Comparative effectiveness of after-school programs to increase physical activity.

BACKGROUND: We conducted a comparative effectiveness analysis to evaluate the difference in the amount of physical activity children engaged in when enrolled in a physical activity-enhanced after-school program based in a community recreation center versus a standard school-based after-school program. METHODS: The study was a natural experiment with 54 elementary school children attending the community ASP and 37 attending the school-based ASP. Accelerometry was used to measure physical activity. Data were collected at baseline, 6 weeks, and 12 weeks, with 91% retention. RESULTS: At baseline, 43% of the multiethnic sample was overweight/obese, and the mean age was 7.9 years (SD = 1.7). Linear latent growth models suggested that the average difference between the two groups of children at Week 12 was 14.7 percentage points in moderate-vigorous physical activity (P < .001). Cost analysis suggested that children attending traditional school-based ASPs-at an average cost of $17.67 per day-would need an additional daily investment of $1.59 per child for 12 weeks to increase their moderate-vigorous physical activity by a model-implied 14.7 percentage points. CONCLUSIONS: A low-cost, alternative after-school program featuring adult-led physical activities in a community recreation center was associated with increased physical activity compared to standard-of-care school-based after-school program.

The tumor necrosis factor-α gene -238G>A polymorphism, dietary fat intake, obesity risk and serum lipid concentrations in black and white South African women.

BACKGROUND/OBJECTIVES: This study explored interactions between dietary fat intake and the tumor necrosis factor-α gene (TNFA) -238G>A polymorphism (rs361525) on adiposity and serum lipid concentrations in apparently healthy premenopausal black and white South African (SA) women. SUBJECTS/METHODS: Normal-weight (N=107) and obese (N=120) black, and normal-weight (N=89) and obese (N=62) white SA women underwent measurements of body composition, fasting lipids and dietary intake, and were genotyped for the -238G>A polymorphism. RESULTS: Black women had a higher -238GA genotype frequency than white women (P<0.001), but there were no differences between body mass index groups. Black women with the -238A allele had a greater body fat % than those with the GG genotype (P<0.001). Further, in black women, with increasing polyunsaturated:saturated fat ratio and omega-6 (n-6):omega-3 (n-3) ratio, high-density lipoprotein-cholesterol (HDL-C) concentrations decreased, and total cholesterol (T-C):HDL-C ratio increased in those with the GA genotype but not the GG genotype. In addition, with increasing n-3 polyunsaturated fatty acid intake (percentage of total energy intake, %E), T-C:HDL-C ratio decreased in those with the GA genotype, but not in those with the GG genotype. In white SA women, with increasing eicosapentaenoic acid (%E) intake, low-density lipoprotein-cholesterol concentrations decreased in those with the GG genotype but not the GA genotype. CONCLUSIONS: The -238G>A polymorphism was associated with body fatness in black women. Interactions between -238G>A genotypes and dietary fat intake on serum lipids and adiposity differed depending on dietary fat intake, but those for serum lipids were not the same in black and white SA women.

Visual stimulus deprivation and manipulation of auditory timing signals on pacing strategy.

In this study the effect of complete visual stimulus deprivation and manipulation of auditory timing signals during this deprivation on pacing strategy during an exercise bout were examined. 7 moderately trained men completed four 40-km cycling time trials under laboratory conditions in either normal light or absolute darkness, with either correct or manipulated auditory timing signals and without any other timing cues. The subjects were told to perform the time trial in the fastest time possible. There was no significant difference among trials for time to perform the trial, power output, heart rate, or ratings of perceived exertion, indicating that brain-control mechanisms responsible for pacing are not affected by manipulation of light or auditory signals.

Noradrenaline synthesis, release and vesicular transport in the rat brain following subarachnoid haemorrhage.

The present study was designed to estimate the release of noradrenaline, and to evaluate the efficiency of noradrenaline vesicular transport, as indicated from measures of dihydroxyphenylglycol (DHPG), and synthesis in the medulla and hypothalamus following subarachnoid haemorrhage in rats. Subarachnoid haemorrhage was induced by the injection of homologous blood into the cisterna magna (n = 11). Sham operated animals served as controls (n = 11). Three days following subarachnoid haemorrhage, medulla and hypothalamus were dissected and placed in an in vitro superfusion system. Exposure to K(+) (50 mM) for 2 min served as a stimulus for the release of the neurotransmitter noradrenaline, its precursor (dihydroxyphenylalanine [DOPA]) and intraneuronal metabolite, DHPG. Basal noradrenaline overflow from both the medulla and hypothalamus were similar in the two groups of rats but basal DOPA overflow from the medulla was significantly reduced in the subarachnoid haemorrhage animals (0.97 +/- 0.15 vs. 1.97 +/- 0.38 pg/10 min/mg, p < 0.01). Administration of K(+) induced the release of noradrenaline, the response from the medulla in the subarachnoid haemorrhage group being attenuated (p < 0.01) compared with the sham operated animals (174% and 240%, respectively). K(+) induced a similar release of noradrenaline from the hypothalamus in both groups of rats (239% in sham animals and 283% in the subarachnoid haemorrhage group). The overflow of DHPG from both the hypothalamus and medulla was similar in both groups of animals. Our results suggest that the diminution in noradrenaline release from the medulla occurs as a result of a reduction in the rate of noradrenaline synthesis and release.

Beneficial effect of renin-angiotensin system for maintaining blood pressure control following subarachnoid haemorrhage.

Subarachnoid haemorrhage is a serious condition often accompanied by delayed cerebral ischaemia. Earlier reports have provided evidence suggesting a role for angiotensin II in the development of cerebral vasospasm following subarachnoid bleeding. We sought to examine the influence of angiotensin II blockade with losartan on blood pressure and survival in animals following experimental subarachnoid haemorrhage, induced in conscious rats by injecting homologous blood via a catheter placed along the surface of the brain. We combined measurements of plasma renin activity with blood pressure recording in order to examine renin-angiotensin system activation following experimental subarachnoid haemorrhage. Following subarachnoid injury an approximately three-fold increase in plasma renin activity occurred (3.4 +/- 1.0 vs. 10.1 +/- 1.8 ng angiotensin I produced/ml/h, p < 0.01). In animals treated with losartan (20 mg/kg) prior to the induction of subarachnoid haemorrhage blood pressure fell dramatically following the cerebral injury (124 +/- 5 vs. 94 +/- 7 mmHg, p < 0.001), whereas blood pressure remained unchanged in control animals. Survival was markedly reduced in those animals treated with losartan. Given the pronounced decrease in blood pressure and impaired survival following subarachnoid haemorrhage in animals treated with losartan, it would appear that the acute activation of the renin-angiotensin system following this insult is in fact a desirable, compensatory response.

Nutritional strategies for promoting fat utilization and delaying the onset of fatigue during prolonged exercise.

Carbohydrate ingestion before and during endurance exercise delays the onset of fatigue (reduced power output). Therefore, endurance athletes are recommended to ingest diets high in carbohydrate (70% of total energy) during competition and training. However, increasing the availability of plasma free fatty acids has been shown to slow the rate of muscle and liver glycogen depletion by promoting the utilization of fat. Ingested fat, in the form of long-chain (C16-22) triacylglycerols, is largely unavailable during acute exercise, but medium-chain (C8-10) triacylglycerols are rapidly absorbed and oxidized. We have shown that the ingestion of medium-chain triacylglycerols in combination with carbohydrate spares muscle carbohydrate stores during 2 h of submaximal (< 70% VO2 peak) cycling exercise, and improves 40 km time-trial performance. These data suggest that by combining carbohydrate and medium-chain triacylglycerols as a pre-exercise supplement and as a nutritional supplement during exercise, fat oxidation will be enhanced, and endogenous carbohydrate will be spared. We have also examined the chronic metabolic adaptations and effects on substrate utilization and endurance performance when athletes ingest a diet that is high in fat (> 70% by energy). Dietary fat adaptation for a period of at least 2-4 weeks has resulted in a nearly two-fold increase in resistance to fatigue during prolonged, low- to moderate-intensity cycling (< 70% VO2 peak). Moreover, preliminary studies suggest that mean cycling 20 km time-trial performance following prolonged submaximal exercise is enhanced by 80 s after dietary fat adaptation and 3 days of carbohydrate loading. Thus the relative contribution of fuel substrate to prolonged endurance activity may be modified by training, pre-exercise feeding, habitual diet, or by artificially altering the hormonal milieu or the availability of circulating fuels. The time course and dose-response of these effects on maximizing the oxidative contribution of fat for exercise metabolism and in exercise performance have not been systematically studied during moderate- to high-intensity exercise in humans.

A transgenic mouse model of the slow-channel syndrome.

To investigate the effect of acetylcholine receptor (AChR) mutations on neuromuscular transmission and to develop a model for the human neuromuscular disease, the slow-channel syndrome, we generated transgenic mice with abnormal AChRs using a delta subunit with a mutation in the ion channel domain. In three transgenic lines, nerve-evoked end-plate currents and spontaneous miniature end-plate currents (MEPCs) had prolonged decay phases and MEPC amplitudes were reduced by 33%. Single nerve stimuli elicited repetitive compound muscle action potentials in vivo. Transgenic mice were abnormally sensitive to the neuromuscular blocker, curare. These observations demonstrate that we can predictably alter AChR function, synaptic responses, and muscle fiber excitation in vivo by overexpressing subunits containing well-defined mutations. Furthermore these data support the hypothesis that the electrophysiological findings in the neuromuscular disorder, the slow-channel syndrome, are due to mutant AChRs.

Plasma lipid concentrations in children with cystic fibrosis: the value of a high-fat diet and pancreatic supplementation.

Impaired digestion of dietary fat is an almost universal feature of cystic fibrosis (CF) which results in low concentrations of essential fatty acids in plasma lipids. We have evaluated the effect of a high-lipid diet and pancreatic enzyme supplementation, using enteric-coated microsphere preparations, on plasma lipid concentrations in paediatric CF patients. Absorption of dietary lipid was comparable between control and CF subjects. This resulted in plasma cholesterol, triacylglycerol, total phosphatidylcholine and individual phosphatidylcholine molecular species concentrations in CF patients which were in the same range as those in controls. Normal values for these variables were also found in patients with clinically detectable liver disease. These results show that present dietary management of CF patients supports normal plasma lipid concentrations.