Three minutes of all-out intermittent exercise per week increases skeletal muscle oxidative capacity and improves cardiometabolic health.

We investigated whether a training protocol that involved 3 min of intense intermittent exercise per week--within a total training time commitment of 30 min including warm up and cool down--could increase skeletal muscle oxidative capacity and markers of health status. Overweight/obese but otherwise healthy men and women (n = 7 each; age = 29±9 y; BMI = 29.8±2.7 kg/m2) performed 18 training sessions over 6 wk on a cycle ergometer. Each session began with a 2 min warm-up at 50 W, followed by 3×20 s "all-out" sprints against 5.0% body mass (mean power output: ∼450-500 W) interspersed with 2 min of recovery at 50 W, followed by a 3 min cool-down at 50 W. Peak oxygen uptake increased by 12% after training (32.6±4.5 vs. 29.1±4.2 ml/kg/min) and resting mean arterial pressure decreased by 7% (78±10 vs. 83±10 mmHg), with no difference between groups (both p<0.01, main effects for time). Skeletal muscle biopsy samples obtained before and 72 h after training revealed increased maximal activity of citrate synthase and protein content of cytochrome oxidase 4 (p<0.01, main effect), while the maximal activity of ß-hydroxy acyl CoA dehydrogenase increased in men only (p<0.05). Continuous glucose monitoring measured under standard dietary conditions before and 48-72 h following training revealed lower 24 h average blood glucose concentration in men following training (5.4±0.6 vs. 5.9±0.5 mmol/L, p<0.05), but not women (5.5±0.4 vs. 5.5±0.6 mmol/L). This was associated with a greater increase in GLUT4 protein content in men compared to women (138% vs. 23%, p<0.05). Short-term interval training using a 10 min protocol that involved only 1 min of hard exercise, 3x/wk, stimulated physiological changes linked to improved health in overweight adults. Despite the small sample size, potential sex-specific adaptations were apparent that warrant further investigation.

No effect of short-term green tea extract supplementation on metabolism at rest or during exercise in the fed state.

UNLABELLED: Supplementation with green tea extract (GTE) in animals has been reported to induce numerous metabolic adaptations including increased fat oxidation during exercise and improved performance. However, data regarding the metabolic and physiological effects of GTE during exercise in humans are limited and equivocal. PURPOSE: To examine the effects of short-term GTE treatment on resting energy expenditure (REE), wholebody substrate utilization during exercise and time trial performance. METHODS: Fifteen active men (24 ± 3 y; VO(2)peak = 48 ± 7 ml · kg · min(-1); BMI = 26 ± 3 kg · m(2)((-1))) ingested GTE (3x per day = 1,000 mg/d) or placebo (PLA) for 2 day in a double-blind, crossover design (each separated by a 1 week wash-out period). REE was assessed in the fasted state. Subjects then ingested a standardized breakfast (~5.0 kcal · kg(-1)) and 90 min later performed a 60 min cycling bout at an intensity corresponding to individual maximal fat oxidation (44 ± 11% VO(2)peak), followed by a 250 kJ TT. RESULTS: REE, whole-body oxygen consumption (VO2) and substrate oxidation rates during steady-state exercise were not different between treatments. However, mean heart rate (HR) was lower in GTE vs. PLA (115 ± 16 vs. 118 ± 17 beats · min(-1); main effect, p = .049). Mixed venous blood [glycerol] was higher during rest and exercise after GTE vs. PLA (p = .006, main effect for treatment) but glucose, insulin and free-fatty acids were not different. Subsequent time trial performance was not different between treatments (GTE = 25:38 ± 5:32 vs. PLA = 26:08 ± 8:13 min; p = .75). CONCLUSION: GTE had minimal effects on whole-body substrate metabolism but significantly increased plasma glycerol and lowered heart rate during steady-state exercise, suggesting a potential increase in lipolysis and a cardiovascular effect that warrants further investigation.

Mapping of the Plasmodium chabaudi resistance locus char2.

Animals congenic for the char2 host response locus to the murine malarial parasite Plasmodium chabaudi have been bred, and they demonstrated a phenotypic difference from the parental lines. These congenic lines have been crossed back to the parental line to generate recombinants across the congenic intervals. The recombinants were inbred, and the subcongenic intervals were fixed. These lines were then challenged with parasites and assessed as being either resistant or susceptible. From the analysis of many subcongenic lines, it has become obvious that there are at least two loci underlying the char2 locus and that both of these mediate resistance when the haplotype derives from the resistant C57BL/6 strain.

On the utility of data from the International HapMap Project for Australian association studies.

We compare patterns of linkage disequilibrium (LD) for 633 SNPs in two regions between samples collected in two Australian states and HapMap samples collected from Utah residents of Northern and Western (NW) European ancestry (CEU). Patterns of LD in the Australian and HapMap samples are similar, and tag SNPs chosen using HapMap genotypes perform almost as well on Australian samples as tags chosen using Australian genotypes.