Skeletal muscle respiratory capacity, endurance, and glycogen utilization

1975 ◽  
Vol 228 (4) ◽  
pp. 1029-1033 ◽  
Author(s):  
RH Fitts ◽  
FW Booth ◽  
WW Winder ◽  
JO Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Treadmill Running ◽  
Mitochondrial Content ◽  
Respiratory Capacity ◽  
Leg Muscles ◽  
Glycogen Utilization ◽  
Exercise Induced ◽  
Gastrocnemius Muscles ◽  
The Relationship

This study was undertaken to evaluate the relationship between physical performance capacity and the mitochondrial content of skeletal muscle. Four groups of rats were trained by means of treadmill running 5 days/wk for 13 wk. One group ran 10 min/day, a second group ran 30 min/day, a third group ran 60 min/day, and a fourth group ran 120 min/day. The magnitude of the exercise-induced adaptive increase in gastrocnemius muscle respiratory capacity varied over a twofold range in the four groups. There were significant correlations between the levels of three mitochondrial markers (cytochrome c, citrate synthase, respiratory capacity) in the animals' gastrocnemius muscles and the duration of a run to exhaustion. There was also a significant correlation between the amounts of glycogen remaining in liver and skeletal muscle after a 30-min-long exercise test and the respiratory capacity of the animal's leg muscles. These findings are compatible with the interpretation that a close relationshiop exists between skeletal muscle mitochondrial content and the capacity to perform endurance exercise.

Muscle respiratory capacity and VO2 max in identically trained young and old rats

1987 ◽  
Vol 63 (1) ◽  
pp. 257-261 ◽  
Author(s):  
G. D. Cartee ◽  
R. P. Farrar
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Treadmill Running ◽  
Whole Body ◽  
Vo2 Max ◽  
Respiratory Enzymes ◽  
Respiratory Capacity ◽  
Palmitate Oxidation ◽  
Age Related ◽  
Old Rats

Old rats have a decreased hindlimb muscle respiratory capacity and whole-body maximal O2 consumption (VO2 max). The decline in spontaneous physical activity in old rats might contribute to these age-related changes. The magnitude of the age-related decline is not uniform in all skeletal muscle respiratory enzymes, and the decrease in palmitate oxidation is particularly great. This study was designed to determine if young and old rats subjected to the same exercise-training protocol would attain similar values for VO2 max and several markers of muscle respiratory capacity. Four- and 18-mo-old Fischer 344 rats underwent an identical 6-mo program of treadmill running. After training, both age groups had increased VO2 max above sedentary age-matched controls. However, the old trained rats had a lower VO2 max than identically trained young rats. In contrast to VO2 max, the two trained groups attained similar values for gastrocnemius citrate synthase, cytochrome oxidase, 3-hydroxyacyl-CoA dehydrogenase, palmitate oxidation, and total carnitine concentration. Thus, when the young and old rats performed an identical exercise protocol within the capacity of the old animals, differences in skeletal muscle respiratory capacity were eliminated. The dissimilarity in VO2 max between the identically trained groups was apparently caused by age-related differences in factors other than muscle respiratory capacity.

PGC-1α's relationship with skeletal muscle palmitate oxidation is not present with obesity despite maintained PGC-1α and PGC-1β protein

2008 ◽  
Vol 294 (6) ◽  
pp. E1060-E1069 ◽  
Author(s):  
Graham P. Holloway ◽  
Christopher G. R. Perry ◽  
A. Brianne Thrush ◽  
George J. F. Heigenhauser ◽  
David J. Dyck ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Transcription Factors ◽  
Network Formation ◽  
Citrate Synthase ◽  
Acid Oxidation ◽  
Mitochondrial Content ◽  
Palmitate Oxidation ◽  
Mitofusin 1 ◽  
The Relationship

Reduced skeletal muscle mitochondrial content and fatty acid oxidation are associated with obesity and insulin resistance. Although the exact mechanisms remain elusive, this may result from impaired mitochondrial biogenesis or reductions in the mitochondrial reticulum network. Therefore, the purpose of this study was to determine whether the protein contents of various transcription factors, including PGC-1α and PGC-1β and proteins associated with mitochondrial fusion events, were reduced in skeletal muscle of nine obese (BMI = 37.6 ± 2.2 kg/m−2) compared with nine age-matched lean (BMI = 23.3 ± 0.7 kg/m−2) women. The protein contents of PGC-1α, PGC-1β, PPARα, and tFAM were not reduced with obesity. In contrast, PPARγ was increased (+22%, P < 0.05) with obesity, and there was a trend toward an increase (+31%, P = 0.13) in PPARδ/β. In lean individuals, PGC-1α protein correlated with citrate synthase (CS; r = 0.67) and rates of palmitate oxidation ( r = 0.87), whereas PGC-1β correlated with PPARγ ( r = 0.90), PPARδ/β ( r = 0.63), and cytochrome c oxidase IV (COX-IV; r = 0.63). In obese individuals, the relationship between PGC-1α and CS was maintained ( r = 0.65); however, the associations between PGC-1α and palmitate oxidation ( r = −0.38) and PGC-1β with PPARγ ( r = 0.14), PPARδ/β ( r = 0.21), and COX-IV ( r = 0.01) were lost. In addition, mitofusin-1 (MFN-1), MFN-2, and dynamin-related protein-1 (DRP-1) total protein contents were not altered with obesity ( P > 0.05). These data suggest that altered regulation, and not reductions in the protein contents of transcription factors, is associated with insulin resistance. Also, it does not appear that alterations in the proteins associated with mitochondrial network formation and degradation can account for the observed decrease in mitochondrial content.

scholarly journals Atorvastatin impairs liver mitochondrial function in obese Göttingen Minipigs but heart and skeletal muscle are not affected

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Liselotte Bruun Christiansen ◽  
Tine Lovsø Dohlmann ◽  
Trine Pagh Ludvigsen ◽  
Ewa Parfieniuk ◽  
Michal Ciborowski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Obese Group ◽  
Control Group ◽  
Dependent Manner ◽  
Respiratory Capacity ◽  
Protein Carbonyl Content ◽  
Functional Changes ◽  
Mitochondrial Respiratory

AbstractStatins lower the risk of cardiovascular events but have been associated with mitochondrial functional changes in a tissue-dependent manner. We investigated tissue-specific modifications of mitochondrial function in liver, heart and skeletal muscle mediated by chronic statin therapy in a Göttingen Minipig model. We hypothesized that statins enhance the mitochondrial function in heart but impair skeletal muscle and liver mitochondria. Mitochondrial respiratory capacities, citrate synthase activity, coenzyme Q10 concentrations and protein carbonyl content (PCC) were analyzed in samples of liver, heart and skeletal muscle from three groups of Göttingen Minipigs: a lean control group (CON, n = 6), an obese group (HFD, n = 7) and an obese group treated with atorvastatin for 28 weeks (HFD + ATO, n = 7). Atorvastatin concentrations were analyzed in each of the three tissues and in plasma from the Göttingen Minipigs. In treated minipigs, atorvastatin was detected in the liver and in plasma. A significant reduction in complex I + II-supported mitochondrial respiratory capacity was seen in liver of HFD + ATO compared to HFD (P = 0.022). Opposite directed but insignificant modifications of mitochondrial respiratory capacity were seen in heart versus skeletal muscle in HFD + ATO compared to the HFD group. In heart muscle, the HFD + ATO had significantly higher PCC compared to the HFD group (P = 0.0323). In the HFD group relative to CON, liver mitochondrial respiration decreased whereas in skeletal muscle, respiration increased but these changes were insignificant when normalizing for mitochondrial content. Oral atorvastatin treatment in Göttingen Minipigs is associated with a reduced mitochondrial respiratory capacity in the liver that may be linked to increased content of atorvastatin in this organ.

Muscle blood flow during exercise in sedentary and trained hypothyroid rats

1995 ◽  
Vol 269 (6) ◽  
pp. H1949-H1954 ◽  
Author(s):  
R. M. McAllister ◽  
M. D. Delp ◽  
K. A. Thayer ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Muscle Blood Flow ◽  
Treadmill Running ◽  
Exercise Intolerance ◽  
Vastus Lateralis Muscle ◽  
Blood Flows ◽  
Vastus Intermedius

Hypothyroidism is characterized by exercise intolerance. We hypothesized that active muscle blood flow during in vivo exercise is inadequate in the hypothyroid state. Additionally, we hypothesized that endurance exercise training would restore normal blood flow during acute exercise. To test these hypotheses, rats were made hypothyroid (Hypo) over 3-4 mo with propylthiouracil. A subset of Hypo rats was trained (THypo) on a treadmill at 30 m/min (15% grade) for 60 min/day 5 days/wk over 10-15 wk. Hypothyroidism was evidenced by approximately 80% reductions in plasma triiodothyronine levels in Hypo and THypo and by 40-50% reductions in citrate synthase activities in high oxidative muscles in Hypo compared with euthyroid (Eut) rats. Training efficacy was indicated by increased (25-100%) citrate synthase activities in muscles of THypo vs. Hypo. Regional blood flows were determined by the radiolabeled microsphere method before exercise and at 1-2 min of treadmill running at 15 m/min (0% grade). Preexercise muscle blood flows were generally similar among groups. During exercise, however, flows were lower in Hypo than in Eut for high oxidative muscles such as the red section of vastus lateralis [277 +/- 24 and 153 +/- 13 (SE) ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01] and vastus intermedius (317 +/- 32 and 187 +/- 20 ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01) muscles. Training (THypo) did not normalize these flows (168 +/- 24 and 181 +/- 24 ml.min-1.100 g-1 for red section of vastus lateralis and vastus intermedius muscles, respectively). Blood flows to low oxidative muscle, such as the white section of vastus lateralis muscle, were similar among groups (21 +/- 5, 25 +/- 4, and 34 +/- 7 ml.min-1.100 g-1 for Eut, Hypo, and THypo, respectively; P = NS). These findings indicate that hypothyroidism is associated with reduced blood flow to skeletal muscle during exercise, suggesting that impaired delivery of nutrients to and/or removal of metabolites from skeletal muscle contributes to the poor exercise tolerance characteristic of hypothyroidism.

IL-6 is not essential for exercise-induced increases in glucose uptake

2013 ◽  
Vol 114 (9) ◽  
pp. 1151-1157 ◽  
Author(s):  
Hayley M. O'Neill ◽  
Rengasamy Palanivel ◽  
David C. Wright ◽  
Tara MacDonald ◽  
James S. Lally ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Steady State ◽  
Glucose Uptake ◽  
Substrate Utilization ◽  
Treadmill Running ◽  
Glucose Clearance ◽  
Skeletal Muscle Glucose Uptake ◽  
Exercise Induced ◽  
Similar Body

Interleukin-6 (IL-6) increases glucose uptake in resting skeletal muscle. IL-6 is released from skeletal muscle during exercise; however; it is not known whether this IL-6 response is important for exercise-induced increases in skeletal muscle glucose uptake. We report that IL-6 knockout (KO) mice, 4 mo of age, have similar body weight to wild-type (WT), and, under resting conditions, oxygen consumption, food intake, substrate utilization, glucose tolerance, and insulin sensitivity are not different. Maximal exercise capacity is also similar to WT. We investigated substrate utilization and glucose clearance in vivo during steady-state treadmill running at 70% of maximal running speed and found that WT and IL-6 KO mice had similar rates of substrate utilization, muscle glucose clearance, and phosphorylation of AMP-activated protein kinase T172. These data provide evidence that IL-6 does not play a major role in regulating substrate utilization or skeletal muscle glucose uptake during steady-state endurance exercise.

scholarly journals Divergent skeletal muscle respiratory capacities in rats artificially selected for high and low running ability: a role for Nor1?

2012 ◽  
Vol 113 (9) ◽  
pp. 1403-1412 ◽  
Author(s):  
Erin J. Stephenson ◽  
Nigel K. Stepto ◽  
Lauren G. Koch ◽  
Steven L. Britton ◽  
John A. Hawley
Keyword(s):  
Skeletal Muscle ◽  
Metabolic Regulation ◽  
Citrate Synthase ◽  
Uncoupling Protein ◽  
Serum Insulin ◽  
Orphan Receptor ◽  
Western Society ◽  
Orphan Nuclear Receptor ◽  
Respiratory Capacity ◽  
Relative Contribution

Inactivity-related diseases are becoming a huge burden on Western society. While there is a major environmental contribution to metabolic health, the intrinsic properties that predispose or protect against particular health traits are harder to define. We used rat models of inborn high running capacity (HCR) and low running capacity (LCR) to determine inherent differences in mitochondrial volume and function, hypothesizing that HCR rats would have greater skeletal muscle respiratory capacity due to an increase in mitochondrial number. Additionally, we sought to determine if there was a link between the expression of the orphan nuclear receptor neuron-derived orphan receptor (Nor)1, a regulator of oxidative metabolism, and inherent skeletal muscle respiratory capacity. LCR rats were 28% heavier ( P < 0.0001), and fasting serum insulin concentrations were 62% greater than in HCR rats ( P = 0.02). In contrast, HCR rats had better glucose tolerance and reduced adiposity. In the primarily oxidative soleus muscle, maximal respiratory capacity was 21% greater in HCR rats ( P = 0.001), for which the relative contribution of fat oxidation was 20% higher than in LCR rats ( P = 0.02). This was associated with increased citrate synthase (CS; 33%, P = 0.009) and β-hydroxyacyl-CoA (β-HAD; 33%, P = 0.0003) activities. In the primarily glycolytic extensor digitum longus muscle, CS activity was 29% greater ( P = 0.01) and β-HAD activity was 41% ( P = 0.0004) greater in HCR rats compared with LCR rats. Mitochondrial DNA copy numbers were also elevated in the extensor digitum longus muscles of HCR rats (35%, P = 0.049) and in soleus muscles (44%, P = 0.16). Additionally, HCR rats had increased protein expression of individual mitochondrial respiratory complexes, CS, and uncoupling protein 3 in both muscle types (all P < 0.05). In both muscles, Nor1 protein was greater in HCR rats compared with LCR rats ( P < 0.05). We propose that the differential expression of Nor1 may contribute to the differences in metabolic regulation between LCR and HCR phenotypes.

Adaptations of skeletal muscle to endurance exercise and their metabolic consequences

1984 ◽  
Vol 56 (4) ◽  
pp. 831-838 ◽  
Author(s):  
J. O. Holloszy ◽  
E. F. Coyle
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Muscle Glycogen ◽  
Lactate Production ◽  
Strenuous Exercise ◽  
Mitochondrial Content ◽  
Respiratory Capacity ◽  
Endurance Exercise Training

Regularly performed endurance exercise induces major adaptations in skeletal muscle. These include increases in the mitochondrial content and respiratory capacity of the muscle fibers. As a consequence of the increase in mitochondria, exercise of the same intensity results in a disturbance in homeostasis that is smaller in trained than in untrained muscles. The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity. These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.

Mitochondrial Protein Content and in Vivo Synthesis Rates in Skeletal Muscle from Critically Ill Rats

1996 ◽  
Vol 91 (4) ◽  
pp. 475-481 ◽  
Author(s):  
Olav E. Rooyackers ◽  
Alexande R H. Kersten ◽  
Anton J. M. Wagenmakers
Keyword(s):  
Skeletal Muscle ◽  
Critical Illness ◽  
Cytochrome C ◽  
Protein Content ◽  
Cytochrome C Oxidase ◽  
Citrate Synthase ◽  
Mitochondrial Protein ◽  
Substantial Reduction ◽  
Mitochondrial Content

1. Recently we reported decreased activities of two mitochondrial marker enzymes (citrate synthase and cytochrome c oxidase) in skeletal muscle from a rat model of critical illness (zymosan injection). In the present study we investigated (i) whether these decreases in enzyme activity reflect a reduction in mitochondrial content and (ii) whether this potential reduction in mitochondrial content was the result of decreased mitochondrial protein synthesis rates. 2. Mitochondrial protein content was calculated from the activities of cytochrome c oxidase in whole-muscle homogenates and purified mitochondria. Synthesis rates of mitochondrial protein in vivo were studied by measuring the incorporation of [3H]phenylalanine into mitochondrial protein using the flooding dose technique. 3. Mitochondrial protein content was reduced to 54% of that measured in the pair-fed rats and to 71% of that measured in control rats fed ad libitum 2 days after the zymosan treatment The decreased mitochondrial protein content observed 2 days after zymosan challenge was preceded by a reduced rate of synthesis of mitochondrial protein 16 h after treatment. Both changes were of greater magnitude than the general muscle wasting and the decreased rate of synthesis of mixed protein observed in the zymosan-treated rats. 4. We conclude that the acute phase of critical illness in zymosan-treated rats is characterized by a substantial reduction in muscle mitochondria that is at least in part caused by a decreased rate of synthesis of mitochondrial protein. This derangement in mitochondrial protein metabolism may be related to the impaired muscle function observed during and after critical illness.

Effects of hyperthyroidism on muscle blood flow during exercise in rats

1995 ◽  
Vol 268 (1) ◽  
pp. H330-H335 ◽  
Author(s):  
R. M. McAllister ◽  
J. C. Sansone ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Citrate Synthase ◽  
Muscle Blood Flow ◽  
Left Ventricular ◽  
Submaximal Exercise ◽  
Treadmill Running ◽  
Exercise Intolerance ◽  
Blood Flows

Hyperthyroidism is associated with exercise intolerance. Previous research, however, has shown that cardiac output is either normal or enhanced during exercise in the hyperthyroid state. We therefore hypothesized that blood flow to working skeletal muscle is augmented in hyperthyroid animals during in vivo submaximal exercise and, consequently, that noncardiovascular factors are responsible for intolerance to exercise. To test this hypothesis, rats were made hyperthyroid (Hyper) over 6–12 wk with injections of triiodothyronine (300 micrograms/kg). Hyperthyroidism was evidenced by left ventricular hypertrophy [euthyroid (Eut), 2.12 +/- 0.05 mg/g body wt; Hyper, 2.78 +/- 0.06; P < 0.005], 25–60% increases in citrate synthase activities in Hyper hindlimb muscles over those of Eut rats, and higher preexercise heart rates (Eut, 415 +/- 18 beats/min; Hyper, 479 +/- 19; P < 0.025). Regional blood flows were determined by the radiolabeled microsphere method, preexercise, and at 1–2 min of treadmill running at 15 m/min (0% grade). Total hindlimb muscle blood flow preexercise was unaffected (Eut, 31 +/- 4 ml.min-1.(100) g-1, n = 11; Hyper, 40 +/- 6, n = 9; not significant) but was higher (P < 0.025) in Hyper (127 +/- 17, n = 9) compared with Eut (72 +/- 11, n = 9) during treadmill running. During exercise, flows to individual muscles and muscle sections were approximately 50–150% higher in Hyper compared with Eut rats. Visceral blood flows were largely similar between groups. These findings indicate that hyperthyroidism is associated with augmented blood flow to skeletal muscle during submaximal exercise. Thus hypoperfusion of skeletal muscle does not account for the poor exercise tolerance characteristic of hyperthyroidism.

Skeletal muscle respiratory capacity is enhanced in rats consuming an obesogenic Western diet

2012 ◽  
Vol 302 (12) ◽  
pp. E1541-E1549 ◽  
Author(s):  
Erin J. Stephenson ◽  
Donny M. Camera ◽  
Trisha A. Jenkins ◽  
Sepideh Kosari ◽  
Jong Sam Lee ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Energy Demand ◽  
Citrate Synthase ◽  
Blood Glucose Concentration ◽  
Control Diet ◽  
Fasting Blood Glucose ◽  
Western Diet ◽  
Mitochondrial Enzymes ◽  
Serum Triglycerides ◽  
Respiratory Capacity

Obesity-induced lipid oversupply promotes skeletal muscle mitochondrial biogenesis. Previous investigations have utilized extreme high-fat diets (HFD) to induce such mitochondrial perturbations despite their disparity from human obesogenic diets. Here, we evaluate the effects of Western diet (WD)-induced obesity on skeletal muscle mitochondrial function. Long-Evans rats were given ad libitum access to either a WD [40% energy (E) from fat, 17% protein, and 43% carbohydrate (30% sucrose); n = 12] or a control diet (CON; 16% of E from fat, 21% protein, and 63% carbohydrate; n = 12) for 12 wk. Rats fed the WD consumed 23% more E than CON ( P = 0.0001), which was associated with greater increases in body mass (23%, P = 0.0002) and adiposity (17%, P = 0.03). There were no differences in fasting blood glucose concentration or glucose tolerance between diets, although fasting insulin was increased by 40% ( P = 0.007). Fasting serum triglycerides were also elevated in WD (86%, P = 0.001). The maximal capacity of the electron transfer system was greater following WD (37%, P = 0.02), as were the maximal activities of several mitochondrial enzymes (citrate synthase, β-hydroxyacyl-CoA dehydrogenase, carnitine palmitoyltransferase). Protein expression of citrate synthase, UCP3, and individual respiratory complexes was greater after WD ( P < 0.05) despite no differences in the expression of peroxisome proliferator-activated receptor (PPAR)α, PPARδ, or PPARγ coactivator-1 mRNA or protein abundance. We conclude that the respiratory capacity of skeletal muscle is enhanced in response to the excess energy supplied by a WD. This is likely due to an increase in mitochondrial density, which at least in the short term, and in the absence of increased energy demand, may protect the tissue from lipid-induced impairments in glycemic control.

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