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The purpose of this systematic review was to synthesize the results from current literature examining the effects of prior exercise on the postprandial triglyceride (TG) response to evaluate current literature and provide future direction. A quantitative review was performed using meta-analytic methods to quantify individual effect sizes. A moderator analysis was performed to investigate potential variables that could influence the effect of prior exercise on postprandial TG response. Two hundred and seventy-nine effects were retrieved from 165 studies for the total TG response and 142 effects from 87 studies for the incremental area under the curve TG response. There was a moderate effect of exercise on the total TG response (Cohen's d = −0.47; p <.0001). Moderator analysis revealed exercise energy expenditure significantly moderated the effect of prior exercise on the total TG response (p <.0001). Exercise modality (e.g., cardiovascular, resistance, combination of both cardiovascular and resistance, or standing), cardiovascular exercise type (e.g., continuous, interval, concurrent, or combined), and timing of exercise prior to meal administration significantly affected the total TG response (p <.001). Additionally, exercise had a moderate effect on the incremental area under the curve TG response (Cohen's d = −0.40; p <.0001). The current analysis reveals a more homogeneous data set than previously reported. The attenuation of postprandial TG appears largely dependent on exercise energy expenditure (∼2 MJ) and the timing of exercise. The effect of prior exercise on the postprandial TG response appears to be transient; therefore, exercise should be frequent to elicit an adaptation. [ABSTRACT FROM AUTHOR]

The influence of menstrual cycle phase and fitness status on metabolism during high-intensity interval exercise (HIIE) was assessed. Twenty-five females (24.4 (3.6) years) were categorized by normal menstrual cycle (n = 14) vs. oral contraceptive (OC) use (n = 11) and by aerobic fitness, high-fitness females (HFF; n = 13) vs. low-fitness females (LFF; n = 12). HIIE was four sets of four repetitions with a 3 min rest between intervals on a cycle ergometer at a power output halfway between the ventilatory threshold and V̇O2peak and performed during follicular (FOL: days 2–7 or inactive pills) and luteal phases (LUT: day ∼21 or 3rd week of active pills). Substrate oxidation was assessed via indirect calorimetry, blood lactate via finger stick, and recovery of skeletal muscle oxidative metabolism (mV̇O2) via continuous-wave near-infrared spectroscopy. HFF oxidized more fat (g·kg−1) during the full session (FOL: p = 0.050, LUT: p = 0.001), high intervals (FOL: p = 0.048, LUT: p = 0.001), low intervals (FOL: p = 0.032, LUT: p = 0.024), and LUT recovery (p = 0.033). Carbohydrate oxidation area under the curve was greater in HFF during FOL (FOL: p = 0.049, LUT: p = 0.124). Blood lactate was lower in LFF in FOL (p ≤ 0.05) but not in LUT. Metabolic flexibility (Δ fat oxidation g·kg−1·min−1) was greater in HFF than LFF during intervals 2–3 in FOL and 1–4 in LUT (p ≤ 0.05). Fitness status more positively influences exercise metabolic flexibility during HIIE than cycle phase or OC use. [ABSTRACT FROM AUTHOR]

We propose a new VO2max test using a progressive staged protocol on an Assault Fitness AssaultBike. Twelve healthy males performed a traditional ramp cycle ergometer test (TRAD) and a progressively staged AssaultBike protocol (AB) in a counterbalanced order. AB elicited higher immediate post-exercise lactate, absolute and relative VO2max, and maximum heart rate than TRAD (P = 0.006, P = 0.014, P = 0.007, and P = 0.001, respectively). The protocol outlined herein may provide a more accurate assessment of VO2max due to greater skeletal muscle mass recruitment that is more representative of the whole body. [ABSTRACT FROM AUTHOR]

Aim: We compared the impact of artificially- and sugar-sweetened beverages co-ingested with a mixed meal on postprandial fat and carbohydrate oxidation, blood glucose, and plasma insulin and triglyceride concentrations. Methods: Eight college-aged, healthy males completed three randomly assigned trials, which consisted of a mixed macronutrient meal test with 20oz of Diet-Coke (AS), Coca-Cola (NS), or water (CON). One week separated each trial and each participant served as his own control. Resting energy expenditure (REE) via indirect calorimetry, blood pressure, and blood samples were obtained immediately before, 5, 10, 30, 60, 120, and 180 min after meal and beverage ingestion. A two-way (treatment × time) repeated-measures ANOVA was conducted to assess REE, fat and carbohydrate oxidation rates, blood glucose, and plasma insulin and triglyceride concentrations. Results: There was a significant main effect of treatment on total fat oxidation (P = 0.006), fat oxidation was significantly higher after AS (P = 0.006) and CON (P = 0.001) compared to following NS. There was a significant main effect of treatment on total carbohydrate oxidation (P = 0.005), carbohydrate oxidation was significantly lower after AS (P = 0.014) and CON (P = 0.001) compared to following NS. Plasma insulin concentration AUC was significantly lower after AS (P = 0.019) and trended lower in CON (P = 0.054) compared to following NS. Conclusion: Ingestion of a mixed meal with an artificially-sweetened beverage does not impact postprandial metabolism, whereas a sugar-sweetened beverage suppresses fat oxidation and increases carbohydrate oxidation compared to artificially-sweetened beverage and water. [ABSTRACT FROM AUTHOR]

Purpose: We compared aerobic capacity ( V ˙ O 2 max ), mitochondrial capacity ( m V ˙ O 2 ), anaerobic power, strength, and muscle endurance in healthy, active men from strength (STR), endurance (END) and high-intensity functional training (HIFT) backgrounds. Methods: Twenty-four men (n = 8/group) completed a cycle ergometer test to determine V ˙ O 2 max , followed by a 3-min all-out test to determine peak (PP) and end power (EP), and to estimate anaerobic [work done above EP (WEP)] and aerobic work capacity. Strength was determined by knee extensor maximal voluntary contraction at various flexion angles. The endurance index (EI) of the vastus lateralis (VL) was assessed by measuring muscle contraction acceleration during electrical twitch mechanomyography. m V ˙ O 2 max of the VL was assessed using near-infrared spectroscopy to estimate muscle oxygen consumption during transient femoral artery occlusions. Results: V ˙ O 2 max was significantly different among groups (p <.05). PP was significantly higher in HIFT and STR versus END (p <.05). EP was significantly higher in HIFT and END compared to STR (p <.05). WEP was significantly higher in STR compared to END (p <.05), whereas total work done was significantly higher in HIFT and END compared to STR (p <.05). m V ˙ O 2 max and EI were comparable between HIFT and END but significantly lower in STR versus END (p <.05). Torque production was significantly lower in END compared to STR and HIFT at all flexion angles (p <.05), with no difference between STR and HIFT. Conclusion: HIFT participants can exert similar power outputs and absolute strength compared to strength focused participants but exhibit fatigue resistance and mitochondrial capacity comparable to those who train for endurance. [ABSTRACT FROM AUTHOR]

We sought to delineate the effects of acute and chronic exercise on the regulation of intracellular nitric oxide (N[O.sub.i]) production in putative endothelial progenitor cells (EPCs). Putative EPC colony-forming units (CFU-EC) were cultured from blood drawn before and after 30 min of treadmill exercise at 75% of maximal oxygen uptake in active (n = 8) and inactive (n = 8) men. CFU-EC were similar between groups at baseline, but increased after exercise in active men only (P = 0.04). CFU-EC expressed Dower NADPH oxidase subunit [gp91.sup.phox] mRNA and elevated endothelial nitric oxide synthase mRNA in active relative to inactive men at baseline (P < 0.05). Acute exercise reduced [gp91.sup.phox] mRNA in CFU-EC of both groups (P < 0.05), whereas [p47.sup.phox] mRNA levels were reduced in the inactive group only (P = 0.02). There were no differences between groups or with acute exercise in xanthine oxidase, superoxide dismutase isoforms, or gluthathione peroxidase-1 mRNA levels. N[O.sub.i] was significantly greater in CFU-EC of active men at baseline (P = 0.004). N[O.sub.i] increased in CFU-EC of inactive men with acute exercise, and in vitro experiments with apocynin indicated the increased N[O.sub.i] production was caused by suppression of NADPH oxidase. However, the increases in N[O.sub.i] with the different treatments in the inactive group did not reach the baseline levels in the active group (P < 0.05). We conclude that acute exercise increases N[O.sub.i] in cells generated by the CFU-EC assay through an NADPH oxidase-inhibition mechanism in sedentary men. However, differences due to chronic exercise must involve additional factors. Our findings support exercise as a means to improve putative EPC function and suggest a novel mechanism that may explain this effect. physical activity; angiogenesis; oxidative stress doi: 10.1152/ajpheart.00347.2009.