Effect of swimming session duration and repetition on metabolic markers in rats.

The aim of this study was to investigate the profile of metabolites in male rats subjected to 50-60 min of swimming on three protocols: group A, a single 50 min swimming session; group B, one session a day for three days (5 min on day 1, 15 min on day 2 and 30 min on day 3); and group C, one session a day for 5 days, with increasing duration from 5 min on day 1, 15, 30, 45 and 60 min on consecutive days. The interval between sessions was 24 h. Measurements were made after the last swimming session. Controls did not swim. The glycogen content of liver and gastrocnemius and soleus muscle was depleted in the three groups that swam, but blood glucose concentration was significantly increased only in group B. Serum lactate concentrations were greater than the controls in groups A and B. There were significant increases in serum free fatty acid concentrations in all groups that swam. The increases in plasma free fatty acids may have resulted from lipolysis stimulated by endogenous catecholamines in groups A and C, since basal lipolysis measured in vitro was unchanged by swimming. The large increase in basal lipolysis in group B may have contributed to the rise in plasma free fatty acids. Adipocytes from rats in groups A and B were supersensitive to epinephrine, whereas those from group C were not. We conclude that the metabolic alterations were less pronounced after the last of five swimming sessions over 5 days than after a single session, even though session duration and the contribution of the physical component were similar. Glucose mobilization, but probably not utilization, was similar in the three groups that swam. The mechanisms of lipid mobilization from adipose tissue differed, depending on the stress paradigm. The metabolic changes in groups A and B indicated that three daily swimming sessions were insufficient to cause adaptation. The results contrast with previous findings for foot-shock stress, which leads to sensitization rather than adaptation in response to repeated stimuli.

Stress-induced alteration in the lipolytic response to beta-adrenoceptor agonists in rat white adipocytes.

We analysed the sensitivity to beta-adrenoceptor agonists in epididymal adipose cells from rats submitted to a stress protocol previously reported to induce alterations in sensitivity to catecholamines in cardiac tissue from rats. Food intake and body weight were lower, whereas adipocytes basal lipolysis was higher (control: 0.59 +/- 0.04; stress: 1.00 +/- 0.11, micromol glycerol/100 mg total lipids/100 min) in stressed compared to control rats. The responses to isoprenaline (pD(2) control: 7.46 +/- 0.11; stress: 8.11 +/- 0.17), adrenaline (pD(2) control: 5.78 +/- 0. 20; stress: 6.13 +/- 0.18), and salbutamol (pD(2) control: 5.64 +/- 0.28; stress: 5.92 +/- 0.34) were sensitized, and the lipolytic responses to norepinephrine (pD(2) control: 6.98 +/- 0.13; stress: 6. 41 +/- 0.12) and to BRL37344 (pD(2) control: 8.43 +/- 0.19; stress: 7.54 +/- 0.21) were desensitized. Responses to the higher concentration (100 microm) of isoprenaline (control: 1.80 +/- 0.18; stress: 2.24 +/- 0.10 micromol glycerol/100 mg total lipids/100 min), epinephrine (control: 1.64 +/- 0.17; stress: 2.24 +/- 0.14 micromol glycerol/100 mg total lipids/100 min), salbutamol (control: 0.65 +/- 0.11; stress: 1.21 +/- 0.41 micromol glycerol/100 mg total lipids/100 min), and d-butyryl-cAMP (control: 1.59 +/- 0.17; stress: 2.72 +/- 0.25) were significantly enhanced in adipocytes from stressed rats. pD(2) or maximum response to CGP12177 were not altered. Supersensitivity to isoprenaline was abolished by 50 nm ICI118,551 but was not modified by 100 nm metoprolol. However, subsensitivity to norepinephrine and to BRL37344 was abolished by 100 nM metoprolol. Our results suggest that in epididymal adipocytes from stressed rats there is a desensitization of the response to adrenoceptor agonists mediated by beta(1)-adrenoceptors together with a sensitization of the response mediated by beta(2)-adrenoceptors. beta(3)-adrenoceptors seem to be resistant to the stress effect.