1 An investigation was made into the effects of conditioned running (1 h and 2h at 20mmin-'), which accelerates lipolysis, on the concentrations of tryptophan (Trp) in plasma, liver and brain and on 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) levels in brain. 2 Running caused time-dependent increases in plasma free Trp and brain Trp of the rat, leading to increased brain 5-HT turnover as revealed by higher amounts of its metabolite, 5-HIAA. The ratio of brain Trp to plasma free Trp was decreased after 2 h of running. 3 Liver Trp content rose only after 3 h of running, while liver unesterified fatty acid (UFA) concentrations remained unmodified. 4 A comparison between food deprivation and running (both of which promote lipolysis) was performed. Running for 2 h affected to the same extent plasma Trp disposition when compared with 24 h food deprivation. Nevertheless, the ratio of brain Trp to plasma free Trp was decreased in the food-deprived rats, when compared to the runners. 5 Valine, an inhibitor ofentry ofTrp into the brain decreased its level there to the same extent in both controls and I h runners. 6 Nicotinic acid, which inhibits fat catabolism, completely abolished the plasma UFA increase induced by 1 h of running. The drug did not affect plasma free Trp, brain Trp, 5-HT or 5-HIAA but enhanced plasma total Trp level. 7 Naloxone, an opiate antagonist, which decreased running-induced lipolysis, did not alter plasma Trp disposition.8 Desipramine, an antidepressant compound, affected only peripheral Trp concentrations of the runners. Plasma free and total Trp concentrations were increased in desipramine-treated runners, compared with saline-treated runners. In addition, desipramine increased the ratio of brain Trp to plasma free Trp of the runners. Brain 5-HT and 5-HIAA were increased in both desipramine-treated controls and runners. 9 The results suggest that running, which like food deprivatiQn accelerates lipolysis, increases brain Trp content and then 5-HT turnover. Comparison of these two physiological situations suggests that effectiveness of brain Trp entry is much more altered by fasting.

Eleven weight-trained athletes (age X +/- SD = 33 +/- 5 yrs, weight = 72 +/- 10 kg) with a maximal performance in bench press at the beginning of the study (116 +/- 19 kg) were studied at rest, after a standardized submaximal training session, and after a maximal session once a month for 4 months to study the blood metabolites and hormonal changes during weight lifting. The submaximal load was six series of eight bench presses at 70% of maximal performance presses, and the maximal load was the maximal number of repetitions at the same work load. The levels of several metabolites (lactate, glycerol, triglycerides, beta-OH-butyrate) and hormones (norepinephrine and epinephrine) increased (P less than 0.05) after submaximal work and more after maximal work. Glucose, FFA, acetoacetate, insulin, testosterone, and cortisol did not change significantly or consistently. Lactate after maximal work was higher after the 4th training month (P less than 0.05). Other variables did not change much with training while the maximal number of repetitions in the last series increased slightly (P less than 0.05). In general, the changes observed were smaller than the ones reported for endurance or interval running, which use larger muscle groups. Nevertheless, weight lifting induced changes in blood metabolites which reflect a mobilization of both carbohydrates and lipids stores for energy.

No abstract

An investigation was made into the effects of running (1 h at 20 m/min) on central serotonergic and dopaminergic metabolism in trained rats. Methodology involved continuous withdrawal of cerebrospinal fluid (CSF) from the third ventricle of conscious rats and measurements of tryptophan (TRP), 5-hydroxyindoleacetic acid (5-HIAA), and homovanillic acid (HVA) levels during a 2 h post-exercise period. All three compounds were increased during the hour following exercise and returned to their basal values within an hour later. CSF flow rate was stable when metabolite levels were elevated. Brain determinations indicated that CSF metabolite variations only qualitatively paralleled brain changes. Indeed, post-exercise TRP, 5-HIAA, and HVA levels were increased to a greater extent in brain when compared to CSF. It is suggested that increased serotonergic and dopaminergic metabolism, caused by motor activity, may be involved in the behavioral effects of exercise.

The expression of myosin isoforms was studied in regenerated rat soleus muscle during either normal or altered postural activity. Regeneration was induced following injury by venom from the Notechis scutatus scutatus snake. Immunohistochemical analysis showed that, in regenerating soleus muscle after 3 wk of hindlimb suspension, nearly all fibers reacted positively with the myosin heavy chain (MHC) antibody associated with fast-twitch muscle fibers (fast MHC). When 3 wk of recovery with normal weight-bearing activity followed hindlimb suspension, the regeneration soleus muscle exhibited a nearly homogeneous staining with the MHC antibody associated with the slow-twitch muscle fibers (slow MHC). These findings were in accordance with quantitative analysis of the electrophoretic separation of the native myosin isoforms. Immunohistochemical data showed that removal of weight bearing in the 21-day old regenerated soleus muscles resulted in an increase in fast MHC expression. Together, the results of the present study clearly demonstrate that the postural load is an important component in the induction of slow MHC in regenerating muscle and that the control of the expression of MHC in muscle comprising a homogeneous population of fibers deriving from satellite cells appears more homogeneous and more complete than in a nondegenerated one.

No abstract

The aim of this study was to analyze the effects of treadmill training (2 h/day, 5 days/wk, 30 m/min, 7% grade for 5 wk) on the expression of myosin heavy chain (MHC) isoforms during and after regeneration of a fast-twitch white muscle [extensor digitorum longus (EDL)]. Male Wistar rats were randomly assigned to a sedentary (n = 10) or an endurance-trained (ET; n = 10) group. EDL muscle degeneration and regeneration were induced by two subcutaneous injections of a snake toxin. Five days after induction of muscle injury, animals were trained over a 5-wk period. It was verified that approximately 40 days after venom treatment, central nuclei were present in the treated EDL muscles from sedentary and ET rats. The changes in the expression of MHCs in EDL muscles were detected by using a combination of biochemical and immunocytochemical approaches. Compared with contralateral nondegenerated muscles, relative concentrations of types I, IIa, and IIx MHC isoforms in ET rats were greater in regenerated EDL muscles (146%, P < 0.05; 76%, P < 0.01; 87%, P < 0.01, respectively). Their elevation corresponded to a decrease in the relative concentration of type IIb MHC (-36%, P < 0.01). Although type I accounted for only 3.2% of total myosin in regenerated muscles from the ET group, the cytochemical analysis showed that the proportion of positive staining with the slow MHC antibody was markedly greater in regenerated muscles than in contralateral ones. Collectively, these results demonstrate that the regenerated EDL muscle is sensitive to endurance training and suggest that the training-induced shift in MHC isoforms observed in these muscles resulted from an additive effect of regeneration and repeated exercise.

Blood pressure, heart rate, and plasma catecholamine concentrations were measured in 9 normotensive volunteers during a randomized cross-over study of oral nifedipine (10 mg X 5) and placebo; measurements were made at rest and during maximal anaerobic exercise. At rest nifedipine reduced blood pressure and increased heart rate and plasma noradrenaline, whereas plasma adrenaline did not change. During exercise, the blood pressure response was similar in nifedipine and placebo treated subjects; however, heart rate was significantly higher with nifedipine. Plasma noradrenaline increased more during exercise in nifedipine-treated subjects. By contrast, nifedipine inhibited the increase in plasma adrenaline induced by exercise. The results suggest that peripheral vasodilatation induced by nifedipine is responsible for increased sympathetic nerve activity, both at rest and during exercise, and that nifedipine inhibits adrenaline secretion in man.