Carbohydrate metabolism during exercise in females : effect of reduced fat availability

This study examined the effect of reduced plasma free fatty acid (FFA) availability on carbohydrate metabolism during exercise. Six untrained women cycled for 60 minutes at approximately 58% of maximum oxygen uptake after ingestion of a placebo (CON) or nicotinic acid (NA), 30 minutes before exercise (7.4 &plusmn; 0.5 mg·kgp>−1p> body weight), and at 0 minutes (3.7 &plusmn; 0.3 mg·kgp>−1p>) and 30 minutes (3.7 &plusmn; 0.3 mg·kgp>−1p>) of exercise. Glucose kinetics were measured using a primed, continuous infusion of [6,6-p>2p>H] glucose. Plasma FFA (CON, 0.86 &plusmn; 0.12; NA, 0.21 &plusmn; 0.11 mmol·Lp>−1p> at 60 minutes, P < .05) and glycerol (CON, 0.34 &plusmn; 0.05; NA, 0.10 &plusmn; 0.04 mmol·Lp>−1p> at 60 minutes, P < .05) were suppressed throughout exercise. Mean respiratory exchange ratio (RER) during exercise was higher (P < .05) in NA (0.89 &plusmn; 0.02) than CON (0.83 &plusmn; 0.02). Plasma glucose and glucose production were similar between trials. Total glucose uptake during exercise was greater (P < .05) in NA (1,876 &plusmn; 161 μmol·kgp>−1p>) than in CON (1,525 &plusmn; 107 μmol·kgp>−1p>). Total fat oxidation was reduced (P < .05) by approximately 32% during exercise in NA. Total carbohydrate oxidized was approximately 42% greater (P < .05) in NA (412 &plusmn; 40 mmol) than CON (290 &plusmn; 37 mmol), of which, approximately 16% (20 &plusmn; 10 mmol) could be attributed to glucose. Plasma insulin and glucagon were similar between trials. Catecholamines were higher (P < .05) during exercise in NA. In summary, during prolonged moderate exercise in untrained women, reduced FFA availability results in a compensatory increase in carbohydrate oxidation, which appears to be due predominantly to an increase in glycogen utilization, although there was a small, but significant, increase in whole body glucose uptake.

Food cost and availability in a rural setting in Australia

Introduction: The burden of chronic diseases is rapidly increasing worldwide. In&nbsp; Australia rural populations have a greater burden of disease. Chronic diseases are largely preventable with diet as a key risk factor. With respect to diet-related chronic disease, dietary risk may be due to poor food access, namely, poor availability and/or the high cost of healthy food. It is likely that poor food access is an issue in rural areas. Objective: To assess food access in rural south-west (SW) Victoria, Australia.

Methods: A total of 53 supermarkets and grocery stores in 42 towns participated in a survey of food cost and availability in the rural area of SW Victoria. The survey assessed availability and cost of a Healthy Food Access Basket (HFAB) which was designed to meet the nutritional needs of a family of 6 for 2 weeks.

Results: Seventy-two percent of the eligible shops in SW Victoria were surveyed. The study found that the complete HFAB was significantly more likely to be available in a town with a chain-owned store (p<0.00). The complete HFAB was less likely to be available from an independently owned store in a town with only one grocery shop (p<0.004). The average cost of the HFAB across SW Victoria was AU$380.30 &plusmn; $25.10 (mean &plusmn; SD). There was a mean range in difference of cost of the HFAB of $36.92. In particular, high variability was found in the cost of fruits and vegetables.

Conclusions: Cost and availability of healthy food may be compromised in rural areas. Implications: Improvements in food access in rural areas could reduce the high burden of disease suffered by rural communities.

Glycogen availability does not affect the TCA cycle or TAN pools during prolonged, fatiguing exercise

The hypothesis that fatigue during prolonged exercise arises from insufficient intramuscular glycogen, which limits tricarboxylic acid cycle (TCA) activity due to reduced TCA cycle intermediates (TCAI), was tested in this experiment. Seven endurance-trained men cycled at approximately 70% of peak O(2) uptake (Vo(2 peak)) until exhaustion with low (LG) or high (HG) preexercise intramuscular glycogen content. Muscle glycogen content was lower (P < 0.05) at fatigue than at rest in both trials. However, the increase in the sum of four measured TCAI (>70% of the total TCAI pool) from rest to 15 min of exercise was not different between trials, and TCAI content was similar after 103 +/- 15 min of exercise (2.62 +/- 0.31 and 2.59 +/- 0.28 mmol/kg dry wt for LG and HG, respectively), which was the point of volitional fatigue during LG. Subjects cycled for an additional 52 +/- 9 min during HG, and although glycogen was markedly reduced (P < 0.05) during this period, no further change in the TCAI pool was observed, thus demonstrating a clear dissociation between exercise duration and the size of the TCAI pool. Neither the total adenine nucleotide pool (TAN = ATP + ADP + AMP) nor IMP was altered compared with rest in either trial, whereas creatine phosphate levels were not different when values measured at fatigue were compared with those measured after 15 min of exercise. These data demonstrate that altered glycogen availability neither compromises TCAI pool expansion nor affects the TAN pool or creatine phosphate or IMP content during prolonged exercise to fatigue. Therefore, our data do not support the concept that a decrease in muscle TCAI during prolonged exercise in humans compromises aerobic energy provision or is the cause of fatigue.

Carbohydrate ingestion reduces skeletal muscle acetylcarnitine availability but has no effect on substrate phosphorylation at the onset of exercise in man

This study investigated the effect of reduced acetylcarnitine availability on oxidative metabolism during the transition from rest to steady-state exercise. Eight male subjects completed two randomised exercise trials at 68 % of the peak rate of O2 uptake (V̇O2,peak). On one occasion subjects ingested 1 g (kg body mass)−1 glucose 75 min prior to exercise (CHO), whereas the other trial acted as a control (CON). Muscle samples were obtained pre- and 75 min post-ingestion, and following 1 and 10 min of exercise. Plasma glucose and insulin were elevated (P < 0.05), and plasma free fatty acids (FFA) were lower at the onset of exercise in CHO. Acetylcarnitine (CON, 4.8 &plusmn; 1.8; CHO, 1.5 &plusmn; 0.9 mmol (kg dry mass (d.m.))−1, P < 0.05) and acetyl CoA (CON, 13.2 &plusmn; 2.3; CHO, 6.3 &plusmn; 0.6 μmol (kg d.m.)−1, P < 0.05) were lower at rest, whereas pyruvate dehydrogenase activation (PDHa) was greater in CHO compared with CON (CON, 0.78 &plusmn; 0.07; CHO, 1.44 &plusmn; 0.19 mmol min−1 (kg wet mass (w.m.))−1). Respiratory exchange ratio (RER) was significantly elevated during exercise in CHO. The acetyl groups increased at similar rates at the onset of exercise (1 min) and there was no difference in substrate phosphorylation as determined from lactate accumulation and phosphocreatine degradation between trials. Subsequently, oxidative metabolism during the transition from rest to steady-state exercise was not affected by prior carbohydrate ingestion. Although exercise resulted in the rapid activation of PDH in both trials, PDHa was greater at 1 min in CHO (CON, 2.36 &plusmn; 0.22; CHO, 2.91 &plusmn; 0.18 mmol min−1 (kg w.m.)−1). No differences in muscle metabolite levels and PDHa were observed after 10 min of moderate exercise between trials. In summary, at rest, carbohydrate ingestion induced multiple metabolic changes which included decreased acetylcarnitine availability and small increases in PDHa. The prior changes in PDHa and acetylcarnitine availability had no effect on substrate phosphorylation and oxidative metabolism at the onset of exercise. These data suggest that acetylcarnitine availability is unlikely to be the site of metabolic inertia during the transition from rest to steady-state moderate intensity exercise.

Adaptations to short-term high-fat diet persist during exercise despite high carbohydrate availability

Purpose: Five days of a high-fat diet produce metabolic adaptations that increase the rate of fat oxidation during prolonged exercise. We investigated whether enhanced rates of fat oxidation during submaximal exercise after 5 d of a high-fat diet would persist in the face of increased carbohydrate (CHO) availability before and during exercise.


Methods: Eight well-trained subjects consumed either a high-CHO (9.3 g·kg-1·d-1 CHO, 1.1 g·kg-1·d-1 fat; HCHO) or an isoenergetic high-fat diet (2.5 g·kg-1·d-1 CHO, 4.3 g·kg-1·d-1 fat; FAT-adapt) for 5 d followed by a high-CHO diet and rest on day 6. On day 7, performance testing (2 h steady-state (SS) cycling at 70% peak O2 uptake [[latin capital V with dot above]O2peak] + time trial [TT]) of 7 kJ·kg-1) was undertaken after a CHO breakfast (CHO 2 g·kg-1) and intake of CHO during cycling (0.8 g·kg-1·h-1).


Results: FAT-adapt reduced respiratory exchange ratio (RER) values before and during cycling at 70% [latin capital V with dot above]O2peak; RER was restored by 1 d CHO and CHO intake during cycling (0.90 &plusmn; 0.01, 0.80 &plusmn; 0.01, 0.91 &plusmn; 0.01, for days 1, 6, and 7, respectively). RER values were higher with HCHO (0.90 &plusmn; 0.01, 0.88 &plusmn; 0.01 (HCHO > FAT-adapt, P < 0.05), 0.95 &plusmn; 0.01 (HCHO > FAT-adapt, P < 0.05)). On day 7, fat oxidation remained elevated (73 &plusmn; 4 g vs 45 &plusmn; 3 g, P < 0.05), whereas CHO oxidation was reduced (354 &plusmn; 11 g vs 419 &plusmn; 13 g, P < 0.05) throughout SS in FAT-adapt versus HCHO. TT performance was similar for both trials (25.53 &plusmn; 0.67 min vs 25.45 &plusmn; 0.96 min, NS).


Conclusion: Adaptations to a short-term high-fat diet persisted in the face of high CHO availability before and during exercise, but failed to confer a performance advantage during a TT lasting ~ 25 min undertaken after 2 h of submaximal cycling.

The ΔF508-CFTR mutation results in increased biofilm formation by Pseodomonas aeruginosa by increasing iron availability

Enhanced antibiotic resistance of Pseudomonas aeruginosa in the cystic fibrosis (CF) lung is thought to be due to the formation of biofilms. However, there is no information on the antibiotic resistance of P. aeruginosa biofilms grown on human airway epithelial cells or on the effects of airway cells on biofilm formation by P. aeruginosa. Thus we developed a coculture model and report that airway cells increase the resistance of P. aeruginosa to tobramycin (Tb) by >25-fold compared with P. aeruginosa grown on abiotic surfaces. Therefore, the concentration of Tb required to kill P. aeruginosa biofilms on airway cells is 10-fold higher than the concentration achievable in the lungs of CF patients. In addition, CF airway cells expressing ΔF508-CFTR significantly enhanced P. aeruginosa biofilm formation, and ΔF508 rescue with wild-type CFTR reduced biofilm formation. Iron (Fe) content of the airway in CF is elevated, and Fe is known to enhance P. aeruginosa growth. Thus we investigated whether enhanced biofilm formation on ΔF508-CFTR cells was due to increased Fe release by airway cells. We found that airway cells expressing ΔF508-CFTR released more Fe than cells rescued with WT-CFTR. Moreover, Fe chelation reduced biofilm formation on airway cells, whereas Fe supplementation enhanced biofilm formation on airway cells expressing WT-CFTR. These data demonstrate that human airway epithelial cells promote the formation of P. aeruginosa biofilms with a dramatically increased antibiotic resistance. The ΔF508-CFTR mutation enhances biofilm formation, in part, by increasing Fe release into the apical medium.

Effect of increased blood glucose availability on glucose kinetics during exercise

This study examined the effect of increased blood glucose availability on glucose kinetics during exercise. Five trained men cycled for 40 min at 77 &plusmn; 1% peak oxygen uptake on two occasions. During the second trial (Glu), glucose was infused at a rate equal to the average hepatic glucose production (HGP) measured during exercise in the control trial (Con). Glucose kinetics were measured by a primed continuous infusion ofd-[3-3H]glucose. Plasma glucose increased during exercise in both trials and was significantly higher in Glu. HGP was similar at rest (Con, 11.4&thinsp;&plusmn;&thinsp;1.2; Glu, 10.6&thinsp;&plusmn;&thinsp;0.6 μmol ⋅ kg−1 ⋅ min−1). After 40 min of exercise, HGP reached a peak of 40.2 &plusmn; 5.5 μmol ⋅ kg−1 ⋅ min−1in Con; however, in Glu, there was complete inhibition of the increase in HGP during exercise that never rose above the preexercise level. The rate of glucose disappearance was greater (P < 0.05) during the last 15 min of exercise in Glu. These results indicate that an increase in glucose availability inhibits the rise in HGP during exercise, suggesting that metabolic feedback signals can override feed-forward activation of HGP during strenuous exercise.

Skeletal muscle fat metabolism after exercise in humans: influence of fat availability

The mechanisms facilitating increased skeletal muscle fat oxidation following prolonged, strenuous exercise remain poorly defined. The aim of this study was to examine the influence of plasma free fatty acid (FFA) availability on intramuscular malonyl-CoA concentration and the regulation of whole-body fat metabolism during a 6-h postexercise recovery period. Eight endurance-trained men performed three trials, consisting of 1.5 h high-intensity and exhaustive exercise, followed by infusion of saline, saline + nicotinic acid (NA; low FFA), or Intralipid and heparin [high FFA (HFA)]. Muscle biopsies were obtained at the end of exercise (0 h) and at 3 and 6 h in recovery. Ingestion of NA suppressed the postexercise plasma FFA concentration throughout recovery (P < 0.01), except at 4 h. The alteration of the availability of plasma FFA during recovery induced a significant increase in whole-body fat oxidation during the 6-h period for HFA (52.2 &plusmn; 4.8 g) relative to NA (38.4 &plusmn; 3.1 g; P < 0.05); however, this response was unrelated to changes in skeletal muscle malonyl-CoA and acetyl-CoA carboxylase (ACC)β phosphorylation, suggesting mechanisms other than phosphorylation-mediated changes in ACC activity may have a role in regulating fat metabolism in human skeletal muscle during postexercise recovery. Despite marked changes in plasma FFA availability, no significant changes in intramuscular triglyceride concentrations were detected. These data suggest that the regulation of postexercise skeletal muscle fat oxidation in humans involves factors other than the 5&prime;AMP-activated protein kinase-ACCβ-malonyl-CoA signaling pathway, although malonyl-CoA-mediated regulation cannot be excluded completely in the acute recovery period.

Adolescent television viewing and unhealthy snack food consumption: the mediating role of home availability of unhealthy snack foods

Objective
To examine whether home availability of energy-dense snack foods mediates the association between television (TV) viewing and energy-dense snack consumption among adolescents.
Design
Cross-sectional.
Setting
Secondary schools in Victoria, Australia.
Subjects
Adolescents (n 2984) from Years 7 and 9 of secondary school completed a web-based survey, between September 2004 and July 2005, assessing their energy-dense snack food consumption, school-day and weekend-day TV viewing and home availability of energy-dense snack foods.
Results
School-day and weekend-day TV viewing were positively associated with energy-dense snack consumption among adolescent boys (β = 0·003, P < 0·001) and girls (β = 0·03, P < 0·001). Furthermore, TV viewing (school day and weekend day) were positively associated with home availability of energy-dense snack foods among adolescent boys and girls and home availability of energy-dense snack foods was positively associated with energy-dense snack food consumption among boys (β = 0·26, P < 0·001) and girls (β = 0·28, P < 0·001). Home availability partly mediated the association between TV viewing and energy-dense snack consumption.
Conclusions
The results of the present study suggest that TV viewing has a significant role to play in adolescent unhealthy eating behaviours. Future research should assess the efficacy of methods to reduce adolescent energy-dense snack food consumption by targeting parents to reduce home availability of energy-dense foods and by reducing TV viewing behaviours of adolescents.

Fishy business : effect of omega-3 fatty acids on zinc transporters and free zinc availability in human neuronal cells

Omega-3 (ω-3) fatty acids are one of the two main families of long chain polyunsaturated fatty acids (PUFA). The main omega-3 fatty acids in the mammalian body are &alpha;-linolenic acid (ALA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). Central nervous tissues of vertebrates are characterized by a high concentration of omega-3 fatty acids. Moreover, in the human brain, DHA is considered as the main structural omega-3 fatty acid, which comprises about 40% of the PUFAs in total. DHA deficiency may be the cause of many disorders such as depression, inability to concentrate, excessive mood swings, anxiety, cardiovascular disease, type 2 diabetes, dry skin and so on. On the other hand, zinc is the most abundant trace metal in the human brain. There are many scientific studies linking zinc, especially excess amounts of free zinc, to cellular death. Neurodegenerative diseases, such as Alzheimer's disease, are characterized by altered zinc metabolism. Both animal model studies and human cell culture studies have shown a possible link between omega-3 fatty acids, zinc transporter levels and free zinc availability at cellular levels. Many other studies have also suggested a possible omega-3 and zinc effect on neurodegeneration and cellular death. Therefore, in this review, we will examine the effect of omega-3 fatty acids on zinc transporters and the importance of free zinc for human neuronal cells. Moreover, we will evaluate the collective understanding of mechanism(s) for the interaction of these elements in neuronal research and their significance for the diagnosis and treatment of neurodegeneration.