scholarly journals Protective effects of low-intensity exercise on metabolic oxidative capacity and capillarization in skeletal muscle of non-obese diabetic rats

2020 ◽  
Vol 41 (5) ◽  
pp. 227-236
Author(s):  
Mohammad A. QATAMISH ◽  
Saad M. AL-NASSAN ◽  
Hiroyo KONDO ◽  
Hidemi FUJINO
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Capacity ◽  
Diabetic Rats ◽  
Protective Effects ◽  
Low Intensity ◽  
Low Intensity Exercise ◽  
Obese Diabetic Rats

scholarly journals LOW-INTENSITY EXERCISE ENHANCES MUSCULAR ANDROGEN/ANDROGEN RECEPTOR TO INHIBIT MYOSTATIN PATHWAY

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S85-S86
Author(s):  
Bo-Kyung Son ◽  
Masato Eto ◽  
Miya Oura ◽  
Masahiro Akishita
Keyword(s):  
Skeletal Muscle ◽  
Androgen Receptor ◽  
Electric Pulse ◽  
Negative Regulator ◽  
Muscle Size ◽  
C2c12 Myotubes ◽  
Protein Levels ◽  
Low Intensity ◽  
Low Intensity Exercise ◽  
Response To Exercise

Abstract Background: Physical exercise is well documented to induce muscle size, strength, and energy metabolism. Although the contribution of systemic or local androgen in exercise-adapted muscle hypertrophy has been suggested, less is known about the molecular pathway of androgen in response to exercise. In the present study, we examined roles of androgen/androgen receptor (AR) after exercise, especially for the suppression of myostatin, a potent negative regulator of muscle mass. Methods and Results: To examine the effects of exercise, we employed low-intensity exercise in mice and electric pulse stimulation (EPS) in C2C12 myotubes. Both mRNA and protein levels of AR significantly increased in skeletal muscle of low-intensity exercised mice and C2C12 myotubes exposed to EPS. Production of testosterone and DHT from EPS-treated C2C12 myotubes was markedly increased. Of interest, we found that myostatin was clearly inhibited by EPS, and its inhibition was significantly abrogated by flutamide, a specific antagonist of AR. Furthermore, IL-6 and phospho-STAT3 (pSTAT3) expression, the downstream pathway of myostatin, were decreased by EPS and this was also reversed by flutamide. Similar downregulation of myostatin and IL-6 was seen in skeletal muscle of low-intensity exercised mice. Conclusion: Muscle AR expression and androgen production were increased by exercise and EPS treatment. As a mechanistical insight, it is suggested that AR inhibited myostatin expression transcriptionally, which downregulates IL-6/pSTAT3 pathway and thus contributes to the prevention of muscle degradation.

scholarly journals Defining the contribution of skeletal muscle pyruvate dehydrogenase α1 to exercise performance and insulin action

2018 ◽  
Vol 315 (5) ◽  
pp. E1034-E1045 ◽  
Author(s):  
Kristoffer Svensson ◽  
Jessica R. Dent ◽  
Shahriar Tahvilian ◽  
Vitor F. Martins ◽  
Abha Sathe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Energy Expenditure ◽  
Exercise Performance ◽  
Pyruvate Dehydrogenase ◽  
High Intensity ◽  
High Intensity Exercise ◽  
Low Intensity ◽  
Low Intensity Exercise ◽  
Muscle Contractile

The pyruvate dehydrogenase complex (PDC) converts pyruvate to acetyl-CoA and is an important control point for carbohydrate (CHO) oxidation. However, the importance of the PDC and CHO oxidation to muscle metabolism and exercise performance, particularly during prolonged or high-intensity exercise, has not been fully defined especially in mature skeletal muscle. To this end, we determined whether skeletal muscle-specific loss of pyruvate dehydrogenase alpha 1 ( Pdha1), which is a critical subunit of the PDC, impacts resting energy metabolism, exercise performance, or metabolic adaptation to high-fat diet (HFD) feeding. For this, we generated a tamoxifen (TMX)-inducible Pdha1 knockout (PDHmKO) mouse, in which PDC activity is temporally and specifically ablated in adult skeletal muscle. We assessed energy expenditure, ex vivo muscle contractile performance, and endurance exercise capacity in PDHmKO mice and wild-type (WT) littermates. Additionally, we studied glucose homeostasis and insulin sensitivity in muscle after 12 wk of HFD feeding. TMX administration largely ablated PDHα in skeletal muscle of adult PDHmKO mice but did not impact energy expenditure, muscle contractile function, or low-intensity exercise performance. Additionally, there were no differences in muscle insulin sensitivity or body composition in PDHmKO mice fed a control or HFD, as compared with WT mice. However, exercise capacity during high-intensity exercise was severely impaired in PDHmKO mice, in parallel with a large increase in plasma lactate concentration. In conclusion, although skeletal muscle PDC is not a major contributor to resting energy expenditure or long-duration, low-intensity exercise performance, it is necessary for optimal performance during high-intensity exercise.

Effects of physical exercise on phospholipid fatty acid composition in skeletal muscle

1998 ◽  
Vol 274 (3) ◽  
pp. E432-E438 ◽  
Author(s):  
Agneta Andersson ◽  
Anders Sjödin ◽  
Roger Olsson ◽  
Bengt Vessby
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Acid Composition ◽  
The Body ◽  
Muscle Membrane ◽  
Peripheral Insulin Sensitivity ◽  
Low Intensity ◽  
Low Intensity Exercise

The effects of low-intensity exercise on the fatty acid composition in skeletal muscle and in serum were studied in 19 sedentary, middle-aged Swedish men. During a 10-wk period, all subjects were given a standardized diet with an identical fat composition. After 4 wk on this diet, they were randomly allocated to a daily exercise program (55% peak oxygen uptake) or to continue to live a sedentary life for the remaining 6 wk. Aerobic capacity (submaximal bicycle test) and peripheral insulin sensitivity (hyperinsulinemic euglycemic clamp) improved with training, whereas the body weight as well as the body composition (underwater weighing and bioimpedance) were unchanged. The proportions of palmitic acid (16:0) and linoleic acid [18:2(n-6)] and the sum of n-6 fatty acids [18:2(n-6), 20:3(n-6), 20:4(n-6)] were decreased in skeletal muscle phospholipids, whereas the proportion of oleic acid [18:1(n-9)] was increased, by training. The fatty acid profile in skeletal muscle triglycerides remained unchanged. We conclude that regular low-intensity exercise influences the fatty acid composition of the phospholipids in skeletal muscle, which hypothetically may contribute to changes of the skeletal muscle membrane fluidity and influence the peripheral insulin sensitivity.

scholarly journals Resveratrol shows neuronal and vascular-protective effects in older, obese, streptozotocin-induced diabetic rats

2016 ◽  
Vol 115 (11) ◽  
pp. 1911-1918 ◽  
Author(s):  
Hnin Ei Phyu ◽  
Jordon Candice Irwin ◽  
Rebecca Kate Vella ◽  
Andrew Stuart Fenning
Keyword(s):  
Diabetes Mellitus ◽  
Water Consumption ◽  
Vascular Reactivity ◽  
Clinical Symptoms ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Tactile Allodynia ◽  
Protective Effects ◽  
Ventricular Compliance ◽  
Obese Diabetic Rats

AbstractDiabetes-induced CVD is the most significant complication of prolonged hyperglycaemia. The aim of this study was to determine whether resveratrol, a polyphenol antioxidant compound, when administered at a dose that can be reasonably obtained through supplementation could prevent the development of cardiovascular complications in older, obese, diabetic rats. Diabetes was induced in 6-month old, obese, male Wistar rats via a single intravenous dose of streptozotocin (65 mg/kg). Randomly selected animals were administered resveratrol (2 mg/kg) via oral gavage daily for 8 weeks. Body weights, blood glucose levels, food intake and water consumption were monitored, and assessments of vascular reactivity, tactile allodynia and left ventricular function were performed. Resveratrol therapy significantly improved tactile allodynia and vascular contractile functionality in diabetic rats (P<0·05). There were no significant changes in standardised vasorelaxation responses, plasma glucose concentrations, water consumption, body weight, left ventricular hypertrophy, kidney hypertrophy, heart rate or left ventricular compliance with resveratrol administration. Resveratrol-mediated improvements in vascular and nerve function in old, obese, diabetic rats were associated with its reported antioxidant effects. Resveratrol did not improve cardiac function nor mitigate the classic clinical symptoms of diabetes mellitus (i.e. hyperglycaemia, polydypsia and a failure to thrive). This suggests that supplementation with resveratrol at a dose achievable with commercially available supplements would not produce significant cardioprotective effects in people with diabetes mellitus.

scholarly journals Effects of β2-agonist administration and exercise on contractile activation of skeletal muscle fibers

1996 ◽  
Vol 81 (4) ◽  
pp. 1610-1618 ◽  
Author(s):  
Gordon S. Lynch ◽  
Alan Hayes ◽  
Siun P. Campbell ◽  
David A. Williams
Keyword(s):  
Skeletal Muscle ◽  
Muscle Wasting ◽  
Therapeutic Potential ◽  
Fiber Type ◽  
Muscle Fibers ◽  
Low Intensity ◽  
Skeletal Muscle Fibers ◽  
Contractile Activation ◽  
Low Intensity Exercise ◽  
And Control

Lynch, Gordon S., Alan Hayes, Siun P. Campbell, and David A. Williams. Effects of β2-agonist administration and exercise on contractile activation of skeletal muscle fibers. J. Appl. Physiol. 81(4): 1610–1618, 1996.—Clenbuterol, a β2-adrenoceptor agonist, has therapeutic potential for the treatment of muscle-wasting diseases, yet its effects, especially at the single-fiber level, have not been fully characterized. Male C57BL/10 mice were allocated to three groups: Control-Treated mice were administered clenbuterol (2 mg ⋅ kg−1 ⋅ day−1) via their drinking water for 15 wk; Trained-Treated mice underwent low-intensity training (unweighted swimming, 5 days/wk, 1 h/day) in addition to receiving clenbuterol; and Control mice were sedentary and untreated. Contractile characteristics were determined on membrane-permeabilized fibers from the extensor digitorum longus (EDL) and soleus muscles. Fast fibers from the EDL and soleus muscles of Treated mice exhibited decreases in Ca2+ sensitivity. Endurance exercise offset clenbuterol’s effects, demonstrated by similar Ca2+ sensitivities in the Trained-Treated and Control groups. Long-term clenbuterol treatment did not affect the normalized maximal tension of fast or slow fibers but increased the proportion of fast fibers in the soleus muscle. Training increased the proportion of fibers with high and intermediate succinate dehydrogenase activity in the EDL and soleus muscles, respectively. If clenbuterol is to be used for treating muscle-wasting disorders, some form of low-intensity exercise might be encouraged such that potentially deleterious slow-to-fast fiber type transformations are minimized. Indeed, in the mouse, low-intensity exercise appears to prevent these effects.

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