The role of gene regulation in obesity and its complications: introduction.
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Biomedical subjects
Publications and source records attributed to P Boisvert.
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Measurements of local sweat rate (back) determined with a closed-pouch collector made of polyethylene (110 cm2) were compared with those obtained from a ventilated capsule using an infrared photometric hygrometer technique. Eight young male subjects underwent three exercise sessions each for 60 min at 45% VO2max on a cycle ergometer at an ambient temperature of 35 degrees C and 35% relative humidity. When the onset and transient sweating periods (0-20 min) are excluded from calculations, the difference between the mean values obtained by the collector and the sweat capsule during the 20-60 time period is only 0.06 +/- 0.04 mg x cm-2 x min-1 (5%). Although a significant correlation (r = .74, p < .05) was obtained between methods, individual differences in sweat-rate measurements varied on average +/-0.22 mg x cm-2 x min-1 (+/-19%). Designed more specifically for sweat-content analysis, the pouch collector may serve as a satisfactory field method to approximate the local sweat rate and excretion induced by prolonged exercise in a hot environment.
The aim of this study was to observe the effect of alcohol ingestion on body temperature and local sweat rate during endogenous and exogenous heat stress. After ingesting either alcohol (1.2 g alcohol/kg of body weight) or a placebo drink, 8 subjects exercised for 60 minutes at 45% VO2max in a warm environment (35 degrees C, 45% RH). Varying patterns of response were observed in these subjects, with no consistent effect on the thermoregulatory response seen. The absence of any significant change in skin and body temperature and in sweat rate suggests that the capacity of the body to struggle against exogenous and endogenous heat is not fundamentally altered by alcohol ingestion. The difference in individual response observed in our experiment is in accord with the previous lack of clearcut effect of alcohol reported in the literature.
Alcohol consumption at rest is associated with disturbed water and salt regulation reflected by changed responses in the hydromineral hormones. This study investigated the effect of alcohol on endocrine systems involved in body fluid and electrolyte regulation under conditions of physical exercise in the heat, a situation in which under normal circumstances, the hydromineral hormones are stimulated in an attempt to preserve physiological homeostasis. Eight healthy male volunteers participated in two trials, which differed only in the presence or absence of alcohol (1.2 g alcohol.kg-1 body mass) in a cocktail drink. After consuming the cocktail, the subjects exercised for 60 min on a cycle ergometer (45% maximal oxygen consumption) at 35 degrees C. Compared to the control situation alcohol consumption (maximal plasma concentrations reaching about 1.08 g.l-1) produced an increase in body fluid loss (P < 0.05), but did not induce significant differences in plasma volume changes. Plasma volume decreased in both sessions during exercise (P < 0.01) and a significant rebound (P < 0.001) occurred during recovery. Osmolality was significantly higher (P < 0.001) during rest, exercise and recovery periods compared to the placebo trials, but no effect of alcohol on plasma Na+ and K+ concentrations was observed. In the alcohol test conditions, the arginine vasopressin (AVP) response to exercise was significantly dampened (P < 0.05). In contrast, alcohol had no effect on aldosterone or atrial natriuretic peptide (ANP). These results demonstrated that alcohol ingestion augmented body fluid losses due to a suppressive effect on AVP during physical exercise conducted in a warm environment. The increase in osmolality due to alcohol did not influence the aldosterone and ANP responses, which would suggest that total osmolality does not play a major role in the regulation of these hormones.
The purpose of this study was to compare the "NaCl equivalent" values determined by the Wescor's sweat conductivity analyzer (Sweat-Chek) with the sweat Na+ and Cl- concentration values measured by conventional methods. The sweat was induced by 60-min exercise and collected by a closed-pouch collector. The "NaCl equivalent" values determined by the sweat conductivity analyzer (mean: 75 mmol.L-1, range: 38 - 122, n = 72) were significantly (P < 0.05) greater than Na+ concentration values (mean: 71 mmol.L-1, range: 24 - 123, n = 72) measured by flame photometry and Cl-concentration values (mean: 61 mmol.L-1, range: 18 - 100, n = 48) measured by coulometric titration. The difference were most accentuated for low concentration values. The 95% confidence-agreement intervals around the mean differences between methods were 11 mmol.L-1 (14%) for both Na+ and Cl-. The Sweat-Chek conductivity analyzer is a portable instrument which approximates the actual Na+ and Cl- concentrations in sweat but with a positive bias probably due to the other unmeasured anions present in sweat.
The purpose of this study was to modify a previously described local sweat collector to facilitate the investigation of sweat rate and composition in a warm (30 degrees C) and humid (relative humidity 80%) environment. The adherence of the collector to the skin was improved and a pouch was appended at the lower end of the collector. The limitations of the closed collector were examined by comparing the local sweat rate and the quantity of electrolyte excreted in sweat with those obtained using a second collector with a wide opening (to permit free evaporation) and by changes in the body mass. Eight subjects performed exercise on a cycle ergometer consisting of four equal periods of 15 min each, at 60% maximal oxygen consumption, with a rest of 5 min between each period. The sweat produced on a local skin area (85 cm2, upper posterior thorax region) was collected at the end of each period, before measuring the body mass on a sensitive (+/- 1 g) platform balance. The mean local sweat rate [2.61 (SEM 0.19) mg.cm-2.min-1] was 2.4 times greater than the pro-rated whole body mass loss but the two were strongly correlated (r = 0.82, P < 0.01). Compared to the open collector, the greater quantity of electrolyte excreted into the closed collector would suggest that the conditions which prevailed in the closed collector, such as a higher local skin temperature, may have affected the function of the sweat gland.(ABSTRACT TRUNCATED AT 250 WORDS)
We investigated the role of the exercise-induced elevation of plasma prolactin (PRL) concentration on sweat rate and composition during prolonged exercise in men. Two groups of healthy young males (20-26 yr old) showing a high (high responders; n = 8) or a low (low responders; n = 7) response of plasma PRL concentration to exercise were studied during a 60-min period of exercise on a cycle ergometer (65% maximum O2 consumption) in warm conditions (26.2 +/- 0.1 degrees C; 57 +/- 1% relative humidity), 1 h after receiving 1.25 mg bromocriptine (BRC) per os or a placebo. In high responders, administration of BRC totally abolished the threefold increase in plasma PRL observed in response to exercise with placebo [placebo, 10 +/- 2 (rest) and 30 +/- 2 micrograms/l (exercise); BRC, 9 +/- 1 (rest) and 8 +/- 1 microgram/l (exercise)]. The latter was associated with a significant decrease in sweat rate (2.7 +/- 0.5 to 1.9 +/- 0.3 microliter.cm-2.min-1) and a significant increase in sweat Na+ concentration (57 +/- 7 to 68 +/- 5 mmol/l). BRC also reduced the small response in plasma PRL concentration observed in low responders [placebo, 10 +/- 1 (rest) and 15 +/- 1 microgram/l (exercise); BRC, 9 +/- 1 (rest) and 7 +/- 1 microgram/l (exercise)], but this was not associated with any change in sweat rate (2.2 +/- 0.2 to 1.9 +/- 0.3 microliter.cm-2.min-1) or in sweat Na+ concentration (63 +/- 10 to 64 +/- 9 mmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)
The effective control of hypophysial prolactin (PRL) secretion with a pharmacological agent is a prerequisite for the investigation of the role of hyperprolactinemia observed during exercise. Using bromocriptine, a potent inhibitor of PRL secretion, this study established the proper experimental conditions whereby any significant increase in plasma PRL level can be prevented and basal circulating levels maintained during physical exercise. On three occasions at weekly intervals, 15 male adults, separated into two groups, exercised on an ergocycle (40 min at 65% VO2max) either 1 or 3 h after ingesting either placebo or 1.25 or 2.50 mg of bromocriptine mesylate (Parlodel; Sandoz Canada Inc., Dorval, Qué.). Under all conditions, the plasma PRL elevation observed during exercise after placebo was prevented by the administration of bromocriptine. Resting plasma PRL levels were maintained when exercise was performed 1 h after bromocriptine ingestion, but were significantly reduced when exercise was performed 3 h after administration of either bromocriptine dosages. Considering the primary and secondary effects observed, 1.25 mg of bromocriptine administered 1 h before exercise provides suitable experimental conditions to investigate the role of the increase in plasma PRL during physical exercise.
Apart from in cystic fibrosis, where sweat analysis provides valuable diagnostic information, sweat yields remain an overlooked biological fluid. Technical problems (dilution, condensation, contamination, evaporation, etc.) linked to currently available collection procedures are of concern and thwart their use. To overcome some of these technical difficulties, an original sweat-collection technique is described. A collection capsule is created inside a flexible, adhesive and disposable anchoring membrane pasted onto the skin. A fluid-tight window is positioned in the upper part of the pocket and gives access to its content. Through the collection window, complete emptying of the sweat collector can be achieved repeatedly by suction using a vacutainer tube inserted in a tube holder equipped with a long dull needle. With prior addition of a suitable marker, fractional samplings can also be performed using a precision micropipette. This collecting method allows for kinetic studies on sweat rate and sweat content. The limited bias-inducing manipulations linked to the described technique, coupled with the ease of performing kinetic studies on sweat volume and content, make this original tool a reliable and accurate sweat-collection technique.
Factors associated with heat-induced increase in blood prolactin (PRL) were investigated. Ten male volunteers (23.7 +/- 2.2 yr) were exposed to exogenous heating (head-out immersion) in 41 degrees C water (control 37 degrees C) for 30 min with and without face fanning and cooling. In seven of the subjects, endogenous heating was produced by a 45-min exercise in a warm environment (41 degrees C; control 10 degrees C) with and without selective face fanning. Venous blood was collected before and after each trial; blood hormones were analyzed by radioimmunologic techniques. Heat loading, whether exogenous or endogenous in origin, induced significant increases in blood PRL, beta-endorphin, and vasoactive intestinal peptide (VIP) levels. Blood thyrotropin (TSH) level decreased significantly during water immersion and more significantly with face cooling. From measurement in peripheral blood, the differential beta-endorphin, VIP, and TSH responses to selective face ventilation during exogenous and endogenous heat exposures suggest that blood PRL released in heat derives from secretory stimuli that are independent of these prolactinotropic factors.
Physiological and metabolic output responses to facial cooling during a graded maximal exercise and a prolonged submaximal exercise lasting 30 min at 65% VO2 max were investigated in five male subjects. Pedalling on a cycle ergometer was performed both with and without facial cooling (10 degrees C, 4.6 M.S-1). Facial cooling at the end of greated maximal exercise apparently had no effect on plasma lactate (LA), maximal oxygen consumption (VO2 max), maximal heart rate (HR max), rectal temperature (Tre), work load, lactate threshold (LT), ventilatory threshold (VT) and onset of blood lactate accumulation (OBLA). However, the response to facial cooling after prolonged submaximal exercise is significantly different for heart rate and work load. The results suggest that facial wind stimulation during maximal exercise does not produce a stress high enough to alter the metabolic and physiological responses.
Physiological and metabolic output responses to facial cooling during a graded maximal exercise and a prolonged submaximal exercise lasting 30 min at 65% VO2 max were investigated in five male subjects. Pedalling on a cycle ergometer was performed both with and without facial cooling (10 degrees C, 4.6 m s-1). Facial cooling at the end of graded maximal exercise apparently had no effect on plasma lactate (LA), maximal oxygen consumption (VO2 max), maximal heart rate (HR max), rectal temperature (Tre), work-load, lactate threshold (LT), ventilatory threshold (VT) and onset of blood lactate accumulation (OBLA). However, the response to facial cooling after prolonged submaximal exercise is significantly different for heart rate and work-load. The results suggest that facial wind stimulation during maximal exercise does not produce a stress high enough to alter the metabolic and physiological responses.
This study was designed to verify if the decrease in blood prolactin (PRL) induced by selective face cooling during exercise could be part of a response to specific body thermal stress. Five healthy trained male cyclists presenting a significant plasma PRL elevation to exercise were, on three occasions and at weekly interval, submitted to a submaximal exercise (approx. 65% VO2max) on ergocycle with and without selective face cooling. In absence of face cooling a first trial served to establish reference values for workload, heart rate and plasma PRL levels, the latter increasing markedly (450% of resting values) in these conditions. On a second trial but with workload maintained at reference values (222 +/- 9 W), a significant bradycardia was observed with face cooling; furthermore, plasma PRL response to exercise was significantly reduced (to 31% of original response). On a third trial with face cooling, workload had to be significantly augmented (242 +/- 10 W) to maintain heart rate at reference level (78% HRmax); in addition, plasma PRL response to exercise was almost unchanged compared to the reference-value level. The absence of a significant face cooling-induced decrease in sympathetic tonus, as evaluated through peripheral plasma catecholamines response, does not indicate a role for the autonomic nervous system in the face cooling-induced reduction of both heart rate and PRL responses during exercise. Assay of circulating peripheral beta-endorphins could indicate that the face cooling-induced PRL blunted response does not necessarily involve an opioid mediation.(ABSTRACT TRUNCATED AT 250 WORDS)
Selective face ventilation, known to interfere with bloodstreamed temperature signals, should alter exercise-induced prolactinemic (PRL) responses if, as recently suggested, the latter responses are associated with body temperature increases generated by working muscles. To test this hypothesis, 15 trained adult male and female volunteers were submitted to 45-min hyperthermic treadmill runs with and without selective face ventilation. Tympanic (Tt) and rectal (Tr) temperatures were measured in these experiments, and serum immunoreactive PRL was assayed on venous blood sampled immediately before and immediately after the exercise. Hyperthermic running induced significant Tr elevations whether selective face ventilation was present or not. In the absence of face ventilation, serum PRL rose markedly in 11 of the 15 hyperthermic runners, the lack of response in 4 runners confirming that exercise per se is not necessarily hyperprolactinotrophic. When the 11 responders (11/15) ran with face ventilation, serum PRL response was abolished in 6 of them, indicating a significant interference from face ventilation on temperature signals streamed through carotid blood; serum PRL-maintained responses in 5 of these 11 ventilated runners suggest the absence of a learning effect. It is concluded that the blood-streamed temperature signals arising from working muscles represent an important but not a unique determinant of blood PRL response during aerobic running. The contribution of TRH and plasma volume changes to blood PRL variations during hyperthermic running appeared nonsignificant.
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A short anatomical and physiological review of the vidian nerve is presented. The authors have described the surgical technique they use which is somewhat similar to the one described by Nomura. Eight cases are presented which had been unsuccessfully treated by multiple radical nasal polypectomies. The results are comparable to those published in the literature and it appears that vidian neurectomy has merit in the treatment of recurrent nasal polyposis but must be used in association with radical polypectomy.
It has been suggested that immune responses and resultant generation or release of inflammatory mediators play a role in otitis media with effusion (OME). To explore the potential of one such mediator to contribute to OME, the effects of histamine injected into the middle ear cavity were examined. Injection of histamine into the guinea pig middle ear was found to produce dilation and endothelial disjunction in capillaries, leading to striking mucosal edema and effusion which persisted for at least several hours. This response could be partially blocked by pretreatment with either H1 or H2 antihistamines. It is suggested that histamine released during immune responses in the middle ear may contribute to the formation of effusion and submucosal edema as observed in OME.