TY - JOUR
T1 - Skeletal muscle and hormonal adaptation to physical training in the rat
T2 - role of the sympatho-adrenal system
AU - Henriksson, J
AU - Svedenhag, J
AU - Richter, Erik A.
AU - Christensen, N J
AU - Galbo, H
PY - 1985
Y1 - 1985
N2 - The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training-induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague-Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham-operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h X day-1, 4 days X week-1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochrome c oxidase, and 3-hydroxyacyl-CoA dehydrogenase. In sham-operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training-induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham-operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training-induced increase in muscle mitochondrial enzymes. The training-induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated by adrenomedullary hormones.
AB - The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training-induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague-Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham-operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h X day-1, 4 days X week-1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochrome c oxidase, and 3-hydroxyacyl-CoA dehydrogenase. In sham-operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training-induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham-operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training-induced increase in muscle mitochondrial enzymes. The training-induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated by adrenomedullary hormones.
KW - 3-Hydroxyacyl CoA Dehydrogenases
KW - Adaptation, Physiological
KW - Adrenal Medulla
KW - Animals
KW - Body Weight
KW - Citrate (si)-Synthase
KW - Electron Transport Complex IV
KW - Epinephrine
KW - Heart
KW - Male
KW - Muscle Contraction
KW - Muscles
KW - Norepinephrine
KW - Organ Size
KW - Physical Exertion
KW - Rats
KW - Rats, Inbred Strains
KW - Succinate Dehydrogenase
KW - Sympathetic Nervous System
U2 - 10.1111/j.1748-1716.1985.tb07569.x
DO - 10.1111/j.1748-1716.1985.tb07569.x
M3 - Journal article
C2 - 2984895
VL - 123
SP - 127
EP - 138
JO - Acta Physiologica Scandinavica
JF - Acta Physiologica Scandinavica
SN - 0001-6772
IS - 2
ER -