Lipoprotein-lipase activity of human skeletal-muscle and adipose tissue after intensive physical exercise

Seven young, healthy subjects performed bicycle exercise with a working load leading to exhaustion after one hour of work. The tests were done in the afternoon in the fed state. The serum insulin concentrations decreased from 22 to 4 mU/1 and plasma glucagon increased from 241 to 340 pg/1 already after 30 min of work. The level of adipose tissue lipoprotein lipase activity (LPLA) did not fall as had been expected, but increased. The skeletal muscle LPLA was unchanged. The results indicate that during the first hour of heavy exercise the heparin-releasable LPLA in tissues is not influenced by the work induced changes in serum hormone levels.     

Physical activity and exercise in the regulation of human adipose tissue physiology

Physical activity and exercise are key components of energy expenditure and therefore of energy balance. Changes in energy balance alter fat mass. It is therefore reasonable to ask: What are the links between physical activity and adipose tissue function? There are many complexities. Physical activity is a multifaceted behavior of which exercise is just one component. Physical activity influences adipose tissue both acutely and in the longer term. A single bout of exercise stimulates adipose tissue blood flow and fat mobilization, resulting in delivery of fatty acids to skeletal muscles at a rate well-matched to metabolic requirements, except perhaps in vigorous intensity exercise. The stimuli include adrenergic and other circulating factors. There is a period following an exercise bout when fatty acids are directed away from adipose tissue to other tissues such as skeletal muscle, reducing dietary fat storage in adipose. With chronic exercise (training), there are changes in adipose tissue physiology, particularly an enhanced fat mobilization during acute exercise. It is difficult, however, to distinguish chronic "structural" changes from those associated with the last exercise bout. In addition, it is difficult to distinguish between the effects of training per se and negative energy balance. Epidemiological observations support the idea that physically active people have relatively low fat mass, and intervention studies tend to show that exercise training reduces fat mass. A much-discussed effect of exercise versus calorie restriction in preferentially reducing visceral fat is not borne out by meta-analyses. We conclude that, in addition to the regulation of fat mass, physical activity may contribute to metabolic health through beneficial dynamic changes within adipose tissue in response to each activity bout.     

Deiodinating activity in the brown adipose tissue of rats following short cold exposure after strenuous exercise

Interscapular brown adipose tissue (IBAT) activity is controlled by the sympathetic nervous system, and factors that influence thermogenesis appear to act centrally to modify the sympathetic outflow to IBAT. Cold exposure produces a rise in IBAT temperature as a result of the increase in sympathetic outflow to IBAT. This is associated with an increased thyroid activity. 3,5,3'-triiodothyronine (T3) and T4 levels increase during strenuous exercise, and, at the end of the exercise bout, a decrease of T3 and T4 levels, with an increase in TSH during the following 4-5 days, is seen. We evaluated the effect of strenuous exercise on 5'-deiodinase (5'-D) activity in IBAT in normal environmental conditions and after short (30 min) cold exposure. 5'-D activity is lower in rats at basal condition. Short cold exposure (SCE) increases 5'-D in IBAT both in exercising rats and in sedentary rats. However, this increase is lower in exercising animals. Strenuous exercise can reduce 5'-D activity in normal environmental conditions and after SCE. Probably, other compensatory mechanisms of heat production are active in exercising rodents.     

Interstitial glycerol concentrations in human skeletal muscle and adipose tissue during graded exercise

AIM: It is not clear how lipolysis changes in skeletal muscle and adipose tissue during exercise of different intensities. We aimed at estimating this by microdialysis and muscle biopsy techniques. METHODS: Nine healthy, young men were kicking with both legs at 25% of maximal power (Wmax) for 45 min and then simultaneously with one leg at 65% and the other leg at 85% Wmax for 35 min. RESULTS: Glycerol concentrations in skeletal muscle and adipose tissue interstitial fluid and in arterial plasma increased (P<0.001) during low intensity exercise and increased (P<0.05) even more during moderate intensity exercise. The difference between interstitial muscle and arterial plasma water glycerol concentration, which indicates the direction of the glycerol flux, was positive (P<0.05) at rest (21 +/- 9 microM) and during exercise at 25% Wmax (18 +/- 6 microM). The difference decreased (P<0.05) with increasing exercise intensity and was not significantly different from zero during exercise at 65% (-11 +/- 17 microM) and 85% (-12 +/- 13 microM) Wmax. In adipose tissue, the difference between interstitial and arterial plasma water glycerol increased (P<0.001) with increasing intensity. The net triacylglycerol breakdown, measured chemically from the biopsy, did not differ significantly from zero at any exercise intensity although directional changes were similar to microdialysis changes. CONCLUSIONS: Skeletal muscle releases glycerol at rest and at low exercise intensity but not at higher intensities. This can be interpreted as skeletal muscle lipolysis peaking at low exercise intensities but could also indicate that glycerol is taken up in skeletal muscle at a rate which is increasing with exercise intensity.     

Lipoprotein lipase of human postheparin plasma and adipose tissue in relation to physical training

Adipose tissue lipoprotein lipase and postheparin plasma triglyceride lipase activities were measured in 28 men differing in their physical training activity. They were divided into 4 subclasses based on their training intensity. The two most active classes (17 subjects) having regular heavy exercise at least 4 times a week were considered as the actively training group, and the other two (11 subjects) classes not training regularly as the control group. In postheparin plasma, the lipoprotein lipase activities were not different between the two groups, whereas training subjects had significantly (P<0.02) lower hepatic lipase activities. Adipose tissue lipoprotein lipase activity was in the training group at about 70% higher level on an average than in the controls (P<0.10). A significant positive correlation (r=0.38, P<0.05) was obtained between the adipose tissue lipoprotein lipase activity and the level of physical activity. Our data suggest that even moderate inter-group differences in the physical training activity are reflected as measurable alterations in the adipose tissue lipoprotein lipase activity in man.     

Interleukin-6 production in human subcutaneous abdominal adipose tissue: the effect of exercise

The interleukin-6 (IL-6) output from subcutaneous, abdominal adipose tissue was studied in nine healthy subjects before, during and for 3 h after 1 h two-legged bicycle exercise at 60 % maximal oxygen consumption. Seven subjects were studied in control experiments without exercise. The adipose tissue IL-6 output was measured by direct Fick technique. An artery and a subcutaneous vein on the anterior abdominal wall were catheterized. Adipose tissue blood flow was measured using the ¹³³Xe-washout method. In both studies there was a significant IL-6 output in the basal state and no significant change was observed during exercise. Post-exercise the IL-6 output began to increase after 30 min. Three hours post-exercise it was 58.6 ± 22.2 pg (100 g)⁻¹ min⁻¹. In the control experiments the IL-6 output also increased, but it only reached a level of 3.5 ± 0.8 pg (100 g)⁻¹ min⁻¹. The temporal profile of the post-exercise change in the IL-6 output closely resembles the changes in the outputs of glycerol and fatty acids, which we have described previously in the same adipose tissue depot. The difference is that it begins to increase ≈30 min before the glycerol and fatty acid outputs begin to increase. Thus, we suggest that the enhanced IL-6 production post-exercise in abdominal, subcutaneous adipose tissue may act locally via autocrine/paracrine mechanisms influencing lipolysis and fatty acid mobilization rate from this lipid depot.     

AMPK as a metabolic switch in rat muscle,liver and adipose tissue after exercise

An increasing body of evidence has revealed that activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK)-activated protein kinase increases fatty acid oxidation by lowering the concentration of malonyl coenzyme A (CoA), an inhibitor of carnitine palmitoyl transferase 1. Studies carried out primarily in skeletal muscle suggest that AMPK modulates the concentration of malonyl CoA by concurrently phosphorylating and inhibiting acetyl CoA carboxylase (ACC), the rate limiting enzyme in malonyl CoA synthesis, and phosphorylating and activating malonyl CoA decarboxylase (MCD), an enzyme involved in its degradation. We have recently observed that AMPK and MCD activities are increased and ACC activity diminished in skeletal muscle, liver and, surprisingly, in adipose tissue 30 min following exercise (treadmill run) in normal rats. In liver and adipose tissue these changes were associated with a decrease in the activity of glycerol-3-phosphate acyltransferase (GPAT), which catalyses the first committed reaction in glycerolipid synthesis and, which like ACC, is phosphorylated and inhibited by AMPK. Similar changes in ACC, MCD and GPAT were observed following the administration of 5-aminoimidazole 4-carboxamide-riboside (AICAR), further indicating that the exercise-induced alterations in these enzymes were AMPK-mediated. CONCLUSIONS: (1) AMPK plays a major role in regulating lipid metabolism in multiple tissues following exercise. (2) The net effect of its activation is to increase fatty acid oxidation and diminish glycerolipid synthesis. (3) The relevance of these findings to the regulation of muscle glycogen repletion in the post-exercise state and to the demonstrated ability of AMPK activation to decrease adiposity and increase insulin sensitivity in rodents remains to be determined.     

AMPK as a metabolic switch in rat muscle,liver and adipose tissue after exercise

An increasing body of evidence has revealed that activation of adenosine monophosphate (AMP)‐activated protein kinase (AMPK)‐activated protein kinase increases fatty acid oxidation by lowering the concentration of malonyl coenzyme A (CoA), an inhibitor of carnitine palmitoyl transferase 1. Studies carried out primarily in skeletal muscle suggest that AMPK modulates the concentration of malonyl CoA by concurrently phosphorylating and inhibiting acetyl CoA carboxylase (ACC), the rate limiting enzyme in malonyl CoA synthesis, and phosphorylating and activating malonyl CoA decarboxylase (MCD), an enzyme involved in its degradation. We have recently observed that AMPK and MCD activities are increased and ACC activity diminished in skeletal muscle, liver and, surprisingly, in adipose tissue 30 min following exercise (treadmill run) in normal rats. In liver and adipose tissue these changes were associated with a decrease in the activity of glycerol‐3‐phosphate acyltransferase (GPAT), which catalyses the first committed reaction in glycerolipid synthesis and, which like ACC, is phosphorylated and inhibited by AMPK. Similar changes in ACC, MCD and GPAT were observed following the administration of 5‐aminoimidazole 4‐carboxamide‐riboside (AICAR), further indicating that the exercise‐induced alterations in these enzymes were AMPK‐mediated. Conclusions: (1) AMPK plays a major role in regulating lipid metabolism in multiple tissues following exercise. (2) The net effect of its activation is to increase fatty acid oxidation and diminish glycerolipid synthesis. (3) The relevance of these findings to the regulation of muscle glycogen repletion in the post‐exercise state and to the demonstrated ability of AMPK activation to decrease adiposity and increase insulin sensitivity in rodents remains to be determined.     

Lipolytic activity of adipose tissue in children

Bulletin of Experimental Biology and Medicine -     

Human adipose tissue blood flow during prolonged exercise II

Subcutaneous and perirenal adipose tissue blood flows (ATBF) were measured by the¹³³Xe washout method before, during and after 4 h exercise on a bicycle ergometer. The load corresponded to about 50% of max (i.e. about 1.7l/min). Subcutaneous and perirenal ATBF increased at an average to 3–400 and 700% of their initial control values respectively. In six of nine measuring sites ATBF remained increased in the hour following work. During work plasma glycerol concentrations increased 8 fold. The core temperature increased 0.9°C, skin temperature did not change significantly. During passive elevation of body temperature (core temperature +1.5°C; skin temperature +3°C) neither subcutaneous ATBF nor plasma glycerol concentrations changed significantly. It is concluded that the increase in subcutaneous ATBF during exercise is not a reaction to increased body temperature.     

Kinetics of excess CO2 output during and after intensive exercise.

In order to clarify the kinetics of excess CO2 output during and after intensive exercise, six male subjects were each instructed to perform 40-, 60- and 80-s cycle ergometer exercises (282 +/- 9 W, 90 rpm). Ventilation and gas exchange parameters were recorded breath-by-breath, and lactate concentration (La) was repeatedly measured with blood samples from a finger tip. The increase in La from the resting value to peak value and the duration of exercise showed a significant linear relationship (r = 0.91, p<0.01) passing through zero, indicating that lactic acid was produced at a constant rate in working muscles from the beginning of exercise. However, in contrast to this increase in La, excess V.CO2, defined as the difference between V.CO2 and V.O2, showed a temporary negative value after the start of exercise. Subsequently, excess V.CO2 became positive, reaching a peak at 60 s post-exercise, and then decreased down to zero at about 9 min after the end of the 80-s exercise. End-tidal CO2 rose above the pre-exercise level during exercise and at about 3 min post-exercise, and thereafter remained below the pre-exercise level. Excess CO2, calculated by the sum of excess V. CO2 from the start of exercise to the 10th min after the end of exercise, was significantly COrrelated with the increase in La from resting to 10 min post-exercise (r = 0.88, p<0.01). These results suggest that although excessive CO2 output (excess CO2) in response to intensive exercise is related to the increase in lactic acid, the time course of excessive CO2 output (excess V.CO2) is delayed, relative to the production of lactic acid, and is affected by hyperventilation.     

Combining decellularized human adipose tissue extracellular matrix and adipose-derived stem cells for adipose tissue engineering

Repair of soft tissue defects resulting from lumpectomy or mastectomy has become an important rehabilitation process for breast cancer patients. This study aimed to provide an adipose tissue engineering platform for soft tissue defect repair by combining decellularized human adipose tissue extracellular matrix (hDAM) and human adipose-derived stem cells (hASCs). To derive hDAM incised human adipose tissues underwent a decellularization process. Effective cell removal and lipid removal were proved by immunohistochemical analysis and DNA quantification. Scanning electron microscopic examination showed a three-dimensional nanofibrous architecture in hDAM. The hDAM included collagen, sulfated glycosaminoglycan, and vascular endothelial growth factor, but lacked major histocompatibility complex antigen I. hASC viability and proliferation on hDAM were proven in vitro. hDAM implanted subcutaneously in Fischer rats did not cause an immunogenic response, and it underwent remodeling, as indicated by host cell infiltration, neovascularization, and adipose tissue formation. Fresh fat grafts (Coleman technique) and engineered fat grafts (hDAM combined with hASCs) were implanted subcutaneously in nude rats. The implanted engineered fat grafts maintained their volume for 8 weeks, and the hASCs contributed to adipose tissue formation. In summary, the combination of hDAM and hASCs provides not only a clinically translatable platform for adipose tissue engineering, but also a vehicle for elucidating fat grafting mechanisms.     

Sporicidal activity of chemical and physical tissue fixation methods.

AIMS: The effects of alcohol based fixation and microwave stimulated alcohol fixation were investigated on spores of Bacillus stearothermophilus and Bacillus subtilis (var. niger). METHODS: Spores were exposed to 10% formalin, or different concentrations of various alcohol containing fixatives (Kryofix/Spuitfix). Adequate controls were also set up in conjunction with the test solutions. The spores were immersed with and without adjunctive microwave stimulation in the various solutions tested. Possible surviving spores were recovered in revival broth and after incubation, and Gram staining viable counts were performed. RESULTS: Alcohol based fixatives did not have a sporicidal effect on B stearothermophilus or B subtilis (var. niger) spores, and microwave stimulated alcohol fixation at 450 W and up to 75 degrees C did not have a sporicidal effect. CONCLUSIONS: When alcohol based fixatives are used for fixation, precautions should be taken with the material thus treated, as it may contain viable spores or other pathogens, which are destroyed after 24 hours of formalin treatment. Of the physicochemical methods tested involving microwaving, none was successful in eliminating viable spores from the test material.