RESUMEN

Fatigue during prolonged exercise is related to brain monoamines concentrations, but the mechanisms underlying this relationship have not been fully elucidated. We investigated the effects of increased central tryptophan (TRP) availability on physical performance and thermoregulation in running rats that were pretreated with parachlorophenylalanine (p-CPA), an inhibitor of the conversion of TRP to serotonin. On the 3 days before the experiment, adult male Wistar rats were treated with intraperitoneal (ip) injections of saline or p-CPA. On the day of the experiment, animals received intracerebroventricular (icv) injections of either saline or TRP (20.3 µM) and underwent a submaximal exercise test until fatigue. Icv TRP-treated rats that received ip saline presented higher heat storage rate and a 69% reduction in time to fatigue compared with the control animals. Pretreatment with ip p-CPA blocked the effects of TRP on thermoregulation and performance. Moreover, ip p-CPA administration accelerated cutaneous heat dissipation when compared with saline-pretreated rats. We conclude that an elevated availability of central TRP interferes with fatigue mechanisms of exercising rats. This response is modulated by serotonergic pathways, because TRP effects were blocked in the presence of p-CPA. Our data also support that a depletion of brain serotonin facilitates heat loss mechanisms during exercise.

Asunto(s)

RESUMEN

We investigated brain mechanisms modulating fatigue during prolonged physical exercise in cold environments. In a first set of studies, each rat was subjected to three running trials in different ambient temperatures (T(a)). At 8 °C and 15 °C, core body temperature (T(core)) decreased and increased, respectively, whereas at 12 °C, the T(core) did not change throughout the exercise. In another set of experiments, rats were randomly assigned to receive bilateral 0.2 µL injections of 2.5 × 10(-2) M methylatropine or 0.15 M NaCl solution into the ventromedial hypothalamic nuclei (VMH). Immediately after the injections, treadmill exercise was started. Each animal was subjected to two experimental trials at one of the following T(a) : 5 °C, 12 °C or 15 °C. Muscarinic blockade of the VMH reduced the time to fatigue (TF) in cold environments by 35-37%. In all T(a) studied, methylatropine-treated rats did not present alterations in T(core) and tail skin temperature compared with controls. These results indicate that, below the zone of thermoneutrality, muscarinic blockade of the VMH decreases the TF, independent of changes in T(core). In conclusion, our data suggest that VMH muscarinic transmission modulates physical performance, even when the effects of thermoregulatory adjustments on fatigue are minimal.

Asunto(s)

RESUMEN

The effects of blocking ventromedial hypothalamic nucleus (VMH) muscarinic cholinoceptors on cardiovascular responses were investigated in running rats. Animals were anesthetized with pentobarbital sodium and fitted with bilateral cannulae into the VMH. After recovering from surgery, the rats were familiarized to running on a treadmill. The animals then had a polyethylene catheter implanted into the left carotid artery to measure blood pressure. Tail skin temperature (T(tail)), heart rate, and systolic, diastolic and mean arterial pressure were measured after bilateral injections of 0.2 microl of 5 x 10(-9) mol methylatropine or 0.15 M NaCl solution into the hypothalamus. Cholinergic blockade of the VMH reduced time to fatigue by 31 % and modified the temporal profile of cardiovascular and T(tail) adjustments without altering their maximal responses. Mean arterial pressure peak was achieved earlier in methylatropine-treated rats, which also showed a 2-min delay in induction of tail skin vasodilation, suggesting a higher sympathetic tonus to peripheral vessels. In conclusion, muscarinic cholinoceptors within the VMH are involved in a neuronal pathway that controls exercise-induced cardiovascular adjustments. Furthermore, blocking of cholinergic transmission increases sympathetic outflow during the initial minutes of exercise, and this higher sympathetic activity may be responsible for the decreased performance.

Asunto(s)

RESUMEN

Lipoprotein (a) [Lp(a)] is an atherogenic lipoprotein resembling low-density lipoprotein (LDL) but with an additional apoprotein (apo), apo(a). To determine whether plasma Lp(a) levels can influence the clinical presentation and extent of coronary artery disease (CAD), Lp(a), plasma lipids and apolipoproteins were determined in 203 Caucasian subjects with CAD and in 66 subjects without CAD, all confirmed by cinecoronariography. CAD patients were divided into groups according to their clinical history. The extent of the disease was evaluated by a scoring system. Lp(a) was elevated in CAD patients compared to subjects without CAD. However, there was no difference between patients that had myocardial infarction as the first manifestation of the disease and those who had only angina pectoris for at least two years. Plasma Lp(a) levels were correlated with extent of the disease. Among patients with CAD, Lp(a) was higher in females. Lp(a) was also studied separately in 29 Black subjects, 12 without CAD and 17 with CAD. In Black subjects, Lp(a) was higher than in Caucasians but there was no difference between subjects with and without CAD. Among the other risk factors studied, only plasma apo B levels and smoking were correlated with CAD.

Asunto(s)

RESUMEN

Lipoprotein (a) [Lp(a)] is an atherogenic lipoprotein resembling low-density lipoprotein (LDL) but with an additional apoprotein (apo), apo(a). To determine whether plasma Lp(a) levels can influence the clinical presentation and extent of coronary artery disease (CAD), Lp(a), plasma lipids and apolipoproteins were determined in 203 Caucasian subjects with CAD and in 66 subjects without CAD, all confirmed by cinecoronariography. CAD patients were divided into groups according to their clinical history. The extent of the disease was evaluated by a scoring system. Lp(a) was elevated in CAD patients compared to subjects without CAD. However, there was no difference between patients that had myocardial infarction as the first manifestation of the disease and those who had only angina pectoris for at least two years. Plasma lp(a) levels were correlated with extent of the disease. Among patients with CAD, Lp(a) was higher in females. Lp(a) was also studied separately in 29 Black subjects, Lp(a) was higher than in Caucasians but there was no difference between subjects with and without CAD. Among the other risk factors studied, only plasma apo B levels and smoking were correlated with CAD

Asunto(s)

RESUMEN

PURPOSE: To evaluate the plasma concentration of lipoprotein (a) (Lp(a) in subjects with normal or altered coronary angiography, as a risk factor of atherosclerosis in a Brazilian population. PATIENTS AND METHOD: Lp(a) plasma levels were determined by radioimmunoassay in 31 subjects with normal angiography and in 131 subjects with atherosclerosis. Plasma cholesterol, triglycerides, apolipoprotein A, A1 and B were also determined as well as risk factors like systemic arterial hypertension, smoking habit, diabetes and physical activity. RESULTS: Subjects with coronary disease had Lp(a) plasma levels of 41.9 mg/dl, compared to 23.9 mg/dl found in the normal group. Coronary artery disease risk was increased 2.3 times in those with plasma Lp(a) levels equal or above 25 mg/dl, compared to those with levels below this boundary. As to other known risk factors, only smoking habit has shown correlation with coronary artery disease. CONCLUSION: We confirmed the value of Lp(a) as a risk factor of coronary heart disease.

Asunto(s)

Asunto(s)