scholarly journals Allometry of skeletal muscle fine structure allows maintenance of aerobic capacity during ontogenetic growth

2009 ◽  
Vol 212 (21) ◽  
pp. 3564-3575 ◽  
Author(s):  
S. Young ◽  
S. Egginton
Keyword(s):  
Skeletal Muscle ◽  
Fine Structure ◽  
Aerobic Capacity

scholarly journals Systemic oxidative stress is associated with lower aerobic capacity and impaired skeletal muscle energy metabolism in heart failure patients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takashi Yokota ◽  
Shintaro Kinugawa ◽  
Kagami Hirabayashi ◽  
Mayumi Yamato ◽  
Shingo Takada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Aerobic Capacity ◽  
Plantar Flexion ◽  
Exercise Intolerance ◽  
Whole Body ◽  
Resonance Spectroscopy ◽  
Systemic Oxidative Stress

AbstractOxidative stress plays a role in the progression of chronic heart failure (CHF). We investigated whether systemic oxidative stress is linked to exercise intolerance and skeletal muscle abnormalities in patients with CHF. We recruited 30 males: 17 CHF patients, 13 healthy controls. All participants underwent blood testing, cardiopulmonary exercise testing, and magnetic resonance spectroscopy (MRS). The serum thiobarbituric acid reactive substances (TBARS; lipid peroxides) were significantly higher (5.1 ± 1.1 vs. 3.4 ± 0.7 μmol/L, p < 0.01) and the serum activities of superoxide dismutase (SOD), an antioxidant, were significantly lower (9.2 ± 7.1 vs. 29.4 ± 9.7 units/L, p < 0.01) in the CHF cohort versus the controls. The oxygen uptake (VO2) at both peak exercise and anaerobic threshold was significantly depressed in the CHF patients; the parameters of aerobic capacity were inversely correlated with serum TBARS and positively correlated with serum SOD activity. The phosphocreatine loss during plantar-flexion exercise and intramyocellular lipid content in the participants' leg muscle measured by 31phosphorus- and 1proton-MRS, respectively, were significantly elevated in the CHF patients, indicating abnormal intramuscular energy metabolism. Notably, the skeletal muscle abnormalities were related to the enhanced systemic oxidative stress. Our analyses revealed that systemic oxidative stress is related to lowered whole-body aerobic capacity and skeletal muscle dysfunction in CHF patients.

The relationship between human skeletal muscle pyruvate dehydrogenase phosphatase activity and muscle aerobic capacity

2011 ◽  
Vol 111 (2) ◽  
pp. 427-434 ◽  
Author(s):  
Lorenzo K. Love ◽  
Paul J. LeBlanc ◽  
J. Greig Inglis ◽  
Nicolette S. Bradley ◽  
Jon Choptiany ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Endurance Training ◽  
Aerobic Capacity ◽  
Pyruvate Dehydrogenase ◽  
Human Skeletal Muscle ◽  
Citrate Synthase ◽  
Tricarboxylic Acid Cycle ◽  
Carbohydrate Oxidation ◽  
Pyruvate Dehydrogenase Phosphatase

Pyruvate dehydrogenase (PDH) is a mitochondrial enzyme responsible for regulating the conversion of pyruvate to acetyl-CoA for use in the tricarboxylic acid cycle. PDH is regulated through phosphorylation and inactivation by PDH kinase (PDK) and dephosphorylation and activation by PDH phosphatase (PDP). The effect of endurance training on PDK in humans has been investigated; however, to date no study has examined the effect of endurance training on PDP in humans. Therefore, the purpose of this study was to examine differences in PDP activity and PDP1 protein content in human skeletal muscle across a range of muscle aerobic capacities. This association is important as higher PDP activity and protein content will allow for increased activation of PDH, and carbohydrate oxidation. The main findings of this study were that 1) PDP activity ( r2 = 0.399, P = 0.001) and PDP1 protein expression ( r2 = 0.153, P = 0.039) were positively correlated with citrate synthase (CS) activity as a marker for muscle aerobic capacity; 2) E1α ( r2 = 0.310, P = 0.002) and PDK2 protein ( r2 = 0.229, P =0.012) are positively correlated with muscle CS activity; and 3) although it is the most abundant isoform, PDP1 protein content only explained ∼18% of the variance in PDP activity ( r2 = 0.184, P = 0.033). In addition, PDP1 in combination with E1α explained ∼38% of the variance in PDP activity ( r2 = 0.383, P = 0.005), suggesting that there may be alternative regulatory mechanisms of this enzyme other than protein content. These data suggest that with higher muscle aerobic capacity (CS activity) there is a greater capacity for carbohydrate oxidation (E1α), in concert with higher potential for PDH activation (PDP activity).

scholarly journals Skeletal muscle mass and the reduction ofV˙o 2 max in trained older subjects

1997 ◽  
Vol 82 (5) ◽  
pp. 1411-1415 ◽  
Author(s):  
David N. Proctor ◽  
Michael J. Joyner
Keyword(s):  
Skeletal Muscle ◽  
Older Women ◽  
Muscle Mass ◽  
Aerobic Capacity ◽  
Skeletal Muscle Mass ◽  
Muscle Blood Flow ◽  
Older Men ◽  
Analysis Of Covariance ◽  
Active Muscle ◽  
Older Subjects

Proctor, David N., and Michael J. Joyner. Skeletal muscle mass and the reduction ofV˙o 2 max in trained older subjects. J. Appl. Physiol.82(5): 1411–1415, 1997.—The role of skeletal muscle mass in the age-associated decline in maximal O2 uptake (V˙o 2 max) is poorly defined because of confounding changes in muscle oxidative capacity and in body fat and the difficulty of quantifying active muscle mass during exercise. We attempted to clarify these issues by examining the relationship between several indexes of muscle mass, as estimated by using dual-energy X-ray absorptiometry and treadmillV˙o 2 max in 32 chronically endurance-trained subjects from four groups ( n = 8/group): young men (20–30 yr), older men (56–72 yr), young women (19–31 yr), and older women (51–72 yr).V˙o 2 max per kilogram body mass was 26 and 22% lower in the older men (45.9 vs. 62.0 ml ⋅ kg−1 ⋅ min−1) and older women (40.0 vs. 51.5 ml ⋅ kg−1 ⋅ min−1). These age differences were reduced to 14 and 13%, respectively, whenV˙o 2 max was expressed per kilogram of appendicular muscle. When appropriately adjusted for age and gender differences in appendicular muscle mass by analysis of covariance, whole bodyV˙o 2 max was 0.50 ± 0.09 l/min less ( P < 0.001) in the older subjects. This effect was similar in both genders. These findings suggest that the reducedV˙o 2 max seen in highly trained older men and women relative to their younger counterparts is due, in part, to a reduced aerobic capacity per kilogram of active muscle independent of age-associated changes in body composition, i.e., replacement of muscle tissue by fat. Because skeletal muscle adaptations to endurance training can be well maintained in older subjects, the reduced aerobic capacity per kilogram of muscle likely results from age-associated reductions in maximal O2 delivery (cardiac output and/or muscle blood flow).

scholarly journals Low intrinsic running capacity is associated with reduced skeletal muscle substrate oxidation and lower mitochondrial content in white skeletal muscle

2011 ◽  
Vol 300 (4) ◽  
pp. R835-R843 ◽  
Author(s):  
Donato A. Rivas ◽  
Sarah J. Lessard ◽  
Misato Saito ◽  
Anna M. Friedhuber ◽  
Lauren G. Koch ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Aerobic Capacity ◽  
Artificial Selection ◽  
White Muscle ◽  
Metabolic Diseases ◽  
Metabolic Health ◽  
Mitochondrial Content ◽  
Red Muscle ◽  
Selection For

Chronic metabolic diseases develop from the complex interaction of environmental and genetic factors, although the extent to which each contributes to these disorders is unknown. Here, we test the hypothesis that artificial selection for low intrinsic aerobic running capacity is associated with reduced skeletal muscle metabolism and impaired metabolic health. Rat models for low- (LCR) and high- (HCR) intrinsic running capacity were derived from genetically heterogeneous N:NIH stock for 20 generations. Artificial selection produced a 530% difference in running capacity between LCR/HCR, which was associated with significant functional differences in glucose and lipid handling by skeletal muscle, as assessed by hindlimb perfusion. LCR had reduced rates of skeletal muscle glucose uptake (∼30%; P = 0.04), glucose oxidation (∼50%; P = 0.04), and lipid oxidation (∼40%; P = 0.02). Artificial selection for low aerobic capacity was also linked with reduced molecular signaling, decreased muscle glycogen, and triglyceride storage, and a lower mitochondrial content in skeletal muscle, with the most profound changes to these parameters evident in white rather than red muscle. We show that a low intrinsic aerobic running capacity confers reduced insulin sensitivity in skeletal muscle and is associated with impaired markers of metabolic health compared with high intrinsic running capacity. Furthermore, selection for high running capacity, in the absence of exercise training, endows increased skeletal muscle insulin sensitivity and oxidative capacity in specifically white muscle rather than red muscle. These data provide evidence that differences in white muscle may have a role in the divergent aerobic capacity observed in this generation of LCR/HCR.

Fine Structure of Aging Skeletal Muscle

1981 ◽  
pp. 333-346 ◽  
Author(s):  
S. A. Shafiq ◽  
S. Lewis ◽  
B. Leung ◽  
H. S. Schutta
Keyword(s):  
Skeletal Muscle ◽  
Fine Structure

Mean myoglobin oxygen tension during exercise at maximal oxygen uptake

1975 ◽  
Vol 39 (1) ◽  
pp. 135-144 ◽  
Author(s):  
B. J. Clark ◽  
R. F. Coburn
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Uptake ◽  
Aerobic Capacity ◽  
Maximal Oxygen Uptake ◽  
Bicycle Ergometer ◽  
Limiting Factors ◽  
Considerable Variability ◽  
Vo2 Max ◽  
The Subject ◽  
Total Body

Changes in intracellular Po2 in myoglobin containing skeletal muscle during exercise were estimated in normal nonathlete subjects from measurements of shifts of CO between blood and muscle under conditions where the total body CO stores remained constant. Exercise was performed on a bicycle ergometer. In 1.5–2 and 6–7 min runs at Vo2 max with the subject breathing 21% O2, mean MbCO/HbCO increased 146 +/- 7 and 163 +/- 11% of resting values, respectively (P less than 0.05). With the subjects breathing 13–14% O2, in 1.5–2 and 6–7 min runs, Vo2 max fell an average of 4.3 +/- 5.1% and 12.0 +/- 5.2%, respectively, and mean MbCO/HbCO increased to 233 +/- 18% and 210 +/- 52% of resting value, respectively (P less than 0.05). These findings suggest that mean myoglobin Po2 fell during exercise at Vo2 max, with the subjects breathing 21% O2 and the decrease in mean myoglobin Po2 was greater with the subject breathing 13–14% O2. There was considerable variability in different subjects and in some, the data were not consistent with intracellular O2 availability limiting aerobic metabolism. The data support a postulate that there are several limiting factors for the aerobic capacity, including intracellular O2 availability.

scholarly journals Progressive exercise training improves maximal aerobic capacity in individuals with well-healed burn injuries

2019 ◽  
Vol 317 (4) ◽  
pp. R563-R570 ◽  
Author(s):  
Steven A. Romero ◽  
Gilbert Moralez ◽  
Manall F. Jaffery ◽  
Mu Huang ◽  
Matthew N. Cramer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Surface Area ◽  
Body Surface Area ◽  
Aerobic Capacity ◽  
Body Surface ◽  
Burn Injuries ◽  
Maximal Aerobic Capacity ◽  
Area Burned ◽  
Progressive Exercise

Long-term rehabilitative strategies are important for individuals with well-healed burn injuries. Such information is particularly critical because patients are routinely surviving severe burn injuries given medical advances in the acute care setting. The purpose of this study was to test the hypothesis that a 6-mo community-based exercise training program will increase maximal aerobic capacity (V̇o2max) in subjects with prior burn injuries, with the extent of that increase influenced by the severity of the burn injury (i.e., percent body surface area burned). Maximal aerobic capacity (indirect calorimetry) and skeletal muscle oxidative enzyme activity (biopsy of the vastus lateralis muscle) were measured pre- and postexercise training in noninjured control subjects ( n = 11) and in individuals with well-healed burn injuries ( n = 13, moderate body surface area burned; n = 20, high body surface area burned). Exercise training increased V̇o2max in all groups (control: 15 ± 5%; moderate body surface area: 11 ± 3%; high body surface area: 11 ± 2%; P < 0.05), though the magnitude of this improvement did not differ between groups ( P = 0.7). Exercise training also increased the activity of the skeletal muscle oxidative enzymes citrate synthase ( P < 0.05) and cytochrome c oxidase ( P < 0.05), an effect that did not differ between groups ( P = 0.2). These data suggest that 6 mo of progressive exercise training improves V̇o2max in individuals with burn injuries and that the magnitude of body surface area burned does not lessen this adaptive response.

scholarly journals Human skeletal muscle mitochondrial dynamics in relation to oxidative capacity and insulin sensitivity

Diabetologia ◽  
2020 ◽  
Author(s):  
Alexandre Houzelle ◽  
Johanna A. Jörgensen ◽  
Gert Schaart ◽  
Sabine Daemen ◽  
Nynke van Polanen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Quality Control ◽  
Insulin Sensitivity ◽  
Aerobic Capacity ◽  
Mitochondrial Dynamics ◽  
Oxidative Capacity ◽  
Protein Balance ◽  
Diabetes Patients

Abstract Aims/hypothesis Mitochondria operate in networks, adapting to external stresses and changes in cellular metabolic demand and are subject to various quality control mechanisms. On the basis of these traits, we here hypothesise that the regulation of mitochondrial networks in skeletal muscle is hampered in humans with compromised oxidative capacity and insulin sensitivity. Methods In a cross-sectional design, we compared four groups of participants (selected from previous studies) ranging in aerobic capacity and insulin sensitivity, i.e. participants with type 2 diabetes (n = 11), obese participants without diabetes (n = 12), lean individuals (n = 10) and endurance-trained athletes (n = 12); basal, overnight fasted muscle biopsies were newly analysed for the current study and we compared the levels of essential mitochondrial dynamics and quality control regulatory proteins in skeletal muscle tissue. Results Type 2 diabetes patients and obese participants were older than lean participants and athletes (58.6 ± 4.0 and 56.7 ± 7.2 vs 21.8 ± 2.5 and 25.1 ± 4.3 years, p < 0.001, respectively) and displayed a higher BMI (32.4 ± 3.7 and 31.0 ± 3.7 vs 22.1 ± 1.8 and 21.0 ± 1.5 kg/m2, p < 0.001, respectively) than lean individuals and endurance-trained athletes. Fission protein 1 (FIS1) and optic atrophy protein 1 (OPA1) protein content was highest in muscle from athletes and lowest in participants with type 2 diabetes and obesity, respectively (FIS1: 1.86 ± 0.79 vs 0.79 ± 0.51 AU, p = 0.002; and OPA1: 1.55 ± 0.64 vs 0.76 ± 0.52 AU, p = 0.014), which coincided with mitochondrial network fragmentation in individuals with type 2 diabetes, as assessed by confocal microscopy in a subset of type 2 diabetes patients vs endurance-trained athletes (n = 6). Furthermore, lean individuals and athletes displayed a mitonuclear protein balance that was different from obese participants and those with type 2 diabetes. Mitonuclear protein balance also associated with heat shock protein 60 (HSP60) protein levels, which were higher in athletes when compared with participants with obesity (p = 0.048) and type 2 diabetes (p = 0.002), indicative for activation of the mitochondrial unfolded protein response. Finally, OPA1, FIS1 and HSP60 correlated positively with aerobic capacity (r = 0.48, p = 0.0001; r = 0.55, p < 0.001 and r = 0.61, p < 0.0001, respectively) and insulin sensitivity (r = 0.40, p = 0.008; r = 0.44, p = 0.003 and r = 0.48, p = 0.001, respectively). Conclusions/interpretation Collectively, our data suggest that mitochondrial dynamics and quality control in skeletal muscle are linked to oxidative capacity in humans, which may play a role in the maintenance of muscle insulin sensitivity. Clinical Trial registry numbers NCT00943059, NCT01298375 and NL1888

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