scholarly journals Temperament influences mitochondrial capacity in skeletal muscle from 8 through 18 mo of age in Brahman heifers

2020 ◽  
Vol 98 (10) ◽  
Author(s):  
Randi N Owen ◽  
Christine M Latham ◽  
Charles R Long ◽  
Ronald D Randel ◽  
Thomas H Welsh ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Product Quality ◽  
Repeated Measures ◽  
Complex I ◽  
Citrate Synthase ◽  
Serum Cortisol ◽  
System Capacity ◽  
Complex Ii ◽  
Potential Link ◽  
Muscle Groups

Abstract Temperamental cattle tend to yield carcasses of poorer quality, and Brahman cattle are reportedly more temperamental than non-indicus cattle breeds. A potential link between temperament and product quality may be mitochondrial activity. We hypothesized that mitochondrial measures would be greater in temperamental compared with calm heifers and that the relationships between temperament and mitochondria would persist as heifers age. Serum cortisol and skeletal muscle (longissimus thoracis [LT] and trapezius [TRAP]) mitochondrial profiles and antioxidant activities were quantified from the same calm (n = 6) and temperamental (n = 6) Brahman heifers at 8, 12, and 18 mo of age. Data were analyzed using a mixed model ANOVA in SAS (9.4) with repeated measures. Serum cortisol was greater in temperamental compared with calm heifers throughout the study (P = 0.02). Mitochondrial volume density (citrate synthase [CS] activity) increased over time (P < 0.0001) but was similar between temperament and muscle groups. Mitochondrial function (cytochrome c oxidase activity) was greatest in the temperamental LT at 8 mo of age (P ≤ 0.0006), greatest in the temperamental TRAP at 18 mo of age (P ≤ 0.003), and did not differ by temperament at 12 mo of age. Integrative (relative to tissue wet weight) mitochondrial oxidative phosphorylation capacity with complex I substrates (PCI), PCI plus complex II substrate (PCI+II), noncoupled electron transfer system capacity (ECI+II), and E with functional complex II only (ECII) were greater in the TRAP than LT for calm heifers at all ages (P ≤ 0.002), but were similar between muscle groups in temperamental heifers. Overall, calm heifers tended to have greater intrinsic (relative to CS activity) PCI and flux control of PCI+II (P ≤ 0.1) than temperamental heifers, indicating greater utilization of complex I paired with greater coupling efficiency in calm heifers. Within the LT, integrative PCI+II was greater (P = 0.05) and ECI+II tended to be greater (P = 0.06) in temperamental compared with calm heifers. From 8- to 18-mo old, glutathione peroxidase (GPx) activity decreased (P < 0.0001) and superoxide dismutase activity increased (P = 0.02), and both were similar between muscle groups. The activity of GPx was greater in temperamental compared with calm heifers at 8 (P = 0.004) but not at 12 or 18 mo of age. These results detail divergent skeletal muscle mitochondrial characteristics of live Brahman heifers according to temperament, which should be further investigated as a potential link between temperament and product quality.

scholarly journals Enhanced Skeletal Muscle Oxidative Capacity and Capillary-to-Fiber Ratio Following Moderately Increased Testosterone Exposure in Young Healthy Women

2020 ◽  
Vol 11 ◽  
Author(s):  
Daniele A. Cardinale ◽  
Oscar Horwath ◽  
Jona Elings-Knutsson ◽  
Torbjörn Helge ◽  
Manne Godhe ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Complex I ◽  
Citrate Synthase ◽  
Mitochondrial Protein ◽  
Capillary Density ◽  
Oxidative Capacity ◽  
System Capacity ◽  
Endurance Capacity ◽  
Muscle Oxidative Capacity ◽  
Before And After

Background: Recently, it was shown that exogenously administered testosterone enhances endurance capacity in women. In this study, our understanding on the effects of exogenous testosterone on key determinants of oxygen transport and utilization in skeletal muscle is expanded.Methods: In a double-blinded, randomized, placebo-controlled trial, 48 healthy active women were randomized to 10 weeks of daily application of 10 mg of testosterone cream or placebo. Before and after the intervention, VO2 max, body composition, total hemoglobin (Hb) mass and blood volumes were assessed. Biopsies from the vastus lateralis muscle were obtained before and after the intervention to assess mitochondrial protein abundance, capillary density, capillary-to-fiber (C/F) ratio, and skeletal muscle oxidative capacity.Results: Maximal oxygen consumption per muscle mass, Hb mass, blood, plasma and red blood cell volumes, capillary density, and the abundance of mitochondrial protein levels (i.e., citrate synthase, complexes I, II, III, IV-subunit 2, IV-subunit 4, and V) were unchanged by the intervention. However, the C/F ratio, specific mitochondrial respiratory flux activating complex I and linked complex I and II, uncoupled respiration and electron transport system capacity, but not leak respiration or fat respiration, were significantly increased following testosterone administration compared to placebo.Conclusion: This study provides novel insights into physiological actions of increased testosterone exposure on key determinants of oxygen diffusion and utilization in skeletal muscle of women. Our findings show that higher skeletal muscle oxidative capacity coupled to higher C/F ratio could be major contributing factors that improve endurance performance following moderately increased testosterone exposure.

scholarly journals 108 President Oral Presentation Pick: Select skeletal muscle mitochondrial measures in Thoroughbred weanlings are related to race earnings and sire

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 85-85
Author(s):  
Chloey P Guy ◽  
Christine M Latham ◽  
Randi N Owen ◽  
Ashley L Fowler ◽  
Sarah H White-Springer
Keyword(s):  
Skeletal Muscle ◽  
Complex I ◽  
Fixed Effects ◽  
Linear Models ◽  
Citrate Synthase ◽  
Pearson Correlation ◽  
Gluteus Medius ◽  
Volume Density ◽  
Complex Ii ◽  
And Training

Abstract Quantifiable, cellular differences of individuals are not widely used in breeding and training decisions in the equine industry. Our objective was to determine if mitochondrial parameters in weanling Thoroughbreds were related to sire or lifetime race earnings. We hypothesized that weanling skeletal muscle mitochondrial capacity would be positively correlated with race earnings. Gluteus medius muscle samples were collected from racing-bred Thoroughbred weanlings (n = 139; mean ± SD; 6.0 ± 0.4 mo) from 40 different sires over 3 years at 5 different farms and evaluated for mitochondrial volume density (citrate synthase activity; CS) and function (cytochrome c oxidase activity) by colorimetry, and oxidative (P) and electron transport system (E) capacities by high resolution respirometry; two- and three-year-old race earnings were available for a subset of 13 horses. Data were analyzed using mixed linear models with sire, sex, year of collection, and farm as fixed effects. Correlations between lifetime race earnings and mitochondrial measures were determined using Pearson Correlation Statistics. A main effect of sire was observed for weanling intrinsic (relative to CS activity) P with complex I substrates (P = 0.04) and the contribution of mitochondrial leak to O2 consumption (FCRL; P = 0.04). A trend was observed for the effect of sire on intrinsic mitochondrial leak (P = 0.09). Race earnings were positively correlated with integrated (relative to mg protein) leak (r = 0.7684, P = 0.009) and FCRL (r = 0.7035; P = 0.02). A trend for a negative correlation between E with complex II substrates and race earnings was also observed (r = -0.4775, P = 0.09), No other measures were influenced by sire, nor were correlated with race earnings. Our previous work has indicated a preferential use of complex I in breeds bred for short-duration racing (Thoroughbreds) compared to distance racing breeds (Standardbreds) that relied more heavily on complex II. Mitochondrial measures in weanlings may be utilized to inform future breeding and training decisions in horses.

scholarly journals Skeletal muscle mitochondrial function and exercise capacity are not impaired in mice with knockout of STAT3

2019 ◽  
Vol 127 (4) ◽  
pp. 1117-1127
Author(s):  
Jessica R. Dent ◽  
Byron Hetrick ◽  
Shahriar Tahvilian ◽  
Abha Sathe ◽  
Keenan Greyslak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electron Transport ◽  
Complex I ◽  
Physiological Function ◽  
Oxidative Capacity ◽  
Signal Transducer ◽  
Muscle Mitochondria ◽  
Complex Ii ◽  
Skeletal Muscle Mitochondria ◽  
Transcription 3

Signal transducer and activator of transcription 3 (STAT3) was recently found to be localized to mitochondria in a number of tissues and cell types, where it modulates oxidative phosphorylation via interactions with the electron transport proteins, complex I and complex II. Skeletal muscle is densely populated with mitochondria although whether STAT3 contributes to skeletal muscle oxidative capacity is unknown. In the present study, we sought to elucidate the contribution of STAT3 to mitochondrial and skeletal muscle function by studying mice with muscle-specific knockout of STAT3 (mKO). First, we developed a novel flow cytometry-based approach to confirm that STAT3 is present in skeletal muscle mitochondria. However, contrary to findings in other tissue types, complex I and complex II activity and maximal mitochondrial respiratory capacity in skeletal muscle were comparable between mKO mice and floxed/wild-type littermates. Moreover, there were no genotype differences in endurance exercise performance, skeletal muscle force-generating capacity, or the adaptive response of skeletal muscle to voluntary wheel running. Collectively, although we confirm the presence of STAT3 in skeletal muscle mitochondria, our data establish that STAT3 is dispensable for mitochondrial and physiological function in skeletal muscle. NEW & NOTEWORTHY Whether signal transducer and activator of transcription 3 (STAT3) can regulate the activity of complex I and II of the electron transport chain and mitochondrial oxidative capacity in skeletal muscle, as it can in other tissues, is unknown. By using a mouse model lacking STAT3 in muscle, we demonstrate that skeletal muscle mitochondrial and physiological function, both in vivo and ex vivo, is not impacted by the loss of STAT3.

Possible Pathogenic Mechanism of Propofol Infusion Syndrome Involves Coenzyme Q

2015 ◽  
Vol 122 (2) ◽  
pp. 343-352 ◽  
Author(s):  
Arnaud Vincent Vanlander ◽  
Juergen Guenther Okun ◽  
Annick de Jaeger ◽  
Joél Smet ◽  
Elien De Latter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Respiratory Chain ◽  
Citrate Synthase ◽  
Tissue Concentration ◽  
Electron Flow ◽  
Coenzyme Q ◽  
Propofol Infusion Syndrome ◽  
Complex Ii ◽  
Main Site ◽  
Mitochondrial Fatty Acid

Abstract Background: Propofol is a short-acting intravenous anesthetic agent. In rare conditions, a life-threatening complication known as propofol infusion syndrome can occur. The pathophysiologic mechanism is still unknown. Some studies suggested that propofol acts as uncoupling agent, others suggested that it inhibits complex I or complex IV, or causes increased oxidation of cytochrome c and cytochrome aa3, or inhibits mitochondrial fatty acid metabolism. Although the exact site of interaction is not known, most hypotheses point to the direction of the mitochondria. Methods: Eight rats were ventilated and sedated with propofol up to 20 h. Sequential biopsy specimens were taken from liver and skeletal muscle and used for determination of respiratory chain activities and propofol concentration. Activities were also measured in skeletal muscle from a patient who died of propofol infusion syndrome. Results: In rats, authors detected a decrease in complex II+III activity starting at low tissue concentration of propofol (20 to 25 µM), further declining at higher concentrations. Before starting anesthesia, the complex II+III/citrate synthase activity ratio in liver was 0.46 (0.25) and in skeletal muscle 0.23 (0.05) (mean [SD]). After 20 h of anesthesia, the ratios declined to 0.17 (0.03) and 0.12 (0.02), respectively. When measured individually, the activities of complexes II and III remained normal. Skeletal muscle from one patient taken in the acute phase of propofol infusion syndrome also shows a selective decrease in complex II+III activity (z-score: −2.96). Conclusion: Propofol impedes the electron flow through the respiratory chain and coenzyme Q is the main site of interaction with propofol.

scholarly journals Adaptations in Mitochondrial Enzymatic Activity Occurs Independent of Genomic Dosage in Response to Aerobic Exercise Training and Deconditioning in Human Skeletal Muscle

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 237 ◽  
Author(s):  
Andreas Fritzen ◽  
Frank Thøgersen ◽  
Kasper Thybo ◽  
Christoffer Vissing ◽  
Thomas Krag ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Enzymatic Activity ◽  
Endurance Exercise ◽  
Complex I ◽  
Citrate Synthase ◽  
Knee Extensor ◽  
Mitochondrial Complex ◽  
Membrane Markers ◽  
Endurance Exercise Training

Mitochondrial DNA (mtDNA) replication is thought to be an integral part of exercise-training-induced mitochondrial adaptations. Thus, mtDNA level is often used as an index of mitochondrial adaptations in training studies. We investigated the hypothesis that endurance exercise training-induced mitochondrial enzymatic changes are independent of genomic dosage by studying mtDNA content in skeletal muscle in response to six weeks of knee-extensor exercise training followed by four weeks of deconditioning in one leg, comparing results to the contralateral untrained leg, in 10 healthy, untrained male volunteers. Findings were compared to citrate synthase activity, mitochondrial complex activities, and content of mitochondrial membrane markers (porin and cardiolipin). One-legged knee-extensor exercise increased endurance performance by 120%, which was accompanied by increases in power output and peak oxygen uptake of 49% and 33%, respectively (p < 0.01). Citrate synthase and mitochondrial respiratory chain complex I–IV activities were increased by 51% and 46–61%, respectively, in the trained leg (p < 0.001). Despite a substantial training-induced increase in mitochondrial activity of TCA and ETC enzymes, there was no change in mtDNA and mitochondrial inner and outer membrane markers (i.e. cardiolipin and porin). Conversely, deconditioning reduced endurance capacity by 41%, muscle citrate synthase activity by 32%, and mitochondrial complex I–IV activities by 29–36% (p < 0.05), without any change in mtDNA and porin and cardiolipin content in the previously trained leg. The findings demonstrate that the adaptations in mitochondrial enzymatic activity after aerobic endurance exercise training and the opposite effects of deconditioning are independent of changes in the number of mitochondrial genomes, and likely relate to changes in the rate of transcription of mtDNA.

scholarly journals Mitochondrial dysfunction in adults after out-of-hospital cardiac arrest

2019 ◽  
Vol 9 (4_suppl) ◽  
pp. S138-S144
Author(s):  
Sebastian Wiberg ◽  
Nis Stride ◽  
John Bro-Jeppesen ◽  
Mathias J Holmberg ◽  
Jesper Kjærgaard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Arrest ◽  
Mitochondrial Function ◽  
Complex I ◽  
Targeted Temperature Management ◽  
System Capacity ◽  
Temperature Management ◽  
Healthy Controls ◽  
Muscle Biopsies ◽  
Hospital Cardiac Arrest

Background: While preclinical studies suggest that mitochondria play a pivotal role in ischaemia–reperfusion injury, the knowledge of mitochondrial function in human out-of-hospital cardiac arrest remains scarce. The present study sought to compare oxidative phosphorylation capacity in skeletal muscle biopsies from out-of-hospital cardiac arrest patients to healthy controls. Methods: This was a substudy of a randomised trial comparing targeted temperature management at 33°C versus 36°C for out-of-hospital cardiac arrest patients. Skeletal muscle biopsies were obtained from adult resuscitated comatose out-of-hospital cardiac arrest patients 28 hours after initiation of targeted temperature management, i.e. at target temperature prior to rewarming, and from age-matched healthy controls. Mitochondrial function was analysed by high-resolution respirometry. Maximal sustained respiration through complex I, maximal coupled respiration through complex I and complex II and maximal electron transport system capacity was compared. Results: A total of 20 out-of-hospital cardiac arrest patients and 21 controls were included in the analysis. We found no difference in mitochondrial function between temperature allocations. We found no difference in complex I sustained respiration between out-of-hospital cardiac arrest and controls (23 (18–26) vs. 22 (19–26) pmol O2/mg/s, P=0.76), whereas coupled complex I and complex II respiration was significantly lower in out-of-hospital cardiac arrest patients versus controls (53 (42–59) vs. 64 (54–68) pmol O2/mg/s, P=0.01). Furthermore, electron transport system capacity was lower in out-of-hospital cardiac arrest versus controls (63 (51–69) vs. 73 (66–78) pmol O2/mg/s, P=0.005). Conclusions: Mitochondrial oxidative phosphorylation capacity in skeletal muscle biopsies was reduced in out-of-hospital cardiac arrest patients undergoing targeted temperature management compared to age-matched, healthy controls. The role of mitochondria as risk markers and potential targets for post-resuscitation care remains unknown.

Effect of hyperthermia and acidosis on equine skeletal muscle mitochondrial oxygen consumption

2020 ◽  
pp. 1-10
Author(s):  
M.S. Davis ◽  
M.R. Fulton ◽  
A. Popken
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Oxidative Phosphorylation ◽  
Muscle Fatigue ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Complex I ◽  
Mitochondrial Oxygen Consumption ◽  
Biochemical Basis ◽  
Complex Ii

The skeletal muscle of exercising horses develops pronounced hyperthermia and acidosis during strenuous or prolonged exercise, with very high tissue temperature and low pH associated with muscle fatigue or damage. The purpose of this study was to evaluate the individual effects of physiologically relevant hyperthermia and acidosis on equine skeletal muscle mitochondrial function, using ex vivo measurement of oxygen consumption to assess the function of different mitochondrial elements. Fresh triceps muscle biopsies from 6 healthy unfit Thoroughbred geldings were permeabilised to permit diffusion of small molecular weight substrates through the sarcolemma and analysed in a high resolution respirometer at 38, 40, 42, and 44 °C, and pH=7.1, 6.5, and 6.1. Oxygen consumption was measured under conditions of non-phosphorylating (leak) respiration and phosphorylating respiration through Complex I and Complex II. Data were analysed using a one-way repeated measures ANOVA and data are expressed as mean ± standard deviation. Leak respiration was ~3-fold higher at 44 °C compared to 38 °C regardless of electron source (Complex I: 22.88±3.05 vs 8.08±1.92 pmol O2/mg/s), P=0.002; Complex II: 79.14±23.72 vs 21.43±11.08 pmol O2/mg/s, P=0.022), resulting in a decrease in efficiency of oxidative phosphorylation. Acidosis had minimal effect on mitochondrial respiration at pH=6.5, but pH=6.1 resulted in a 50% decrease in mitochondrial oxygen consumption. These results suggest that skeletal muscle hyperthermia decreases the efficiency of oxidative phosphorylation through increased leak respiration, thus providing a specific biochemical basis for hyperthermia-induced muscle fatigue. The effect of myocellular acidosis on mitochondrial respiration was minimal under typical levels of acidosis, but atypically severe acidosis can lead to impairment of mitochondrial function.

scholarly journals RAPID COMMUNICATION: Differential skeletal muscle mitochondrial characteristics of weanling racing-bred horses1

2019 ◽  
Vol 97 (8) ◽  
pp. 3193-3198 ◽  
Author(s):  
Christine M Latham ◽  
Clara K Fenger ◽  
Sarah H White
Keyword(s):  
Skeletal Muscle ◽  
Electron Transport ◽  
Transport System ◽  
Complex I ◽  
Management Practices ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Gluteus Medius ◽  
Electron Transport System ◽  
Mitochondrial Density

Abstract Responses of equine skeletal muscle characteristics to growth and training have been shown to differ between breeds. These differential responses may arise in part because muscle fiber type and mitochondrial density differ between breeds, even in untrained racing-bred horses. However, it is not known when these breed-specific differences manifest. To test the hypothesis that weanling Standardbreds (SB) and Thoroughbreds (TB) would have higher mitochondrial measures than Quarter Horses (QH), gluteus medius samples were collected from SB (mean ± SD; 6.2 ± 1.0 mo; n = 10), TB (6.1 ± 0.5 mo; n = 12), and QH (7.4 ± 0.6 mo; n = 10). Citrate synthase (CS) and cytochrome c oxidase (CCO) activities were assessed as markers of mitochondrial density and function, respectively. Mitochondrial oxidative (P) and electron transport system (E) capacities were assessed by high-resolution respirometry (HRR). Data for CCO and HRR are expressed as integrated (per mg protein and per mg tissue wet weight, respectively) and intrinsic (per unit CS). Data were analyzed using PROC MIXED in SAS v 9.4 with breed as a fixed effect. Mitochondrial density (CS) was higher for SB and TB than QH (P ≤ 0.0007). Mitochondrial function (integrated and intrinsic CCO) was higher in TB and QH than SB (P ≤ 0.01). Integrated CCO was also higher in TB than QH (P &lt; 0.0001). However, SB had higher integrated maximum P (PCI+II) and E (ECI+II) than QH (P ≤ 0.02) and greater integrated and intrinsic complex II-supported E (ECII) than both QH and TB (P ≤ 0.02), whereas TB exhibited higher integrated P with complex I substrates (PCI) than SB and QH (P ≤ 0.003) and higher integrated PCI+II and ECI+II than QH (P ≤ 0.02). In agreement, TB and QH had higher contribution of complex I (CI) to max E than SB (P ≤ 0.001), whereas SB had higher contribution of CII than QH and TB (P ≤ 0.002). Despite having higher mitochondrial density than QH and TB, SB showed lower CCO activity and differences in contribution of complexes to oxidative and electron transport system capacities. Breed differences in mitochondrial parameters are present early in life and should be considered when developing feeding, training, medication, and management practices.

Mitochondrial Dysfunction in Blood Platelets of Patients with Manic Episode of Bipolar Disorder

2019 ◽  
Vol 18 (3) ◽  
pp. 222-231 ◽  
Author(s):  
Jana Hroudová ◽  
Zdeněk Fišar ◽  
Hana Hansíková ◽  
Lucie Kališová ◽  
Eva Kitzlerová ◽  
...  
Keyword(s):  
Complex I ◽  
Citrate Synthase ◽  
Blood Platelets ◽  
Bipolar Affective Disorder ◽  
Manic Episode ◽  
Compensatory Mechanism ◽  
Healthy Controls ◽  
Complex Iv ◽  
Complex Ii ◽  
Complex I Activity

Objectives: The bipolar affective disorder (BAD) pathophysiology is multifactorial and has not been fully clarified. Method: We measured selected mitochondrial parameters in peripheral blood components. The analyses were performed for patients suffering from a manic episode during remission and were compared to those performed for healthy controls. BAD was clinically evaluated using well-established diagnostic scales and questionnaires. Mitochondrial respiration was examined in intact and permeabilized blood platelets using high-resolution respirometry. The citrate synthase (CS) and electron transport system (ETS) complex (complex I, II, and IV) activities were examined in platelets. Results: The CS, complex II and complex IV activities were decreased in the BAD patients, complex I activity was increased, and the ratio of complex I to CS was significantly increased. In the intact platelets, respiration after complex I inhibition and residual oxygen consumption were decreased in the BAD patients compared to the healthy controls. In the permeabilized platelets, a decreased ETS capacity was found in the BAD patients. No significant differences were found between BAD patients in mania and remission. Conclusion: Increased complex I activity can be a compensatory mechanism for decreased CS and complex II and IV activities. We conclude that complex I and its abnormal activity contribute to defects in cellular energy metabolism during a manic episode and that the deficiency in the complex's functioning, but not the availability of oxidative phosphorylation substrates, seems to be responsible for the decreased ETS capacity in BAD patients. The observed parameters can be further evaluated as ‘trait’ markers of BAD.

The insulin action-fiber type relationship in humans is muscle group specific

1995 ◽  
Vol 269 (1) ◽  
pp. E150-E154 ◽  
Author(s):  
M. S. Hickey ◽  
M. D. Weidner ◽  
K. E. Gavigan ◽  
D. Zheng ◽  
G. L. Tyndall ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Action ◽  
Citrate Synthase ◽  
Fiber Type ◽  
Vastus Lateralis ◽  
Oxidative Capacity ◽  
Muscle Groups ◽  
The Relationship ◽  
Male Subjects

The purpose of the present investigation was to determine the relationship between skeletal muscle characteristics, adiposity, and in vivo insulin action. Percutaneous muscle biopsies of the vastus lateralis (VL) and gastrocnemius (G) muscles were obtained from twenty-two sedentary male subjects. Insulin sensitivity (SI) and glucose effectiveness (SG) were determined from minimal model analysis, and indexes of regional and overall adiposity were obtained. SI was positively related to the citrate synthase activity from the VL (r = 0.50, P < 0.01) but unrelated to the citrate synthase activity from the G (r = 0.28). Similarly, SI was inversely related to the percentage of type IIb fibers in the VL (r = -0.47, P < 0.01) but unrelated to the percentage of type IIb fibers in the G (r = 0.06). SG was unrelated to fiber type, oxidative capacity, or adiposity. These data suggest that oxidative capacity and other characteristics related to VL skeletal muscle fiber type are determinants of in vivo insulin action but that this relationship cannot be extended to all muscle groups. Finally, neither skeletal muscle characteristics nor adiposity appears to be a determinant of SG in sedentary males.

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