Rats were trained by daily swimming (1—2 h) during 15 weeks. The training caused a significant increase in heart weight. Cardiac noradrenaline (NA) and adrenal catecholamine (CA) contents were significantly increased in trained animals. When exposed to acute prolonged exercise the endogenous levels of cardiac NA decreased in untrained, but not in trained, rats. Resting cardiac NA turnover, as measured by rate of disappearance of exogenous 3H‐NA, was slower in trained than in untrained rats (T1/2= 52 h and 20 h, respectively). The NA turnover increased during exercise, but still remained slower in trained rats. Figures were obtained indicating a significantly lower initial uptake of exogenous NA in the hearts of trained rats. Resting excretion of CA in the urine was not different in trained and untrained rats, while the increase seen after a period of exercise was much greater in the untrained animals. The results indicate that chronic physical training induces a functional adaptation of the sympathicoadrenal system leading to a better transmitter economy during exercise. The nature of this adaptation remains, however, unsettled.
The effect of prolonged physical training on the noradrenaline content of the heart and the catecholaniine content of the adrenal glands was studied on rats. the trained rats showed a moderate but highly significant cardiac hypertrophy (heart weight of controls: 1.32±0.01, trained rats: 1.41 ±0.01, heart ratio (g heart weight/100 g b.w.) of controls: 0.29 ± 0.003, trained rats: 0.34 ± 0.003). There was no difference in cardiac noradrenaline concentration between trained and untrained rats (controls: 0.69±0.04 μg/g, trained rats: 0.73±0.03 μg/g). There was a highly significant increase in adrenaline content of the adrenal glands espressed as μg adrenaline/kg b.w. (Controls 93±5 μg/kg, trained rats: 122 ± 5 μg/kg). It is concluded that prolonged physical training does not lower the amounts of synipatlictic trans mitter of the heart. It is further suggested that an increased adrenaline content in the adrenal glands might be a manifestation of an adaptation to the increased demands upon the rardio vascular system in rats subjccted to prolonged physical training.
The concentration of triglycerides, phospholipids and carnitine was determined in red and white parts of the gastrocnemius muscle from rats with and without a period of training by running. Also the rate of lipolysis in adipose tissue was determined with and without stimulation in vitro. The concentration of triglycerides was reduced in the red and white muscle tissue but positively correlated to each other in white muscle tissue. This suggests that the white muscle tissue. Correlation analysis revealed no direct relationship between the spontaneous or stimulated rate of lipolysis in vitro and the triglyceride concentration in either type of muscle tissue. This suggests that the level of muscle triglycerides was influenced or deter‐mined by other factors than the rate of mobilization of fatty acids from the adipose tissue per se. The concentrations of carnitine and triglycerides were negatively correlated in red muscle tissue but positively correlated to each other in white muscle tissue. This suggests that the metabolic role of carnitine with regard to triglyceride metabolism differed between the two muscle types. The possibility was discussed that the capacity of the intracellular carnitine transport system for fatty acids into mitochondria of red muscle tissue increased in the course of physical training as part of an adaptation towards enhanced oxidative metabolism.
Physically trained rats were compared with cold-acclimated rats. Trained as well as cold-acclimated rats showed cardiac and adrenal hypertrophy. Cardiac noradrenaline (NA) content was increased in both groups of rats but only the trained rats had an increased cardiac NA concentration. The adrenal NA content was increased in both groups but only the trained rats had an increased adrenal content of adrenaline (A). The spleen of trained rats had an increased NA content, while that of cold-acclimated rats had a decreased NA content. The submandibular glands of cold-acclimated rats were enlarged and had an increased NA content. Trained as well as cold-acclimated rats had lower urinary NA excretions during rest, after exercise and during cold stress when compared with controls. However, only the trained rats had a reduced net increment in NA excretion after exercise, whereas there was no difference between the increments of cold-acclimated and control rats. Six months after cessation of training, ex-trained rats still had an increased heart ratio and a reduced urinary NA excretion after exercise. It is suggested that physical training induces "cross tolerance" to cold stress, while cold-acclimation does not lead to "cross tolerance" to acute exercise.
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