an increase in core temperature. Spike-burst frequency (SBF) increased (P less than 0.05) with moderate exercise (50% HRR), but the magnitude was small. When exercise was extended beyond 30 min and during all recovery periods, SBF decreased significantly. Exercise produced migrating myoelectrical complexes in three experiments and less dramatic pattern changes characterized as "clustered contractions" (regular spike bursts preceded and followed by the absence of spike bursts) in at least nine other experiments. We conclude that exercise does alter jejunal myoelectrical activity, but myoelectrical patterns may be more important in explaining exercise-induced gastrointestinal symptoms than changes in spike-burst frequency or duration.

Animals↗

Coronary vasodilator reserve, capillarity, and mitochondria in trained hypertensive rats.

To test the hypothesis that exercise training can reverse the decrements in coronary reserve, capillary density, and mitochondrial volume density evident during established hypertension, we trained spontaneously hypertensive (SHR) and normotensive (WKY) rats on a treadmill over a 3-mo period. At 7 mo of age we used microspheres to evaluate myocardial perfusion in conscious rats. Exercise training did not alter hypertension or left ventricular hypertrophy but did increase maximal O2 consumption in both SHR and WKY. A decrement in left and right ventricular coronary reserve in SHR, compared with WKY, was indicated by 1) a smaller increment in myocardial perfusion during maximal vasodilation with dipyridamole and 2) a higher minimal coronary vascular resistance per unit mass. Exercise training had no significant effect on any index of myocardial perfusion in SHR or WKY. A 12% decrement in capillary numerical density in the endomyocardium of SHR was not reversed by exercise training. We estimated the volume densities of mitochondria, myofibrils, and sarcoplasm using electron microscopy and point-counting stereology on perfusion-fixed hearts. None of the parameters in either SHR or WKY was changed by exercise training. It is concluded that exercise training does not reverse the decrements in coronary reserve and capillary numerical density associated with hypertension in adult rats. Moreover the previously observed enhancement of mitochondrial volume density due to exercise in young hypertensive rats was not observed in adult SHR.

Animals↗

Peripheral vascular responses to hyperthermia in the rat.

To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70-150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10-15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.

Animals↗