Detraining losses of skeletal muscle capillarization are associated with vascular endothelial growth factor protein expression in rats

Abstract

The purposes of this study were as follows: (1) to examine basal vascular endothelial growth factor (VEGF) protein concentrations following 10 weeks of endurance training and after 7 days of detraining; and (2) to examine the acute VEGF protein response to a single 1 h exercise work bout in trained and detrained animals in relationship to changes in capillary indices following training and detraining. Thirty-three Sprague-Dawley rats were randomized into the following six groups: (1) control-basal; (2) control-acute exercise; (3) trained-basal; (4) trained-acute exercise; (5) detrained-basal; and (6) detrained-acute exercise. Groups 3-6 performed endurance training on a rodent treadmill three times per week for 10 weeks. Following the training intervention, rats in groups 5 and 6 remained cage confined (i.e. detrained) for 7 days. As expected, training increased soleus and plantaris muscle capillarity and attenuated the VEGF response to acute exercise. Seven days of detraining, however, resulted in a regression of capillary contacts and individual capillary-to-fibre ratio in the plantaris and soleus muscles compared with the trained group (P < 0.05). Restoration of the VEGF protein response to acute exercise was evident in both muscles, but only statistically significant in the plantaris muscle (P < 0.05). This is the first study to demonstrate the temporal relationship between VEGF protein expression and skeletal muscle capillarity within the first week of detraining. The findings of the present investigation are consistent with the hypothesis that reduced capillarity impairs oxygen availability to the working muscles. The results indicated that training-induced angiogenic remodelling was reversible following 1 week of detraining and may be modulated by VEGF.

Physiological Capillary Regression is not Dependent on Reducing VEGF Expression

“…This was a robust response seen in several muscles of the distal hindlimb (i.e., soleus, gastrocnemius, plantaris) (Table ), each representing varying degrees of oxidative and glycolytic potential . Consistent with this observation, two prior studies involving exercise training in rats, have also found detraining‐induced capillary regression whilst basal muscle VEGF expression is elevated (Table ). These studies provide the seemingly provocative observation that physiologically mediated capillary regression is not dependent on the withdrawal of VEGF.…”

(–)-Epicatechin is associated with increased angiogenic and mitochondrial signalling in the hindlimb of rats selectively bred for innate low running capacity

“…We were unsuccessful despite numerous attempts to get the LCR rats to run on the treadmill prior to the start of our intervention period at the Wayne State University laboratory. Based on our experience with exercise studies using rodent models [4, 5, 10, 22], the LCR rats became excessively stressed when placed on the treadmill and would not move off of the shock grid despite being shocked intermittently or when the shock grid was turned off. Similarly, when the rats were placed on the treadmill belt and then the treadmill turned on the rats would `ride' the belt and then stand on the shock grid.…”

“…Consistent with standard procedures in our laboratory [4, 5, 10, 22, 23], animals were anesthetized with sodium pentobarbital (60 mg×kg −1 i.p .) and the left plantaris muscle was removed.…”

Effects of Physical Activity and Inactivity on Muscle Fatigue

“…Earlier studies reported that a short period of detraining does not seem to significantly decrease capillary density of the previously trained muscle, possibly due to the concomitant decrease in muscle fiber area (Klausen et al, 1981; Coyle et al, 1984). However, more recent data suggest that only a short period of detraining is adequate to reverse training-induced angiogenic remodeling, as seen by the regression of capillary contacts and individual capillary-to-fiber ratio in the plantaris and soleus muscles of rats (Malek et al, 2010). These authors suggested that this was modulated by vascular endothelial growth factor (VEGF).…”