Sprint interval training (SIT) and traditional endurance training elicit similar physiological adaptations. From the perspective of metabolic function, superior glucose regulation is a common characteristic of endurance-trained adults. Accordingly, we have investigated the hypothesis that short-term SIT will increase insulin sensitivity in sedentary/recreationally active humans. Thirty one healthy adults were randomly assigned to one of three conditions: (1) −1 min −1 : % EE 11 ± 2, 14 ± 3, 23 ± 2 vs. 11 ± 1, 16 ± 2, 25 ± 3; P = 0.79). Combined data from both studies revealed no effect of SIT on fasted circulating concentrations of glucose, insulin, adiponectin, pigment epithelial-derived factor, non-esterified fatty acids or noradrenaline (all P > 0.05). Sixteen minutes of high-intensity exercise over 14 days augments insulin sensitivity but does not affect the thermogenic response to β-AR stimulation. Abbreviations β-AR, beta-adrenergic receptor; EE, energy expenditure; FFM, fat-free mass; GLUT4, glucose transporter 4; NEFA, non-esterified fatty acids; PEDF, pigment epithelial-derived factor; RER, respiratory exchange ratio; SIT, sprint interval training;V O 2 ,peak , peak oxygen uptake.

Improved endurance exercise performance in adult humans after sprint interval training (SIT) has been attributed to mitochondrial biogenesis. However, muscle protein synthesis (MPS) and mitochondrial biogenesis during SIT have not been measured, nor have sex-specific differences. We hypothesized that males and females would have similar rates of MPS, mitochondrial biogenesis, and synthesis of individual proteins during SIT. Deuterium oxide (D2O) was orally administered to 21 adults [11 male, 10 female; mean age, 23±1 yr; body mass index (BMI), 22.8±0.6 kg/m(2); mean± SE] for 4 wk, to measure protein synthesis rates while completing 9 sessions of 4-8 bouts of 30 s duration on a cycle ergometer separated by 4 min of active recovery. Samples of the vastus lateralis were taken before and 48 h after SIT. SIT increased maximum oxygen uptake (VO(2max), males 43.4±2.1-44.0±2.3; females 39.5±0.9-42.5±1.3 ml/kg/min; P=0.002). MPS was greater in the males than in the females in the mixed (~150%; P < 0.001), cytosolic (~135%; P=0.038), and mitochondrial (~135%; P=0.056) fractions. The corresponding ontological clusters of individual proteins were significantly greater in the males than in the females (all P<0.00001). For the first time, we document greater MPS and mitochondrial biogenesis during SIT in males than in females and describe the synthetic response of individual proteins in humans during exercise training.

Epigallocatechin-3-gallate (EGCG), a component of green tea, increases endurance performance in animals and promotes fat oxidation during cycle ergometer exercise in adult humans. Purpose We have investigated the hypothesis that short-term consumption of EGCG delays the onset of the ventilatory threshold (TVE) and increases maximal oxygen uptake (VO2max). Methods In this randomized, repeated measures, double blind study, 19 healthy adults (11 males, 8 females, age: 26 ± 2 years (mean ± SE)) received 7 placebo or 7 EGCG (135 mg) pills. 48-hours prior to data collection participants began consuming 3 pills per day; the last pill was taken 2-hours before exercise testing. TVE and VO2max were determined from breath-by-breath indirect calorimetry data collected during continuous incremental stationary cycle ergometer exercise (20-35 W/min), from rest until volitional fatigue. Each condition/exercise test was separated by a minimum of 14-days. Results Compared with placebo, short-term EGCG consumption increased VO2max (3.123 ± 0.187 vs. 3.259 ± 0.196 L·min-1, P=0.04). Maximal work rate (301 ± 15 vs. 301 ± 16 W, P=0.98), maximal respiratory exchange ratio (1.21 ± 0.01 vs. 1.22 ± 0.02, P=0.27), and maximal heart rate were unaffected (180 ± 3 vs. 180 ± 3 beats·min-1, P=0.87). In a subset of subjects (n=11) maximal cardiac output (determined via open-circuit acetylene breathing) was also unaffected by EGCG (29.6 ± 2.2 vs. 30.2 ± 1.4 L·min-1, P=0.70). Contrary to our hypothesis, EGCG decreased VO2 at TVE (1.57 ± 0.11 vs. 1.48 ± 0.10 L·min-1) but this change was not significant (P=0.06). Conclusion Short-term consumption of EGCG increased VO2max without affecting maximal cardiac output, suggesting that EGCG may increase arterial-venous oxygen difference.

Green tea is purported to promote weight loss. Resting metabolic rate (RMR) and the thermic effect of feeding (TEF) are significant components of total daily energy expenditure and are partially determined by the sympathetic nervous system via catecholamine‐mediated stimulation of β‐adrenergic receptors. Epigallocatechin‐3‐gallate (EGCG: the most bioactive catechin in green tea) inhibits catechol‐O‐methyltransferase, an enzyme contributing to the degradation of catecholamines. Accordingly, we hypothesized that short‐term consumption of a commercially available EGCG supplement (Teavigo) augments RMR and TEF. On two separate occasions, seven placebo or seven EGCG capsules (135 mg/capsule) were administered to 16 adults (9 males, 7 females, age 25 ± 2 years, BMI 24.6 ± 1.2 kg/m2 (mean ± s.e.)). Capsules (three/day) were consumed over 48 h; the final capsule was consumed 2 h prior to visiting the laboratory. Energy expenditure (ventilated hood technique) was determined at rest and for 5 h following ingestion of a liquid meal (caloric content: 40% RMR). Contrary to our hypothesis, RMR was not greater (P = 0.10) following consumption of EGCG (6,740 ± 373 kJ/day) compared with placebo (6,971 ± 352). Similarly, the area under the TEF response curve (Δ energy expenditure) was also unaffected by EGCG (246,808 ± 23,748 vs. 243,270 ± 22,177 kJ; P = 0.88). EGCG had no effect on respiratory exchange ratio at rest (P = 0.29) or throughout the TEF measurement (P = 0.56). In summary, together RMR and TEF may account for up to 85% of total daily energy expenditure; we report that short‐term consumption of a commercially available EGCG supplement did not increase RMR or TEF.

Regular endurance exercise is an effective strategy for healthy weight maintenance, mediated via increased total daily energy expenditure (TDEE), and possibly an increase in resting metabolic rate (RMR: the single largest component of TDEE). Sprint interval training (SIT) is a low-volume alternative to endurance exercise; however, the utility of SIT for healthy weight maintenance is less clear. In this regard, it is feasible that SIT may evoke a thermogenic response above and beyond the estimates required for prevention of weight gain (i.e., >200–600 kJ). The purpose of these studies was to investigate the hypotheses that a single bout of SIT would increase RMR and/or TDEE. Study 1: RMR (ventilated hood) was determined on four separate occasions in 15 healthy men. Measurements were performed over two pairs of consecutive mornings; each pair was separated by 7 days. Immediately following either the first or third RMR measurement (randomly assigned) subjects completed a single bout of SIT (cycle ergometer exercise). RMR was unaffected by a single bout of SIT (7195 ± 285 kJ/day vs. 7147 ± 222, 7149 ± 246 and 6987 ± 245 kJ/day (mean ± SE); P = 0.12). Study 2: TDEE (whole-room calorimeter) was measured in 12 healthy men, on two consecutive days, one of which began with a single bout of SIT (random order). Sprint exercise increased TDEE in every research participant (9169 ± 243 vs. 10,111 ± 260 kJ/day; P < 0.0001); the magnitude of increase was 946 ± 62 kJ/day (∼10%). These data provide support for SIT as a strategy for increasing TDEE, and may have implications for healthy body weight maintenance.