scholarly journals Mitochondria-specific antioxidant supplementation does not influence endurance exercise training-induced adaptations in circulating angiogenic cells, skeletal muscle oxidative capacity or maximal oxygen uptake

2016 ◽  
Vol 594 (23) ◽  
pp. 7005-7014 ◽  
Author(s):  
Daniel D. Shill ◽  
W. Michael Southern ◽  
T. Bradley Willingham ◽  
Kasey A. Lansford ◽  
Kevin K. McCully ◽  
...  
1997 ◽  
Vol 82 (6) ◽  
pp. 1862-1868 ◽  
Author(s):  
Richard M. McAllister ◽  
Brian L. Reiter ◽  
John F. Amann ◽  
M. Harold Laughlin

McAllister, Richard M., Brian L. Reiter, John F. Amann, and M. Harold Laughlin. Skeletal muscle biochemical adaptations to exercise training in miniature swine. J. Appl. Physiol. 82(6): 1862–1868, 1997.—The primary purpose of this study was to test the hypothesis that endurance exercise training induces increased oxidative capacity in porcine skeletal muscle. To test this hypothesis, female miniature swine were either trained by treadmill running 5 days/wk over 16–20 wk (Trn; n = 35) or pen confined (Sed; n = 33). Myocardial hypertrophy, lower heart rates during submaximal stages of a maximal treadmill running test, and increased running time to exhaustion during that test were indicative of training efficacy. A variety of skeletal muscles were sampled and subsequently assayed for the enzymes citrate synthase (CS), 3-hydroxyacyl-CoA dehydrogenase, and lactate dehydrogenase and for antioxidant enzymes. Fiber type composition of a representative muscle was also determined histochemically. The largest increase in CS activity (62%) was found in the gluteus maximus muscle (Sed, 14.7 ± 1.1 μmol ⋅ min−1 ⋅ g−1; Trn, 23.9 ± 1.0; P < 0.0005). Muscles exhibiting increased CS activity, however, were located primarily in the forelimb; ankle and knee extensor and respiratory muscles were unchanged with training. Only two muscles exhibited higher 3-hydroxyacyl-CoA dehydrogenase activity in Trn compared with Sed. Lactate dehydrogenase activity was unchanged with training, as were activities of antioxidant enzymes. Histochemical analysis of the triceps brachii muscle (long head) revealed lower type IIB fiber numbers in Trn (Sed, 42 ± 6%; Trn, 10 ± 4; P < 0.01) and greater type IID/X fiber numbers (Sed, 11 ± 2; Trn, 22 ± 3; P < 0.025). These findings indicate that porcine skeletal muscle adapts to endurance exercise training in a manner similar to muscle of humans and other animal models, with increased oxidative capacity. Specific muscles exhibiting these adaptations, however, differ between the miniature swine and other species.


1990 ◽  
Vol 69 (5) ◽  
pp. 1804-1809 ◽  
Author(s):  
W. H. Martin ◽  
W. M. Kohrt ◽  
M. T. Malley ◽  
E. Korte ◽  
S. Stoltz

To determine whether extremity vasodilatory capacity may be augmented in older persons by endurance exercise training, lower leg blood flow and conductance were characterized plethysmographically at rest and during maximal hyperemia in 9 men and 10 women aged 64 +/- 3 (SD) yr before and after 31 +/- 6 wk of walking and jogging at 70-90% of maximal oxygen uptake for 45 min 3-5 days/wk. Maximal oxygen uptake expressed as milliliters per kilogram per minute improved 25% in men and 21% in women (P less than 0.01). Maximal leg blood flow and conductance increased in all nine men by an average of 39 +/- 33 (P less than 0.001) and 42 +/- 44% (P less than 0.004), respectively. Results were more variable in women and achieved unequivocal statistical significance only for maximal blood flow (+33 +/- 54% for blood flow and +29 +/- 55% for conductance; P less than 0.02 and P = 0.05, respectively). Body weight and skinfold adiposity declined in both sexes (P less than 0.05). Enhancement of vasodilatory capacity was related to weight loss in men and adipose tissue loss in women (r = 0.61 and 0.51, respectively; P less than 0.05). There were no significant changes in exercise capacity, body weight, or maximal blood flow in four male and three female controls aged 66 +/- 4 yr. Thus adaptability of the lower limb circulation to endurance exercise training is retained to at least age 65 yr.


2013 ◽  
Vol 98 (12) ◽  
pp. 4863-4871 ◽  
Author(s):  
Katie Louche ◽  
Pierre-Marie Badin ◽  
Emilie Montastier ◽  
Claire Laurens ◽  
Virginie Bourlier ◽  
...  

Context: Skeletal muscle lipase and intramyocellular triglyceride (IMTG) play a role in obesity-related metabolic disorders. Objectives: The aim of the present study was to investigate the impact of 8 weeks of endurance exercise training on IMTG content and lipolytic proteins in obese male subjects. Design and Volunteers: Ten obese subjects completed an 8-week supervised endurance exercise training intervention in which vastus lateralis muscle biopsy samples were collected before and after training. Main Outcome Measures: Clinical characteristics and ex vivo substrate oxidation rates were measured pre- and posttraining. Skeletal muscle lipid content and lipolytic protein expression were also investigated. Results: Our data show that exercise training reduced IMTG content by 42% (P &lt; .01) and increased skeletal muscle oxidative capacity, whereas no change in total diacylglycerol content and glucose oxidation was found. Exercise training up-regulated adipose triglyceride lipase, perilipin (PLIN) 3 protein, and PLIN5 protein contents in skeletal muscle despite no change in mRNA levels. Training also increased hormone sensitive–lipase Ser660 phosphorylation. No significant changes in comparative gene identification 58, G0/G1 switch gene 2, and PLIN2 protein and mRNA levels were observed in response to training. Interestingly, we noted a strong relationship between skeletal muscle comparative gene identification 58 and mitochondrial respiratory chain complex I protein contents at baseline (r = 0.87, P &lt; .0001). Conclusions: Endurance exercise training coordinately up-regulates fat oxidative capacity and lipolytic protein expression in skeletal muscle of obese subjects. This physiological adaptation probably favors fat oxidation and may alleviate the lipotoxic lipid pressure in skeletal muscle. Enhancement of IMTG turnover may be required for the beneficial metabolic effects of exercise in obesity.


2017 ◽  
Vol 123 (2) ◽  
pp. 460-472 ◽  
Author(s):  
Scott K. Powers

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as “exercise preconditioning.” As few as 3–5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.


2020 ◽  
Vol 129 (3) ◽  
pp. 558-568
Author(s):  
Austin T. Beever ◽  
Thomas R. Tripp ◽  
Jenny Zhang ◽  
Martin J. MacInnis

Near-infrared spectroscopy (NIRS) can be used to measure skeletal muscle oxidative capacity. Here, we demonstrated that NIRS-derived skeletal muscle oxidative capacity of the vastus lateralis was independent of sex, reliable across and within days, and correlated with maximal and submaximal indices of aerobic fitness, including maximal oxygen uptake, lactate threshold, and respiratory compensation point. These findings highlight the utility of NIRS for investigating skeletal muscle oxidative capacity in females and males.


2006 ◽  
Vol 290 (5) ◽  
pp. E998-E1005 ◽  
Author(s):  
Torben Østergård ◽  
Jesper L. Andersen ◽  
Birgit Nyholm ◽  
Sten Lund ◽  
K.Sreekumaran Nair ◽  
...  

First-degree relatives of type 2 diabetic patients (offspring) are often characterized by insulin resistance and reduced physical fitness (V̇o2 max). We determined the response of healthy first-degree relatives to a standardized 10-wk exercise program compared with an age-, sex-, and body mass index-matched control group. Improvements in V̇o2 max(14.1 ± 11.3 and 16.1 ± 14.2%; both P < 0.001) and insulin sensitivity (0.6 ± 1.4 and 1.0 ± 2.1 mg·kg−1·min−1; both P < 0.05) were comparable in offspring and control subjects. However, V̇o2 maxand insulin sensitivity in offspring were not related at baseline as in the controls ( r = 0.009, P = 0.96 vs. r = 0.67, P = 0.002). Likewise, in offspring, exercise-induced changes in V̇o2 maxdid not correlate with changes in insulin sensitivity as opposed to controls ( r = 0.06, P = 0.76 vs. r = 0.57, P = 0.01). Skeletal muscle oxidative capacity tended to be lower in offspring at baseline but improved equally in both offspring and controls in response to exercise training (Δcitrate synthase enzyme activity 26 vs. 20%, and Δcyclooxygenase enzyme activity 25 vs. 23%. Skeletal muscle fiber morphology and capillary density were comparable between groups at baseline and did not change significantly with exercise training. In conclusion, this study shows that first-degree relatives of type 2 diabetic patients respond normally to endurance exercise in terms of changes in V̇o2 maxand insulin sensitivity. However, the lack of a correlation between the V̇o2 maxand insulin sensitivity in the first-degree relatives of type 2 diabetic patients indicates that skeletal muscle adaptations are dissociated from the improvement in V̇o2 max. This could indicate that, in first-degree relatives, improvement of insulin sensitivity is dissociated from muscle mitochondrial functions.


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