Improving the effect of shear on skin viability with wound dressings.

BACKGROUND: Pressure ulcers are a major healthcare problem and caused by pressure and shear-forces. Although shear-force is understood to be a major contributing factor, no preventive interventions are specifically aimed at relieving the effect of shear on skin to improve skin viability. METHODS: A physical model was used to apply a combined loading of 2.4kPa pressure and 14.5N shear-force on skin in humans. Loading was applied on the volar aspect of both forearms for 30min in ten healthy volunteers. One arm received loading on skin with a wound dressing, the other arm (control) received loading directly on skin. The following parameters were determined before and after loading: IL-1α/Total Protein-ratio (used as a measure of skin damage); Cutaneous blood cell flux ((CBF) measure of reactive hyperaemia); Lactate concentration (measure of tissue ischemia). Three different dressings were tested on three different days. The order of dressing application, dressing arm and start of the intervention were randomized. RESULTS: Participants mean age was 22.5±1.6 year with a BMI of 22.3±2.4kg/m(2). IL-1α/Total Protein-ratio of the skin was significantly lower after the application of pressure and shear when the Mepilex® (P<0.01), Allevyn (P<0.05) or Aquacel(TM) dressing (P<0.01) was used compared with the control measurement. The Mepilex® dressing was more effective in reducing post-load IL-1α/Total Protein-ratio compared to the Allevyn dressing (P<0.01). Post-load CBF was significantly lower when the Mepilex® or Aquacel dressing was used (P<0.001). Both dressings induced significantly less post-load CBF than the Allevyn dressing (P<0.01 and P<0.001, respectively). The concentration of lactate was not significantly increased after the application of pressure and shear and could not be used as a measure with this model. CONCLUSION: This is the first in vivo study to demonstrate that the effects of pressure in combination with shear on skin viability can be improved with foam dressings. In this study, the multi-layered dressings perform better than the single-layered dressing.

An intervention study of the effects of calcium intake on faecal fat excretion, energy metabolism and adipose tissue mRNA expression of lipid-metabolism related proteins.

CONTEXT: In various observational studies, an inverse relation between calcium intake and body weight has been observed. A possible explanation could be an increased calcium excretion through the faeces caused by an increased dietary calcium intake. OBJECTIVE: To examine whether an increased calcium intake could lead to changes in faecal fat and energy excretion. DESIGN: Four different isocaloric diets with various calcium contents (400, 1200 and 2500 mg from dairy and 1200 mg from calcium carbonate (1200S)) were administered in a crossover design for 7 days each. SUBJECTS: Five healthy men and five healthy women (age=28+/-2, body mass index=24.1+/-0.4, body fat%=25.6+/-2.4) were recruited by local announcement. MEASUREMENTS: At the end of every intervention period, faecal samples were collected for determination of fat, energy and calcium content, blood samples were obtained for determination of relevant blood parameters; and fat samples were obtained for measurement of the mRNA expression. Furthermore, resting energy expenditure and fat oxidation were measured with the ventilated-hood technique. RESULTS: We observed a non-significant 56% increase in fat excretion (P=0.159) on the 2500 mg diet, compared to the 400 mg diet. The 2500 mg diet significantly reduced the expression of fatty acid synthase (FAS) mRNA (P<0.05) and the calcium content of the diets significantly affected calcium excretion. Furthermore, we saw a significant decrease of serum triglycerides on the 1200S diet (P<0.05). CONCLUSION: In this study, we observed a trend towards a higher fat excretion on the high-calcium diet, but this difference failed to reach statistical significance. It is possible that the relatively high protein content of the experimental diets increased calcium absorption from the intestine, thus decreasing the amount of calcium available for binding to fat and eliminating possible effects of dietary calcium on fat excretion. Furthermore, we observed decreases in FAS mRNA expression and serum triglycerides as a result of a high calcium intake.

Inhibition of adipose tissue lipolysis increases intramuscular lipid use in type 2 diabetic patients.

AIMS/HYPOTHESIS: In the present study, we investigated the consequences of adipose tissue lipolytic inhibition on skeletal muscle substrate use in type 2 diabetic patients. MATERIALS AND METHODS: We studied ten type 2 diabetic patients under the following conditions: (1) at rest; (2) during 60 min of cycling exercise at 50% of maximal workload capacity and subsequent recovery. Studies were done under normal, fasting conditions (control trial: CON) and following administration of a nicotinic acid analogue (low plasma non-esterified fatty acid trial: LFA). Continuous [U-13C]palmitate and [6,6 -2H2]glucose infusions were applied to quantify plasma NEFA and glucose oxidation rates, and to estimate intramuscular triacylglycerol (IMTG) and glycogen use. Muscle biopsies were collected before and after exercise to determine net changes in lipid and glycogen content specific to muscle fibre type. RESULTS: Following administration of the nicotinic acid analogue (Acipimox), the plasma NEFA rate of appearance was effectively reduced, resulting in lower NEFA concentrations in the LFA trial (p<0.001). Plasma NEFA oxidation rates were substantially reduced at rest, during exercise and subsequent recovery in the LFA trial. The lower plasma NEFA oxidation rates were compensated by an increase in IMTG and endogenous carbohydrate use (p<0.05). Plasma glucose disposal rates did not differ between trials. In accordance with the tracer data, a greater net decline in type I muscle fibre lipid content was observed following exercise in the LFA trial (p<0.05). CONCLUSIONS/INTERPRETATION: This study shows that plasma NEFA availability regulates IMTG use, and that adipose tissue lipolytic inhibition, in combination with exercise, could be an effective means of augmenting intramuscular lipid and glycogen use in type 2 diabetic patients in an overnight fasted state.

Relationship between gastro-intestinal complaints and endotoxaemia, cytokine release and the acute-phase reaction during and after a long-distance triathlon in highly trained men.

The aim of the present study was to establish whether gastro-intestinal (GI) complaints observed during and after ultra-endurance exercise are related to gut ischaemia-associated leakage of endotoxins [lipopolysaccharide (LPS)] into the circulation and associated cytokine production. Therefore we collected blood samples from 29 athletes before, immediately after, and 1, 2 and 16 h after a long-distance triathlon for measurement of LPS, tumour necrosis factor-alpha and interleukin-6 (IL-6). As the cytokine response would trigger an acute-phase response, characteristic variables of these responses were also measured, along with creatine kinase (CK) to obtain an indicator of muscle damage. There was a high incidence (93% of all participants) of GI symptoms; 45% reported severe complaints and 7% of the participants abandoned the race because of severe GI distress. Mild endotoxaemia (5-15 pg/ml) was evident in 68% of the athletes immediately after the race, as also indicated by a reduction in IgG anti-LPS levels. In addition, we observed production of IL-6 (27-fold increase immediately after the race), leading to an acute-phase response (20-fold increase in C-reactive protein and 12% decrease in pre-albumin 16 h after the race). The extent of endotoxaemia was not correlated with the GI complaints or the IL-6 response, but did show a correlation with the elevation in C-reactive protein (r(s) 0.389; P=0.037). Creatine kinase levels were increased significantly immediately post-race, and increased further in the follow-up period. Creatine kinase levels did not correlate with those of either IL-6 or C-reactive protein. It is therefore concluded that LPS does enter the circulation after ultra-endurance exercise and may, together with muscle damage, be responsible for the increased cytokine response and hence GI complaints in these athletes.

Carbohydrate ingestion can completely suppress endogenous glucose production during exercise.

The purposes of this study were 1) to investigate the effect of carbohydrate (CHO) ingestion on endogenous glucose production (EGP) during prolonged exercise, 2) to study whether glucose appearance in the circulation could be a limiting factor for exogenous CHO oxidation, and 3) to investigate whether large CHO feedings can reduce muscle glycogen oxidation during exercise. Six well-trained subjects exercised three times for 120 min at 50% maximum workload while ingesting water (FAST), a 4% glucose solution (LO-Glc), or a 22% glucose solution (HI-Glc). A primed continuous intravenous [6, 6-2H2]glucose infusion was given, and the ingested glucose was enriched with [U-13C]glucose. Glucose ingestion significantly elevated CHO oxidation as well as the rates of appearance (Ra) and disappearance. Ra glucose equaled Ra of glucose in gut (Ra gut) during HI-Glc, whereas EGP was completely suppressed. During LO-Glc, EGP was partially suppressed, whereas Ra gut provided most of the total glucose Ra. We conclude that 1) high rates of CHO ingestion can completely block EGP, 2) Ra gut may be a limiting factor for exogenous CHO oxidation, and 3) muscle glycogen oxidation was not reduced by large glucose feedings.

Glucose kinetics during prolonged exercise in highly trained human subjects: effect of glucose ingestion.

1. The objectives of this study were (1) to investigate whether glucose ingestion during prolonged exercise reduces whole body muscle glycogen oxidation, (2) to determine the extent to which glucose disappearing from the plasma is oxidized during exercise with and without carbohydrate ingestion and (3) to obtain an estimate of gluconeogenesis. 2. After an overnight fast, six well-trained cyclists exercised on three occasions for 120 min on a bicycle ergometer at 50 % maximum velocity of O2 uptake and ingested either water (Fast), or a 4 % glucose solution (Lo-Glu) or a 22 % glucose solution (Hi-Glu) during exercise. 3. Dual tracer infusion of [U-13C]-glucose and [6,6-2H2]-glucose was given to measure the rate of appearance (Ra) of glucose, muscle glycogen oxidation, glucose carbon recycling, metabolic clearance rate (MCR) and non-oxidative disposal of glucose. 4. Glucose ingestion markedly increased total Ra especially with Hi-Glu. After 120 min Ra and rate of disappearance (Rd) of glucose were 51-52 micromol kg-1 min-1 during Fast, 73-74 micromol kg-1 min-1 during Lo-Glu and 117-119 micromol kg-1 min-1 during Hi-Glu. The percentage of Rd oxidized was between 96 and 100 % in all trials. 5. Glycogen oxidation during exercise was not reduced by glucose ingestion. The vast majority of glucose disappearing from the plasma is oxidized and MCR increased markedly with glucose ingestion. Glucose carbon recycling was minimal suggesting that gluconeogenesis in these conditions is negligible.