Response of the human triceps surae muscle to electrical stimulation during varying levels of blood flow restriction

2000 ◽  
Vol 82 (1-2) ◽  
pp. 39-44 ◽  
Author(s):  
M. A. Cole ◽  
M. D. Brown
2019 ◽  
Vol 127 (5) ◽  
pp. 1288-1296
Author(s):  
Madoka Yoshikawa ◽  
Takeshi Morifuji ◽  
Tomohiro Matsumoto ◽  
Noriaki Maeshige ◽  
Minoru Tanaka ◽  
...  

This study aimed to clarify the effects of a combined treatment comprising blood flow restriction and low-current electrical stimulation on skeletal muscle hypertrophy in rats. Male Wistar rats were divided into control (Cont), blood flow restriction (Bfr), electrical stimulation (Es), or Bfr with Es (Bfr + Es) groups. Pressure cuffs (80 mmHg) were placed around the thighs of Bfr and Bfr + Es rats. Low-current Es was applied to calf muscles in the Es and Bfr + Es rats. In experiment 1, a 1-day treatment regimen (5-min stimulation, followed by 5-min rest) was delivered four times to study the acute effects. In experiment 2, the same treatment regimen was delivered three times/wk for 8 wk. Body weight, muscle mass, changes in maximal isometric contraction, fiber cross-sectional area of the soleus muscle, expression of phosphorylated and total-ERK1/2, phosphorylated-rpS6 Ser235/236, phosphorylated and total Akt, and phosphorylated-rpS6 Ser240/244 were measured. Bfr and Es treatment alone failed to induce muscle hypertrophy and increase the expression of phosphorylated rpS6 Ser240/244. Combined Bfr + Es upregulated muscle mass, increased the fiber cross-sectional area, and increased phosphorylated rpS6 Ser240/244 expression and phosphorylated rpS6 Ser235/236 expression compared with controls. Combined treatment with Bfr and low-current Es can induce muscle hypertrophy via activation of two protein synthesis signaling pathways. This treatment should be introduced for older patients with sarcopenia and others with muscle weakness. NEW & NOTEWORTHY We investigated the acute and chronic effect of low-current electrical stimulation with blood flow restriction on skeletal muscle hypertrophy and the mechanisms controlling the hypertrophic response. Low-current electrical stimulation could not induce skeletal muscle hypertrophy, but a combination treatment did. Blood lactate and growth hormone levels were increased in the early response. Moreover, activation of ERK1/2 and mTOR pathways were observed in both the acute and chronic response, which contribute to muscle hypertrophy.


Author(s):  
Minoru Tanaka ◽  
Takeshi Morifuji ◽  
Ken Sugimoto ◽  
Hiroshi Akasaka ◽  
Taku Fujimoto ◽  
...  

To clarify the preventive effects of low current electrical stimulation (ES) under blood flow restriction (Bfr) on diabetes-associated capillary regression in skeletal muscles, we assessed the changes in three-dimensional capillary architecture and angiogenic factors. Twenty-four Goto-Kakizaki rats were randomly divided into four groups: the sedentary diabetes mellitus (DM), Bfr (DM+Bfr), electrical stimulation (DM+ES), and Bfr plus ES (DM+Bfr+ES) groups. Six healthy Wistar rats were used as age-matched controls. Bfr was performed using pressure cuffs (80 mmHg) around the thighs of the rats, and low-current ES was applied to the calf muscles of the rats. The current intensity was set at 30% of the maximal isometric contraction (24-30 mA). The treatments were delivered three times a week for eight weeks. In the DM group, the capillary diameter and volume of the soleus muscle decreased, and, the anti-angiogenic factor level increased. Furthermore, DM caused an increase in the hypoxia-inducible factor. Individually, Bfr or ES treatments failed to inhibit the DM-associated capillary regression and increase in anti-angiogenic factor. However, combined treatment with Bfr and ES prevented DM-associated capillary regression via inhibition of the increased anti-angiogenic factor and enhancement of interleukin-15 expression, mitochondrial biogenesis factors, and a pro-angiogenic factor. Therefore, DM-associated capillary regression inhibited by the combined treatment may prevent the effects of the increased anti-angiogenic factor and enhance the pro-angiogenic factor.


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