Skeletal Muscle Oxidative Enzyme Research Articles

Resistance exercise training increases skeletal muscle mitochondrial respiration in chronic obstructive pulmonary disease

AbstractBackgroundChronic obstructive pulmonary disease (COPD) is associated with skeletal muscle mitochondrial dysfunction. Resistance exercise training (RT) is a training modality with a relatively small pulmonary demand that has been suggested to increase skeletal muscle oxidative enzyme activity in COPD. Whether a shift into a more oxidative profile following RT also translates into increased mitochondrial respiratory capacity in COPD is yet to be established.MethodsThis study investigated the effects of 13 weeks of RT on m. vastus lateralis mitochondrial capacity in 11 persons with moderate COPD [45% females, age: 69 ± 4 years (mean ± SD), predicted forced expiratory volume in 1 s (FEV1): 56 ± 7%] and 12 healthy controls (75% females, age: 66 ± 5 years, predicted FEV1: 110 ± 16%). RT was supervised and carried out two times per week. Leg exercises included leg press, knee extension, and knee flexion and were performed unilaterally with one leg conducting high‐load training (10 repetitions maximum, 10RM) and the other leg conducting low‐load training (30 repetitions maximum, 30RM). One‐legged muscle mass, maximal muscle strength, and endurance performance were determined prior to and after the RT period, together with mitochondrial respiratory capacity using high‐resolution respirometry and citrate synthase (CS) activity (a marker for mitochondrial volume density). Transcriptome analysis of genes associated with mitochondrial function was performed.ResultsResistance exercise training led to similar improvements in one‐legged muscle mass, muscle strength, and endurance performance in COPD and healthy individuals. In COPD, mitochondrial fatty acid oxidation capacity and oxidative phosphorylation increased following RT (+13 ± 22%, P = 0.033 and +9 ± 23%, P = 0.035, respectively). Marked increases were also seen in COPD for mitochondrial volume density (CS activity, +39 ± 35%, P = 0.001), which increased more than mitochondrial respiration, leading to lowered intrinsic mitochondrial function (respiration/CS activity) for complex‐1‐supported respiration (−12 ± 43%, P = 0.033), oxidative phosphorylation (−10 ± 42%, P = 0.037), and electron transfer system capacity (−6 ± 52%, P = 0.027). No differences were observed between 10RM and 30RM RT, nor were there any adaptations in mitochondrial function following RT in healthy controls. RT led to differential expression of numerous genes related to mitochondrial function in both COPD and healthy controls, with no difference being observed between groups.ConclusionsThirteen weeks of RT resulted in augmented skeletal muscle mitochondrial respiratory capacity in COPD, accompanied by alterations in the transcriptome and driven by an increase in mitochondrial quantity rather than improved mitochondrial quality.

Systematic Review and Meta-Analysis of Endurance Exercise Training Protocols for Mice.

Inbred and genetically modified mice are frequently used to investigate the molecular mechanisms responsible for the beneficial adaptations to exercise training. However, published paradigms for exercise training in mice are variable, making comparisons across studies for training efficacy difficult. The purpose of this systematic review and meta-analysis was to characterize the diversity across published treadmill-based endurance exercise training protocols for mice and to identify training protocol parameters that moderate the adaptations to endurance exercise training in mice. Published studies were retrieved from PubMed and EMBASE and reviewed for the following inclusion criteria: inbred mice; inclusion of a sedentary group; and exercise training using a motorized treadmill. Fifty-eight articles met those inclusion criteria and also included a “classical” marker of training efficacy. Outcome measures included changes in exercise performance, O2max, skeletal muscle oxidative enzyme activity, blood lactate levels, or exercise-induced cardiac hypertrophy. The majority of studies were conducted using male mice. Approximately 48% of studies included all information regarding exercise training protocol parameters. Meta-analysis was performed using 105 distinct training groups (i.e., EX-SED pairs). Exercise training had a significant effect on training outcomes, but with high heterogeneity (Hedges’ g=1.70, 95% CI=1.47–1.94, Tau2=1.14, I2=80.4%, prediction interval=−0.43–3.84). Heterogeneity was partially explained by subgroup differences in treadmill incline, training duration, exercise performance test type, and outcome variable. Subsequent analyses were performed on subsets of studies based on training outcome, exercise performance, or biochemical markers. Exercise training significantly improved performance outcomes (Hedges’ g=1.85, 95% CI=1.55–2.15). Subgroup differences were observed for treadmill incline, training duration, and exercise performance test protocol on improvements in performance. Biochemical markers also changed significantly with training (Hedges’ g=1.62, 95% CI=1.14–2.11). Subgroup differences were observed for strain, sex, exercise session time, and training duration. These results demonstrate there is a high degree of heterogeneity across exercise training studies in mice. Training duration had the most significant impact on training outcome. However, the magnitude of the effect of exercise training varies based on the marker used to assess training efficacy.

Exercise training in heart transplantation.

Heart transplantation remains the gold standard in the treatment of end-stage heart failure (HF). Heart transplantation patients present lower exercise capacity due to cardiovascular and musculoskeletal alterations leading thus to poor quality of life and reduction in the ability of daily self-service. Impaired vascular function and diastolic dysfunction cause lower cardiac output while decreased skeletal muscle oxidative fibers, enzymes and capillarity cause arteriovenous oxygen difference, leading thus to decreased peak oxygen uptake in heart transplant recipients. Exercise training improves exercise capacity, cardiac and vascular endothelial function in heart transplant recipients. Pre-rehabilitation regular aerobic or combined exercise is beneficial for patients with end-stage HF awaiting heart transplantation in order to maintain a higher fitness level and reduce complications afterwards like intensive care unit acquired weakness or cardiac cachexia. All hospitalized patients after heart transplantation should be referred to early mobilization of skeletal muscles through kinesiotherapy of the upper and lower limbs and respiratory physiotherapy in order to prevent infections of the respiratory system prior to hospital discharge. Moreover, all heart transplant recipients after hospital discharge who have not already participated in an early cardiac rehabilitation program should be referred to a rehabilitation center by their health care provider. Although high intensity interval training seems to have more benefits than moderate intensity continuous training, especially in stable transplant patients, individualized training based on the abilities and needs of each patient still remains the most appropriate approach. Cardiac rehabilitation appears to be safe in heart transplant patients. However, long-term follow-up data is incomplete and, therefore, further high quality and adequately-powered studies are needed to demonstrate the long-term benefits of exercise training in this population.

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

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.

Tocotrienols and Whey Protein Isolates Substantially Increase Exercise Endurance Capacity in Diet -Induced Obese Male Sprague-Dawley Rats.

Background and AimsObesity and impairments in metabolic health are associated with reductions in exercise capacity. Both whey protein isolates (WPIs) and vitamin E tocotrienols (TCTs) exert favorable effects on obesity-related metabolic parameters. This research sought to determine whether these supplements improved exercise capacity and increased glucose tolerance in diet-induced obese rats.MethodsSix week old male rats (n = 35) weighing 187 ± 32g were allocated to either: Control (n = 9), TCT (n = 9), WPI (n = 8) or TCT + WPI (n = 9) and placed on a high-fat diet (40% of energy from fat) for 10 weeks. Animals received 50mg/kg body weight and 8% of total energy intake per day of TCTs and/or WPIs respectively. Food intake, body composition, glucose tolerance, insulin sensitivity, exercise capacity, skeletal muscle glycogen content and oxidative enzyme activity were determined.ResultsBoth TCT and WPI groups ran >50% longer (2271 ± 185m and 2195 ± 265m respectively) than the Control group (1428 ± 139m) during the run to exhaustion test (P<0.05), TCT + WPI did not further improve exercise endurance (2068 ± 104m). WPIs increased the maximum in vitro activity of beta-hydroxyacyl-CoA in the soleus muscle (P<0.05 vs. Control) but not in the plantaris. Citrate synthase activity was not different between groups. Neither supplement had any effect on weight gain, adiposity, glucose tolerance or insulin sensitivity.ConclusionTen weeks of both TCTs and WPIs increased exercise endurance by 50% in sedentary, diet-induced obese rats. These positive effects of TCTs and WPIs were independent of body weight, adiposity or glucose tolerance.

Combined whole-body vibration, resistance exercise, and sustained vascular occlusion increases PGC-1α and VEGF mRNA abundances

We previously reported that high load resistance exercise with superimposed whole-body vibration and sustained vascular occlusion (vibroX) markedly improves cycling endurance capacity, increases capillary-to-fibre ratio and skeletal muscle oxidative enzyme activity in untrained young women. These findings are intriguing, since increases in oxidative muscle phenotype and endurance capacity are typically induced by endurance but not heavy resistance exercise. Here, we tested the hypothesis that vibroX activates genes associated with mitochondrial biogenesis and angiogenesis. Eight healthy, recreationally resistance-trained young men performed either vibroX or resistance exercise (RES) in a randomised, cross-over design. Needle biopsies (M. vastus lateralis) were obtained at rest and 3 h post-exercise. Changes in relative gene expression levels were assessed by real-time quantitative PCR. After vibroX, vascular endothelial growth factor and peroxisome proliferator-activated receptor-γ coactivator 1α mRNA abundances increased to 2- and 4.4-fold, respectively, but did not significantly change above resting values after RES. Other genes involved in mitochondrial biogenesis were not affected by either exercise modality. While vibroX increased the expression of hexokinase II, xanthine dehydrogenase, and manganese superoxide dismutase mRNA, there were no changes in these transcripts after RES. This study demonstrates that high load resistance exercise with superimposed whole-body vibration and sustained vascular occlusion activates metabolic and angiogenic gene programs, which are usually activated after endurance but not resistance exercise. Thus, targeted modification of high load resistance exercise by vibration and vascular occlusion might represent a novel strategy to induce endurance-type muscle adaptations.

New records in aerobic power among octogenarian lifelong endurance athletes

We examined whole body aerobic capacity and myocellular markers of oxidative metabolism in lifelong endurance athletes [n = 9, 81 ± 1 yr, 68 ± 3 kg, body mass index (BMI) = 23 ± 1 kg/m(2)] and age-matched, healthy, untrained men (n = 6; 82 ± 1 y, 77 ± 5 kg, BMI = 26 ± 1 kg/m(2)). The endurance athletes were cross-country skiers, including a former Olympic champion and several national/regional champions, with a history of aerobic exercise and participation in endurance events throughout their lives. Each subject performed a maximal cycle test to assess aerobic capacity (VO(2max)). Subjects had a resting vastus lateralis muscle biopsy to assess oxidative enzymes (citrate synthase and βHAD) and molecular (mRNA) targets associated with mitochondrial biogenesis [peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) and mitochondrial transcription factor A (Tfam)]. The octogenarian athletes had a higher (P < 0.05) absolute (2.6 ± 0.1 vs. 1.6 ± 0.1 l/min) and relative (38 ± 1 vs. 21 ± 1 ml·kg(-1)·min(-1)) VO(2max), ventilation (79 ± 3 vs. 64 ± 7 l/min), heart rate (160 ± 5 vs. 146 ± 8 beats per minute), and final workload (182 ± 4 vs. 131 ± 14 W). Skeletal muscle oxidative enzymes were 54% (citrate synthase) and 42% (βHAD) higher (P < 0.05) in the octogenarian athletes. Likewise, basal PGC-1α and Tfam mRNA were 135% and 80% greater (P < 0.05) in the octogenarian athletes. To our knowledge, the VO(2max) of the lifelong endurance athletes is the highest recorded in humans >80 yr of age and comparable to nonendurance trained men 40 years younger. The superior cardiovascular and skeletal muscle health profile of the octogenarian athletes provides a large functional reserve above the aerobic frailty threshold and is associated with lower risk for disability and mortality.

Endurance exercise induces mRNA expression of oxidative enzymes in human skeletal muscle late in recovery

Exercise-induced adaptations in skeletal muscle oxidative enzymes are suggested to result from the cumulative effects of transient changes in gene expression after each single exercise session. However, for several oxidative enzymes, no changes in mRNA expression are detected up to 8 h after exercise. To test the hypothesis that mRNA expression of many oxidative enzymes is up-regulated late in recovery (10-24 h) after exercise, male subjects (n=8) performed a 90-min cycling exercise (70% VO(2-max)), with muscle biopsies obtained before exercise (pre), and after 10, 18 and 24 h of recovery. The mRNA expression of carnitine-palmitoyltransferase (CPT)I, CD36, 3-hydroxyacyl-CoA-dehydrogenase (HAD), cytochrome (Cyt)c, aminolevulinate-delta-synthase (ALAS)1 and GLUT4 was 100-200% higher at 10-24 h of recovery from exercise than in a control trial. Exercise induced a 100-300% increase in peroxisome proliferator-activated receptor gamma co-activator (PGC)-1alpha, citrate synthase (CS), CPTI, CD36, HAD and ALAS1 mRNA contents at 10-24 h of recovery relative to before exercise. No protein changes were detected in Cytc, ALAS1 or GLUT4. This shows that mRNA expression of several training-responsive oxidative enzymes is up-regulated in human skeletal muscle at 10-24 h of recovery, supporting that exercise-induced adaptations of these oxidative enzymes can be the result of the cumulative effects of transient changes in mRNA expression.

Manipulating training intensity and volume in already well-trained rats: effect on skeletal muscle oxidative and glycolytic enzymes and buffering capacity

Well-trained endurance athletes undergo periods of high-intensity interval training (HIT) or high-volume training (HVT) to improve exercise performance, but little is known about the mechanistic changes that occur during this time. The purpose of this study was to examine the influence of HIT and HVT on the activities of citrate synthase (CS) and phosphofructokinase (PFK), and on intramuscular buffering capacity (betam) in already well-trained rats. At 4 weeks of age, Wistar rats were divided into sedentary (SED; n=18) and exercise training groups (n=38). Following a 10 week preliminary training program, trained rats were divided randomly into 3 further groups that completed 4 additional weeks of continued endurance (CON, n=14), high-intensity training (HIT, n=12), or high-volume training (HVT, n=12). Soleus (SOL), red and white gastrocnemius (RG and WG), and red and white vastus (RV and WV) muscles were removed 24-48 h after a final run-to-fatigue performance test (30 m.min(-1) 25% grade) to determine the activities of CS, PFK, and betam. No differences in run time to exhaustion were found between the groups. However the HIT group possessed CS and PFK activities and betam in WV muscle that were 60%, 24%, and 10% higher, respectively (all p<0.05), compared with the HVT group; differences were not found between the HIT and CON groups. Although no differences in run performance were found, HIT compared with HVT in already well-trained rats resulted in significantly higher oxidative and glycolytic capacities of fast-contracting fibres. No differences were shown in fast-contracting muscle between HIT and CON.

Improved skeletal muscle oxidative enzyme activity and restoration of PGC-1α and PPARβ/δ gene expression upon rosiglitazone treatment in obese patients with type 2 diabetes mellitus

To examine whether rosiglitazone alters gene expression of some key genes involved in mitochondrial biogenesis and oxidative capacity in skeletal muscle of type 2 diabetic patients, and whether this is associated with alterations in skeletal muscle oxidative capacity and lipid content. measured in muscle biopsies obtained from diabetic patients, before and after 8 weeks of rosiglitazone treatment, and matched controls. Furthermore, whole-body insulin sensitivity and substrate utilization were assessed. Ten obese type 2 diabetic patients and 10 obese normoglycemic controls matched for age and BMI. Gene expression and mitochondrial protein content of complexes I-V of the respiratory chain were measured by quantitative polymerase chain reaction and Western blotting, respectively. Histochemical staining was used to quantify lipid accumulation and complex II succinate dehydrogenase (SDH) activity. Insulin sensitivity and substrate utilization were measured during a hyperinsulinemic-euglycemic clamp with indirect calorimetry. Skeletal-muscle mRNA of PGC-1 alpha and PPAR beta/delta--but not of other genes involved in glucose, fat and oxidative metabolism--was significantly lower in diabetic patients (P<0.01). Rosiglitazone significantly increased PGC-1 alpha ( approximately 2.2-fold, P<0.01) and PPAR beta/delta ( approximately 2.6-fold, P<0.01), in parallel with an increase in insulin sensitivity, SDH activity and metabolic flexibility (P<0.01). Surprisingly, none of the measured mitochondrial proteins was reduced in type 2 diabetic patients, nor affected by rosiglitazone treatment. No alterations were seen in muscular fat accumulation upon treatment. These results suggest that the insulin-sensitizing effect of rosiglitazone may involve an effect on muscular oxidative capacity, via PGC-1 alpha and PPAR beta/delta, independent of mitochondrial protein content and/or changes in intramyocellular lipid.

Systemic oxygen transport in rats artificially selected for running endurance

The relative contribution of genetic and environmental influences to individual exercise capacity is difficult to determine. Accordingly, animal models in which these influences are carefully controlled are highly useful to understand the determinants of intrinsic exercise capacity. Studies of systemic O(2) transport during maximal treadmill exercise in two diverging lines of rats artificially selected for endurance capacity showed that, at generation 7, whole body maximal O(2) uptake ((.)V(O(2)(max)) was 12% higher in high capacity (HCR) than in low capacity runners (LCR) during normoxic exercise. The difference in (.)V(O(2)(max) between HCR and LCR was larger during hypoxic exercise. Analysis of the linked O(2) conductances of the O(2) transport system showed that the higher (.)V(O(2)(max) was not due to a higher ventilatory response, a more effective pulmonary gas exchange, or an increased rate of O(2) delivery to the tissue by blood. The main reason for the higher (.)V(O(2)(max) of HCR was an increased tissue O(2) extraction, due largely to a higher tissue diffusive O(2) conductance. The enhanced tissue O(2) diffusing capacity was paralleled by an increased capillary density of a representative locomotory skeletal muscle, the gastrocnemius, in HCR. Activities of skeletal muscle oxidative enzymes citrate synthase and beta-HAD were also higher in HCR than LCR. Thus, the functional characteristics observed during exercise are consistent with the structural and biochemical changes observed in skeletal muscle that imply an enhanced capacity for muscle O(2) uptake and utilization in HCR. The results indicate that the improved (.)V(O(2)(max) is solely due to enhanced muscle O(2) extraction and utilization. However, the question arises as to whether it is possible to maintain a continually expanding capacity for O(2) extraction at the tissue level with successive generations, without a parallel improvement in the capacity to deliver O(2) to the exercising muscles.

Whole‐body fat oxidation determined by graded exercise and indirect calorimetry: a role for muscle oxidative capacity?

During whole-body exercise, peak fat oxidation occurs at a moderate intensity. This study investigated whole-body peak fat oxidation in untrained and trained subjects, and the presence of a relation between skeletal muscle oxidative enzyme activity and whole-body peak fat oxidation. Healthy male subjects were recruited and categorized into an untrained (N=8, VO(2max) 3.5+/-0.1 L/min) and a trained (N=8, VO(2max) 4.6+/-0.2 L/min) group. Subjects performed a graded exercise test commencing at 60 W for 8 min followed by 35 W increments every 3 min. On a separate day, muscle biopsies were obtained from vastus lateralis and a 3 h bicycle exercise test was performed at 58% of VO(2max). Whole-body fat oxidation was calculated during prolonged and graded exercise from the respiratory exchange ratio using standard indirect calorimetry equations. Based on the graded exercise test, whole-body peak fat oxidation was determined. The body composition was determined by DEXA. Whole-body peak fat oxidation (250+/-25 and 462+/-33 mg/min) was higher (P<0.05) and occurred at a higher (P<0.05) relative workload (43.5+/-1.8% and 49.9+/-1.2% VO(2max)) in trained compared with untrained subjects, respectively. Muscle citrate synthase activity and beta-hydroxy-acyl-CoA-dehydrogenase activity were higher (49% and 35%, respectively, P<0.05) in trained compared with untrained subjects. Both lean body mass and maximal oxygen uptake were significantly correlated to whole-body peak fat oxidation (r(2)=0.57, P<0.001), but leg muscle oxidative capacity was not correlated to whole-body peak fat oxidation. In conclusion, whole-body peak fat oxidation occurred at a higher relative exercise load in trained compared with untrained subjects. Whole-body peak fat oxidation was not significantly related to leg muscle oxidative capacity, but was related to lean body mass and maximal oxygen uptake. This may suggest that leg muscle oxidative activity is not the main determinant of whole-body peak fat oxidation.

Dietary fat and body weight set point.

The level of body weight corresponding to the threshold where energy balance is spontaneously stable is influenced by factors contributing to variations in fat balance. In this regard, a high-fat diet is associated with an increase in ad libitum energy intake and can lead to an increase of several kilograms of body weight over a year. On a long-term basis, this spontaneous weight gain is expected to plateau because of the ability of fat gain to promote an increase in fat oxidation up to a level allowing the recovery of energy and fat balance. Recent evidence suggests that lipid-soluble organochlorine pollutants may also make energy and fat balance regulation more vulnerable in obese individuals by accentuating the decrease in plasma thyroid hormone concentrations, skeletal muscle oxidative enzymes, and resting metabolic rate induced by weight loss. These observations support the idea that the body weight set point may fluctuate according to the actual impact of factors influencing fat balance.

SKELETAL MUSCLE LIPID CONTENT AND INSULIN RESISTANCE

PURPOSE This cross-sectional study assessed whole-body insulin sensitivity (by euglycemic-hyperinsulinemic clamp), skeletal muscle triglycerides (IMTG), long-chain acyl CoA (LCACoA) content and fatty acid (FA) transporter protein content in 8 patients with type 2 diabetes (TYPE 2), 6 healthy control subjects matched for age, BMI, % body fat and VO2peak (OLD), 9 well-trained athletes (TRAINED) and 4 age-matched controls (YOUNG). METHODS Muscle biopsies from the v. lateralis were taken prior to and after a 2 h clamp. Oxidative enzyme activities, FA transporters (FAT/CD36 and FABPpm) and IMTG were determined from resting muscle samples, while total LCACoA content was assessed pre- and post-insulin stimulation. RESULTS Whole body insulin-stimulated glucose disposal was lower in TYPE 2 (p < 0.05). Citrate synthase activity was increased in TRAINED (p < 0.05), while βHAD activity was higher in TRAINED compared to TYPE 2 (94%) and OLD (76%). There was no difference in FAT/CD36 protein content between groups. FABPpm protein was decreased in OLD compared to TYPE 2 and YOUNG (p < 0.05). IMTG was elevated in TYPE 2 compared to OLD, YOUNG and TRAINED (p < 0.05). Basal skeletal muscle LCACoA content did not differ between groups, or after insulin-stimulation. CONCLUSION Despite marked differences in whole-body insulin sensitivity, skeletal muscle oxidative enzyme activity and IMTG, total LCACoA content and the FA transporter proteins FAT/CD36 and FABPpm were similar between type 2 diabetics and well-trained endurance athletes. Supported by a grant from EFFEM Foods (Mars) Australia.

INCREASES IN VO2MAX AND ALTERATIONS IN FAT METABOLISM WITH SPRINT INTERVAL TRAINING

Prior research by MacDougall (1998) has indicated that high intensity intervals of 30-s performed three times a week increases VO2 max and skeletal muscle oxidative enzyme activity. However, the effects of these changes on whole body fat oxidation rates have not been investigated. PURPOSE To assess the effects of high-intensity interval training on VO2max and maximum/submaximal fat oxidation rates in males of low cardiovascular fitness. METHODS Five males, age = 25 ± .4 yrs, with an average VO2max = 39.2 ± 6.6 ml*kg-1*min-1 participated in a seven-week high intensity exercise program. Subjects performed 30-s maximum sprint efforts on a cycle ergometer (Wingate protocol) with 2–4 minutes of recovery, three times a week. The training consisted of 4 intervals with 4 min of recovery at week-1, followed by an increase of one interval per week till 10 were performed by week-7 with 2.5 min of recovery. An exercise test with expired gas analysis (Parvo, Consentious Technologies) was used to measure VO2max pre/post training. Submaximal (FatSub) and maximal fat (Fatmax) oxidation rates and the crossover point to carbohydrate metabolism were measured using indirect calorimetry according to Achten (2002). RESULTS There was a post-training increase of 11.7% in VO2max (Pre = 39.2 ± 6.6 ml*kg-1*min-1 vs Post = 43.8 ± 6.1 ml*kg-1*min-1) (p = 0.006). Across treatments post-training FatSub were greater when compared to pre-training (p = 0.037). Further, a nonsignificant increase in Fatmax of 8.6% (p > 0.05) was observed. Post-training, the crossover point nonsignificantly increased by 15.9% when compared to pretraining (p = 0.073). CONCLUSION This preliminary study indicates that high intensity sprint interval training can significantly improve VO2max and FatSub metabolism. Further investigations of the physiological mechanisms by which these adaptations occur are warranted.

Skeletal Muscle Lipid Content and Oxidative Enzyme Activity in Relation to Muscle Fiber Type in Type 2 Diabetes and Obesity

In obesity and type 2 diabetes, skeletal muscle has been observed to have a reduced oxidative enzyme activity, increased glycolytic activity, and increased lipid content. These metabolic characteristics are related to insulin resistance of skeletal muscle and are factors potentially related to muscle fiber type. The current study was undertaken to examine the interactions of muscle fiber type in relation to oxidative enzyme activity, glycolytic enzyme activity, and muscle lipid content in obese and type 2 diabetic subjects compared with lean healthy volunteers. The method of single-fiber analysis was used on vastus lateralis muscle obtained by percutaneous biopsy from 22 lean, 20 obese, and 20 type 2 diabetic subjects (ages 35+/-1, 42+/-2, and 52+/-2 years, respectively), with values for BMI that were similar in obese and diabetic subjects (23.7+/-0.7, 33.2+/-0.8, and 31.8+/-0.8 kg/m2, respectively). Oxidative enzyme activity followed the order of type I > type IIa > type IIb, but within each fiber type, skeletal muscle from obese and type 2 diabetic subjects had lower oxidative enzyme activity than muscle from lean subjects (P < 0.01). Muscle lipid content followed a similar pattern in relation to fiber type, and within each fiber type, muscle from obese and type 2 diabetic subjects had greater lipid content (P < 0.01). In summary, based on single-fiber analysis, skeletal muscle in obese and type 2 diabetic subjects mani-fests disturbances of oxidative enzyme activity and increased lipid content that are independent of the effect of fiber type.

Pulmonary emphysema decreases hamster skeletal muscle oxidative enzyme capacity.

Skeletal muscle oxidative enzyme capacity is impaired in patients suffering from emphysema and chronic obstructive pulmonary disease. This effect may result as a consequence of the physiological derangements because of the emphysema condition or, alternatively, as a consequence of the reduced physical activity level in these patients. To explore this issue, citrate synthase (CS) activity was measured in selected hindlimb muscles and the diaphragm of Syrian Golden hamsters 6 mo after intratracheal instillation of either saline (Con, n = 7) or elastase [emphysema (Emp); 25 units/100 g body weight, n = 8]. Activity level was monitored, and no difference between groups was found. Excised lung volume increased with emphysema (Con, 1.5 +/- 0.3 g; Emp, 3.0 +/- 0.3 g, P < 0.002). Emphysema significantly reduced CS activity in the gastrocnemius (Con, 45.1 +/- 2.0; Emp, 39.2 +/- 0.8 micromol . min-1 . g wet wt-1, P < 0.05) and vastus lateralis (Con, 48.5 +/- 1.5; Emp, 44.9 +/- 0.8 micromol . min-1 . g wet wt-1, P < 0.05) but not in the plantaris (Con, 47.4 +/- 3.9; Emp, 48.0 +/- 2.1 micromol . min-1 . g wet wt-1, P < 0.05) muscle. In contrast, CS activity increased in the costal (Con, 61.1 +/- 1.8; Emp, 65.1 +/- 1.5 micromol . min-1 . g wet wt-1, P < 0.05) and crural (Con, 58.5 +/- 2.0; Emp, 65.7 +/- 2.2 micromol . min-1 . g wet wt-1, P < 0.05) regions of the diaphragm. These data indicate that emphysema per se can induce decrements in the oxidative capacity of certain nonventilatory skeletal muscles that may contribute to exercise limitations in the emphysematous patient.

PULMONARY EMPHYSEMA DECREASES HAMSTER SKELETAL MUSCLE OXIDATIVE ENZYME CAPACITY

Skeletal muscle oxidative enzyme capacity is impaired in patients suffering from emphysema and chronic obstructive pulmonary disease. This effect may result as a consequence of the physiological de...

Skeletal muscle glycolytic and oxidative enzyme capacities are determinants of insulin sensitivity and muscle composition in obese women

Regional fat distribution is an important determinant of insulin resistance in obesity. In the current study, the relationship between skeletal muscle insulin sensitivity, mid-thigh muscle composition, and the metabolic profile of muscle was investigated. Muscle composition was assessed by computed tomography of the mid-thigh, and by activities of marker enzymes of aerobic-oxidative and glycolytic pathways and muscle fiber typing using biopsies of the vastus lateralis muscle. Muscle with reduced Hounsfield attenuation on computed tomography scans was increased in proportion to obesity, and was strongly related to insulin resistance, reduced muscle oxidative capacity, and increased anaerobic and glycolytic capacities by muscle. These findings suggest that as part of its expression of insulin resistance, skeletal muscle of obese individuals is also poorly equipped for substrate oxidation and manifests increased storage of fat.

Physiological and Biochemical Consequences of Detraining in Aerobically Trained Individuals

Detraining is associated with the reversal of many physiological and biochemical adaptations acquired through chronic aerobic exercise. However, highly conditioned individuals appear to retain some of the benefits derived from endurance training despite remaining inactive for as long as 12 weeks. In particular, training-induced gains in skeletal muscle capillarization, myoglobin concentration, and oxidative enzyme capacity are partially retained by well-trained individuals and appear to be responsible for the long-term maintenance of arterial-venous oxygen difference (a-vO2 difference) and maximal aerobic capacity (O2 max) above untrained levels. Conversely, in previously sedentary, moderately trained persons, training related adaptations are completely reversed to pretraining levels after approximately 10 weeks of inactivity.