This study was designed to clarify the effects of cold air exposure on metabolic and hormonal responses during progressive incremental exercise. Eight healthy males volunteered for the study. Informed consent was obtained from every participant. The following protocol was administered to each subject on three occasions in a climatic chamber in which the temperature was 20 degrees, 0 degree or -20 degrees C with relative humidity at 60% +/- 1%. Exercise tests were conducted on an electrically braked ergocycle, and consisted of a progressive incremental maximal exercise. Respiratory parameters were continuously monitored by an automated open-circuit sampling system. Exercise blood lactate (LA), free fatty acids (FFA), glucose levels, bicarbonate concentration (HCO-3), acid-base balance, plasma epinephrine (E) and norepinephrine (NE) were determined from venous blood samples obtained through an indwelling brachial catheter. Maximal oxygen uptake was significantly different between conditions: 72.0 +/- 5.4 ml kg-1 min-1 at 20 degrees C; 68.9 +/- 5.1 ml kg-1 min-1 at 0 degree C and 68.5 +/- 4.6 ml kg-1 min-1 at -20 degrees C. Workload, time to exhaustion, glucose levels and rectal temperature decreased significantly at -20 degrees C. Catecholamines and lactate values were not significantly altered by thermal conditions after maximal exercise but the catecholamines were decreased during rest. Bicarbonate, respiratory quotient, lactate and ventilatory thresholds increased significantly at -20 degrees C. The data support the contention that metabolic and hormonal responses following progressive incremental exercise are altered by cold exposure and they indicate a marked decrease in maximal oxygen uptake, time to exhaustion and workload.
Despite the fact that urogenito-sexual complications significantly impact the quality of life of diabetic patients, a robust in vivo experimental model is lacking. Bladder and erectile function in the Type 2 diabetic Goto-Kakizaki (GK) rat and responses to standard-of-care treatments for each disorder have been assessed. GK rats (n = 25, 18-wk-old, GK/Par colony) and age-matched Wistar rats (n = 23), characterized for their metabolic parameters, were used. Bladder function was assessed by cystometry in conscious rats treated by intravenous solifenacin (1 mg/kg). Subsequently, erectile function was assessed under anesthesia following electrical stimulation of the cavernous nerve in presence of intravenous sildenafil (0.3 mg/kg). GK rats displayed detrusor overactivity with a significant increase in frequency/amplitude of nonvoiding contractions during the filling phase, together with an increase in bladder capacity, intercontraction interval, voided volume, and maximal pressure of voiding contraction. Solifenacin significantly decreased parameters characterizing voiding contractions without modifying voiding efficiency. Erectile function in GK rats was markedly impaired and remained so after sildenafil treatment despite a significant improvement. GK rats display both bladder and erectile dysfunctions and respond at least partially to standard-of-care treatments for each disorder, thus representing a suitable model to investigate the pathophysiology and assess the efficacy of new therapeutic agents for Type 2 diabetes-associated bladder and erectile complications.
Blood prolactin (PRL) variations have been linked to temperature and osmotic changes in several species. The latter factors are here explored to better understand blood PRL responses frequently induced during physical exercise. Since body heat generated by exercise can lead to marked body fluid shifts, it was postulated that PRL changes observed during exercise could be associated with variations in body temperature and/or blood osmolality (OSM). A wide range (38.5–40.5°C) of rectal temperatures (Tr; used here to appreciate core temperatures) were theoretically selected and randomly assigned as targets to male runners. Measured by thermistor probe, target Tr were obtained by a combination of factors: (a) ↑ heat production by treadmill running, and (b) ⇓ heat losses by appropriate clothing (⇓ evaporation) in warmed (⇓ radiation) and hypo ventilated (⇓ convection) laboratory conditions. For each subject, target Tr was attained not prior to 30 min after initiation of running, and had to be maintained for at least 10 min, for a mean ( ± SD) running time of 52.6 ± 10.0 min. In a first protocol, hypohydration was provoked in 26 runners (23.9 ± 4.7 years) by total restriction of water intake. In a second protocol (10 different runners: 22.3 ± 3.3 years), euhydration was maintained by water intake (20 ml/kg body weight). Venous blood was sampled at rest before and immediately after the run. PRL was assayed by RIA; OSM was measured by freezing point depression; sodium was analyzed by flame photometry. At rest, before the heat-producing exercise, mean PRL values were 9.4 ± 3.4 ng/ml for both eu/hypohydrated groups. In the hypohydrated runners, exercise-induced hyperthermia was significantly (r = 0.82; p < 0.0005) associated with blood PRL responses. Moreover, these changes in Tr were also significantly (r = 0.54; p < 0.0025) related to changes in OSM, the latter variations being mostly explained (78 %) by the accompanying hypernatremia. In the euhydrated group of runners, the hyperthermic exercise failed to induce significant changes in OSM (r = 0.22; p > 0.15) and, as expected, variations in blood sodium levels were also not significant under these conditions. However, hyperthermic running in these iso-osmolar conditions did not prevent blood PRL levels from rising (r = 0.77; p < 0.0005). It was thus concluded that, in male trained runners, exercise-induced blood PRL responses could be derived more from thermic than from osmolar stresses.
This study was designed to clarify the effects of dietary modifications on the lactate threshold (LT) and on the onset of blood lactate accumulation (OBLA) during progressive incremental exercise. Six healthy males volunteered for the study. Informed consent was obtained from every participant. The following protocol was administered to each subject on three occasions: a 48-h period of mixed dieting (53% carbohydrates, 30% lipids, 17% proteins) preceding the first exercise test, immediately followed by a 48-h period of either a carbohydrate-rich (68% CHO, 23% lipids, 9% proteins) or a fat-rich (19% CHO, 57% lipids, 26% proteins) iso-caloric diet leading to the second exercise and separated from the third test by a 12-days period. Exercise tests were conducted on an electrically-braked ergocycle, and consisted of a progressive incremental maximal exercise. Respiratory parameters were continuously monitored by an automated open circuit sampling system. Exercise blood lactate (LA), free fatty acids (FFA), glucose levels and acid-base balance were determined from venous blood samples obtained through an indwelling brachial catheter. Peak lactate values, workload and performance time were not significantly altered by imposed diets. Furthermore, dietary modifications had no significant effect on LT, OBLA fixed at 4 mmol and ventilatory threshold. Increased pH and FFA mobilization were observed with fat-rich diet, while CHO-rich diet markedly increased the respiratory exchange ratio (R). It is concluded that LT and OBLA are not significantly altered by fat or CHO enrichment of diets.
8 male collegial athletes were submitted at random to three (55, 70 and 85% of VO2 max) ergocycle exercises of 20-min duration. Venous blood samples were obtained before, during and after ergocycling sessions by antecubital catheterization. Serum prolactin was measured by RIA using specific antiserum. The exercise treatments induced a blood prolactin response proportional to the intensity of the work loads.
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