Luiz Oswaldo Carneiro Rodrigues

Hidratação durante o exercício: a sede é suficiente?

The present work proposes a review about exercise fluid replacement and a discussion whether, during exercise, the fluid ingested according to thirst is sufficient to maintain hydration. Exercise sweat loss, mainly in the heat, can cause dehydration, can alter the hidroelectrolyte balance, disturb thermoregulation, presenting a health risk and/or impairing the athletic performance. It has been asserted that athletes do not drink, spontaneously, the sufficient fluid volume to prevent dehydration during the physical activity. Thus, international recommendations to fluid replacement during physical activities have been proposed. According to the American College of Sports Medicine (ACSM), about 500 mL of fluid on the two hours before the exercise must be ingested. During exercise, they propose that athletes should start fluid replacement since the beginning in regular periods and should drink enough fluid to restore all the sweating losses or ingest the maximal volume tolerated. The National Athletic Trainer’s Association (NATA) proposes the following recommendations: ingestion of 500 to 600 mL of water two or three hours before exercise or other sport drink and ingestion of 200 to 300 mL 10 to 20 minutes before exercise starting. During exercise, the fluid replacement should match the sweating and urine losses and at least should maintain hydration status reaching maximal body weight losses of 2%. After the exercise, fluid replacement must restore all the fluid losses accumulated. In addition, ACSM and NATA asserted about fluid temperature and palatability, beverage carbohydrate and electrolyte additions according to exercise duration and intensity and recommended hydration schedules to provide easier access to fluid ingestion. However, other authors contest the use of hydration schedules based on predetermined fluid volumes and suggest that fluid replacement according to thirst is enough to maintain body homeostasis.ABSTRACTExercise fluid replacement: is thirst enough? The present work proposes a review about exercise fluid repla-cement and a discussion whether, during exercise, the fluid in-gested according to thirst is sufficient to maintain hydration. Exer-cise sweat loss, mainly in the heat, can cause dehydration, canalter the hidroelectrolyte balance, disturb thermoregulation, pre-senting a health risk and/or impairing the athletic performance. Ithas been asserted that athletes do not drink, spontaneously, thesufficient fluid volume to prevent dehydration during the physicalactivity. Thus, international recommendations to fluid replacementduring physical activities have been proposed. According to theAmerican College of Sports Medicine (ACSM), about 500 mL offluid on the two hours before the exercise must be ingested. Dur-ing exercise, they propose that athletes should start fluid replace-ment since the beginning in regular periods and should drinkenough fluid to restore all the sweating losses or ingest the max-imal volume tolerated. The National Athletic Trainer’s Association(NATA) proposes the following recommendations: ingestion of 500to 600 mL of water two or three hours before exercise or othersport drink and ingestion of 200 to 300 mL 10 to 20 minutes be-fore exercise starting. During exercise, the fluid replacement shouldmatch the sweating and urine losses and at least should maintainhydration status reaching maximal body weight losses of 2%. Af-ter the exercise, fluid replacement must restore all the fluid loss-es accumulated. In addition, ACSM and NATA asserted about fluidtemperature and palatability, beverage carbohydrate and electro-lyte additions according to exercise duration and intensity and rec-ommended hydration schedules to provide easier access to fluidingestion. However, other authors contest the use of hydrationschedules based on predetermined fluid volumes and suggest thatfluid replacement according to thirst is enough to maintain bodyhomeostasis.

Heat storage rate and acute fatigue in rats

Thermal environmental stress can anticipate acute fatigue during exercise at a fixed intensity (%VO2max). Controversy exists about whether this anticipation is caused by the absolute internal temperature (Tint, degrees C), by the heat storage rate (HSR, cal/min) or by both mechanisms. The aim of the present study was to study acute fatigue (total exercise time, TET) during thermal stress by determining Tint and HSR from abdominal temperature. Thermal environmental stress was controlled in an environmental chamber and determined as wet bulb globe temperature ( degrees C), with three environmental temperatures being studied: cold (18 degrees C), thermoneutral (23.1 degrees C) or hot (29.4 degrees C). Six untrained male Wistar rats weighing 260-360 g were used. The animals were submitted to exercise at the same time of day in the three environments and at two treadmill velocities (21 and 24 m/min) until exhaustion. After implantation of a temperature sensor and treadmill adaptation, the animals were submitted to a Latin square experimental design using a 2 x 3 factorial scheme (velocity and environment), with the level of significance set at P<0.05. The results showed that the higher the velocity and the ambient temperature, the lower was the TET, with these two factors being independent. This result indicated that fatigue was independently affected by both the increase in exercise intensity and the thermal environmental stress. Fatigue developed at different Tint and HSR showed the best inverse relationship with TET. We conclude that HSR was the main anticipating factor of fatigue.

Muscarinic cholinoceptors in the ventromedial hypothalamic nucleus facilitate tail heat loss during physical exercise

The aim of this study was to evaluate the participation of ventromedial hypothalamic nucleus (VMH) muscarinic cholinoceptors in heat balance and central fatigue during treadmill exercise (24 m min(-1), 5% inclination). The animals were anesthetized with pentobarbital sodium (50 mg/kg body weight i.p.) and fitted with bilateral cannulae into the VMH 1 week prior to the experiments. Tail skin (T(tail)) and core body temperatures (T(b)) were measured after the injection of 0.2 microL of 5 x 10(-9) mol methylatropine (Matr) or 0.15 M NaCl solution (Sal) into the hypothalamus. Methylatropine injection into the VMH greatly increased heat storage rate (HSR) measured until fatigue (19.7+/-4.6 cal min(-1) Matr versus 9.7+/-3.3 cal min(-1) Sal; P<0.05) and attenuated the exercise-induced tail vasodilation as seen by T(tail) (23.98+/-0.43 degrees C Matr versus 25.52+/-0.85 degrees C Sal; at 6.5 min; P<0.05), indicating inhibition of the heat loss process. The 2 min delay and the increased DeltaT(b), which triggered the heat loss mechanisms observed in Matr-treated rats, are associated with increased HSR and may be responsible for the decreased running performance of these animals (21.0+/-2.9 min Matr versus 33.5+/-3.4 min Sal; P<0.001). In fact, a close negative correlation was observed between HSR and time to fatigue (r=-0.61; P<0.01). In conclusion, VMH muscarinic cholinoceptors facilitate tail heat loss mechanisms, and a delay in this adjustment would lead to a decrease in physical exercise performance due to excess heat storage.

Comparison of sweat rate during graded exercise and the local rate induced by pilocarpine

Centrally stimulated sweat rate produced by graded exercise until exhaustion was compared to the local sweat rate induced by pilocarpine, often used as a sweating index for healthy individuals. Nine young male volunteers (22 +/- 4 years) were studied in temperate environment in two situations: at rest and during progressive exercise with 25 W increases every 2 min until exhaustion, on a cycle ergometer. In both situations, sweating was induced on the right forearm with 5 ml 0.5% pilocarpine hydrochloride applied by iontophoresis (1.5 mA, 5 min), with left forearm used as control. Local sweat rate was measured for 15 min at rest. During exercise, whole-body sweat rate was calculated from the body weight variation. Local sweat rate was measured from the time when heart rate reached 150 bpm until exhaustion and was collected using absorbent filter paper. Pharmacologically induced local sweat rate at rest (0.4 +/- 0.2 mg cm-2 min-1) and mean exercise-induced whole-body sweat rate (0.4 +/- 0.1 mg cm-2 min-1) were the same (P > 0.05) but were about five times smaller than local exercise-induced sweat rate (control = 2.1 +/- 1.4; pilocarpine = 2.7 +/- 1.2 mg cm-2 min-1), indicating different sudorific mechanisms. Both exercise-induced whole-body sweat rate (P < 0.05) and local sweat rate (P < 0.05) on control forearm correlated positively with pilocarpine-induced local sweat rate at rest. Assuming that exercise-induced sweating was a result of integrated physiological mechanisms, we suggest that local and whole-body sweat rate measured during graded exercise could be a better sweating index than pilocarpine.

Activation of the central cholinergic pathway increases post-exercise tail heat loss in rats

The aim of this study was to evaluate the effects of stimulation of the central cholinergic pathway on the regulation of post-exercise tail heat loss in rats. Either 2.0microL of 25x10(-3)M physostigmine (Phy) or 0.15M NaCl solution (Sal) were injected into the right lateral cerebral ventricle of both resting (n=8) and post-exercising rats (n=6; 24mmin(-1); 25min; 5% inclination). Tail temperature (Ttail) was measured using a thermistor taped to the tail, and intraperitoneal temperature, an index of core temperature (Tc), was recorded using a telemetry sensor implanted into the peritoneal cavity. In resting rats, Phy induced an increase in both Ttail (26.8+/-0.3 degrees C Phy versus 25.2+/-0.6 degrees C Sal; P<0.05) and in heat loss index (0.26+/-0.03 Phy versus 0.14+/-0.05 Sal; P<0.05; 30min after injection), and a decrease in Tc compared to the Sal injection group (36.6+/-0.2 degrees C Phy versus 37.0+/-0.2 degrees C Sal; P<0.05). In post-exercising rats, Phy injection attenuated the decrease in both T(tail) (28.3+/-0.8 degrees C Phy versus 26.4+/-0.6 degrees C Sal; P<0.05) and heat loss index (0.37+/-0.07 Phy versus 0.19+/-0.02 Sal; P<0.05) without altering Tc. We conclude that activation of the central cholinergic pathway increases post-exercise tail heat loss in rats.

Association between the increase in brain temperature and physical performance at different exercise intensities and protocols in a temperate environment

There is evidence that brain temperature (Tbrain) provides a more sensitive index than other core body temperatures in determining physical performance. However, no study has addressed whether the association between performance and increases in Tbrain in a temperate environment is dependent upon exercise intensity, and this was the primary aim of the present study. Adult male Wistar rats were subjected to constant exercise at three different speeds (18, 21, and 24 m/min) until the onset of volitional fatigue. Tbrain was continuously measured by a thermistor inserted through a brain guide cannula. Exercise induced a speed-dependent increase in Tbrain, with the fastest speed associated with a higher rate of Tbrain increase. Rats subjected to constant exercise had similar Tbrain values at the time of fatigue, although a pronounced individual variability was observed (38.7-41.7°C). There were negative correlations between the rate of Tbrain increase and performance for all speeds that were studied. These results indicate that performance during constant exercise is negatively associated with the increase in Tbrain, particularly with its rate of increase. We then investigated how an incremental-speed protocol affected the association between the increase in Tbrain and performance. At volitional fatigue, Tbrain was lower during incremental exercise compared with the Tbrain resulting from constant exercise (39.3±0.3 vs 40.3±0.1°C; P<0.05), and no association between the rate of Tbrain increase and performance was observed. These findings suggest that the influence of Tbrain on performance under temperate conditions is dependent on exercise protocol.

Sinoaortic denervation prevents enhanced heat loss induced by central cholinergic stimulation during physical exercise

The present study investigated whether the effects of central cholinergic stimulation on thermoregulation during exercise are modulated by arterial baroreceptors. Wistar rats were submitted to sinoaortic denervation (SAD) or sham denervation (SHAM) and then fitted with a chronic guide cannula into the lateral cerebral ventricle. After 2 weeks, a catheter was implanted into the ascending aorta, and a temperature sensor was implanted into the peritoneal cavity. Two days later, the rats were submitted to exercise on a treadmill at 18 m/min until fatigued. Thermoregulatory and cardiovascular responses were measured after injection of 2 μL of 10mM physostigmine (Phy) or 0.15M NaCl solution (Sal) into the cerebral ventricle. In SHAM rats, Phy injection induced a greater exercise-induced increase in blood pressure and lower increase in heart rate than Sal treatment. In the SAD group, the attenuation of heart rate in response to Phy was blocked despite an exaggerated increase in blood pressure. SHAM rats treated with Phy had a higher increase in tail skin temperature compared to Sal injection (31.9 ± 0.4 °C Phy-SHAM vs. 30.1 ± 0.6 °C Sal-SHAM, 5 min after injection; p<0.05), resulting in a lower exercise-induced increase in core temperature. In contrast, SAD blocked the Phy injection effects in thermoregulatory responses during exercise (tail temperature: 30.1 ± 1.2 °C Phy-SAD vs. 29.5 ± 1.2 °C Sal-SAD, 5 min, p = 0.65). Therefore, we conclude that the enhancement of cutaneous heat loss induced by central cholinergic stimulation during exercise is mediated primarily by arterial baroreceptors.

Neurofibromatosis type 1: more frequent and severe then usually thought

OBJECTIVE To study prevalence of clinical features among Brazilian patients diagnosed with neurofibromatosis type 1(NF1), comparing these features with international data to evaluate the severity and visibility of the disease and quantify less frequent manifestations such as short stature, macrocephaly, muscle strength, voice abnormalities and oral motor disorders. METHODS 183 patients diagnosed with NF1, attended at the Neurofibromatosis Outpatient Reference Center, were evaluated for clinical manifestations and complications of NF1. Severity and visibility were verified using the Riccardi and Ablon scales respectively. Voice abnormalities and oral motor disorders were quantified using the Vox-Metria software and maximal voluntary muscle strength (MVMS) was quantified using a handgrip dynamometer. RESULTS Clinical manifestations of NF1 observed were comparable to those described in literature. However, more then 50% of patients presented severity and visibility classified as moderate and severe. The incidence of macrocephaly and short stature was higher among the Brazilian patients. Voice abnormalities and oral motor disorders were quantified for the first time, with hoarseness and oral motor disorders observed in more then 60% the patients. Maximal voluntary muscle strength was found to be reduced in 67% of patients. CONCLUSION The main clinical features of these patients are similar to those reported in previous studies. More then one-half of the patients presented moderate and severe levels of NF1 (severity and visibility), including short stature, macrocephaly, voice abnormalities and oral motor disorders and decreased muscle strength. These results are in disagreement with the traditional concept that NF1 is a benign disease and also disclosed some clinical aspects not previously reported.

Neurofibromatoses: part 1 ? diagnosis and differential diagnosis

Neurofibromatoses (NF) are a group of genetic multiple tumor growing predisposition diseases: neurofibromatosis type 1 (NF1), neurofibromatosis type 2 (NF2) and schwannomatosis (SCH), which have in common the neural origin of tumors and cutaneous signs. They affect nearly 80 thousand of Brazilians. In recent years, the increased scientific knowledge on NF has allowed better clinical management and reduced complication morbidity, resulting in higher quality of life for NF patients. In most cases, neurology, psychiatry, dermatology, clinical geneticists, oncology and internal medicine specialists are able to make the differential diagnosis between NF and other diseases and to identify major NF complications. Nevertheless, due to its great variability in phenotype expression, progressive course, multiple organs involvement and unpredictable natural evolution, NF often requires the support of neurofibromatoses specialists for proper treatment and genetic counseling. This Part 1 offers step-by-step guidelines for NF differential diagnosis. Part 2 will present the NF clinical management.

Thermoregulation in hypertensive men exercising in the heat with water ingestion

Hydration is recommended in order to decrease the overload on the cardiovascular system when healthy individuals exercise, mainly in the heat. To date, no criteria have been established for hydration for hypertensive (HY) individuals during exercise in a hot environment. Eight male HY volunteers without another medical problem and 8 normal (NO) subjects (46 +/- 3 and 48 +/- 1 years; 78.8 +/- 2.5 and 79.5 +/- 2.8 kg; 171 +/- 2 and 167 +/- 1 cm; body mass index=26.8 +/- 0.7 and 28.5 +/- 0.6 kg/m2; resting systolic (SBP)=142.5 and 112.5 mmHg and diastolic blood pressure (DBP)=97.5 and 78.1 mmHg, respectively) exercised for 60 min on a cycle ergometer (40% of VO2peak) with (500 ml 2 h before and 115 ml every 15 min throughout exercise) or without water ingestion, in a hot humid environment (30 masculine C and 85% humidity). Rectal (Tre) and skin (Tsk) temperatures, heart rate (HR), SBP, DBP, double product (DP), urinary volume (Vu), urine specific gravity (Gu), plasma osmolality (Posm), sweat rate (S R), and hydration level were measured. Data were analyzed using ANOVA in a split plot design, followed by the Newman-Keuls test. There were no differences in Vu, Posm, Gu and S R responses between HY and NO during heat exercise with or without water ingestion but there was a gradual increase in HR (59 and 51%), SBP (18 and 28%), DP (80 and 95%), Tre (1.4 and 1.3%), and Tsk (6 and 3%) in HY and NO, respectively. HY had higher HR (10%), SBP (21%), DBP (20%), DP (34%), and Tsk (1%) than NO during both experimental situations. The exercise-related differences in SBP, DP and Tsk between HY and NO were increased by water ingestion (P<0.05). The results showed that cardiac work and Tsk during exercise were higher in HY than in NO and the difference between the two groups increased even further with water ingestion. It was concluded that hydration protocol recommended for NO during exercise could induce an abnormal cardiac and thermoregulatory responses for HY individuals without drug therapy.