Effects of endurance training, stz-induced diabetes and their combination in mice skeletal muscle morphology

Por: Anna-maria Touvra, Heikki Kainulainen, Mika Silvenoinen e Riikka Kivela.

Athens 2004: Pre-olympic Congress

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Introduction

This study investigated the effects of endurance training and streptozotocin (STZ)-induced diabetes on mice skeletal muscle morphology. It is commonly known that STZ-induced diabetes has deleterious effects on skeletal muscle [1], while endurance training has an adaptive effect on skeletal muscle of healthy mice [2]. It is interesting to examine if the stimulus of endurance training (treadmill running) is able to share sufficient adaptations on skeletal muscle morphology and histochemistry of diabetic mice and age-matched nondiabetic controls.


Methods

Twenty male NMRI mice (approximately 40g) were made severely diabetic by single injection of STZ (180mg/kg) and divided into two sedentary groups (n=5 for each group) for 5 (D5) and 25 days (D25) and two age- matched training groups (n=5 for each group) that followed a running training program (5 days; DT5 and 25 days; DT25) on a rodent treadmill (1 h/day, 21m/min, 2.5º incline). Healthy mice were used as a control sedentary group (n=5; C). All animals were sacrificed 24 hours after the last training session.


Results

Body weight (BW) of the diabetic (D) and diabetic training (DT) mice was reduced in post-experimental condition in all groups after 5 and 25 days (D5 and D25 as well as DT5 and DT25). Mean weight of both calf muscles was significantly reduced concurrently in all diabetic groups compared to control group (p<0.001). D25 and DT25 mice showed a significant decrease in fibers expressing myosin heavy chain IIb (MHC IIb; p<0.05) and a significant increase of MHC type IIa isoforms for the DT25 group (p<0.05). D5 and D25 groups had a significant decrease of skeletal muscle fiber cross sectional area (26.8±5.1 and 22.9±3.9 μm2 respectively; p<0.05), while training resulted in non significant differences between DT5 and C groups (27.9±4.6 to 38.7±10.2 μm2). Muscle fiber cross sectional area decreased further for the DT25 group (38.7±10.2; p < 0.01).


Discussion/ Conclusions

In the early onset of STZ-induced diabetes, skeletal muscle can still react to the endurance-training stimulus for the development of muscle morphology. As the disease progresses to a severe state, both endurance training and STZ-induced diabetes act synergistically leading to skeletal muscle atrophy. The increase of histochemical type I fibers (which are smaller in size), demonstrates a shift to a slower contracting muscle fibers (more oxidative fiber profile), contributing to skeletal muscle deterioration [3].

References

[1]. Han X. et al. (1995). Acta Phys Scand, 155(1), 9-16
[2]. Kemi J. O. et al. (2002). J Appl Physiol, 93, 1301-1309
[3]. Klueber K. M. et al. (1994). Anat Rec, 239: 18-34

 

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