Prolonged sitting negatively affects the postprandial plasma triglyceride-lowering effect of acute exercise.

The interaction of prolonged sitting with physical exercise for maintaining health is unclear. We tested the hypothesis that prolonged siting would have a deleterious effect on postprandial plasma lipemia (PPL, postprandial plasma triglycerides) and reduce the ability of an acute exercise bout to attenuate PPL. Seven healthy young men performed three, 5-day interventions [days 1-5 (D1-D5)] in a randomized crossover design with >1 wk between interventions: 1) sitting > 14 h/day with hypercaloric energy balance (SH), 2) sitting >14 h/day with net energy balance (SB), and 3) active walking/standing with net energy balance (WB) and sitting 8.4 h/day. The first high-fat tolerance test (HFTT1) was performed on D3 following 2 days of respective interventions. On the evening of D4 subjects ran on a treadmill for 1 h at ~67% V̇o2max, followed by the second HFTT (HFTT2) on D5. Two days of prolonged sitting increased TG AUCI (i.e., incremental area under the curve for TG), irrespective of energy balance, compared with WB (27% in SH, P = 0.003 and 26% in SB, P = 0.046). Surprisingly, after 4 days of prolonged sitting (i.e.; SH and SB), the acute exercise on D4 failed to attenuate TG AUCI or increase relative fat oxidation in HFTT2, compared with HFTT1, regardless of energy balance. In conclusion, prolonged sitting over 2-4 days was sufficient to amplify PPL, which was not attenuated by acute exercise, regardless of energy balance. This underscores the importance of limiting sitting time even in people who have exercised.

Palmitoleic acid is elevated in fatty liver disease and reflects hepatic lipogenesis.

BACKGROUND: Biochemical evidence has linked the coordinate control of fatty acid (FA) synthesis with the activity of stearoyl-CoA desaturase-1 (SCD1). The ratio of 16:1n-7 to 16:0 [SCD116] in plasma triacylglycerol FA has been used as an index to reflect liver SCD116 activity and has been proposed as a biomarker of FA synthesis, although this use has not been validated by comparison with isotopically measured de novo lipogenesis (DNL(Meas)). OBJECTIVE: We investigated plasma lipid 16:1n-7 and FA indexes of elongation and desaturation in relation to lipogenesis. DESIGN: In this cross-sectional investigation of metabolism, 24 overweight adults, who were likely to have elevated DNL, consumed D2O for 10 d and had liver fat (LF) measured by magnetic resonance spectroscopy. Very-low-density lipoprotein (VLDL)-triacylglycerols and plasma free FA [nonesterified fatty acids (NEFAs)] were analyzed by using gas chromatography for the FA composition (molar percentage) and gas chromatography-mass spectrometry and gas chromatography-combustion isotope ratio mass spectrometry for deuterium enrichment. RESULTS: In all subjects, VLDL-triacylglycerol 16:1n-7 was significantly (P < 0.01) related to DNL(Meas) (r = 0.56), liver fat (r = 0.53), and adipose insulin resistance (r = 0.56); similar positive relations were shown with the SCD116 index, and the pattern in NEFAs echoed that of VLDL-triacylglycerols. Compared with subjects with low LF (3.1 ± 2.7%; n = 11), subjects with high LF (18.4 ± 3.6%; n = 13) exhibited a 45% higher VLDL-triacylglycerol 16:1n-7 molar percentage (P < 0.01), 16% of subjects had lower 18:2n-6 (P = 0.01), and 27% of subjects had higher DNL as assessed by using a published DNL index (ratio of 16:0 to 18:2n-6; P = 0.03), which was isotopically confirmed by DNL(Meas) (increased 2.5-fold; P < 0.01). Compared with 16:0 in the diet, the low amount of dietary 16:1n-7 in VLDL-triacylglycerols corresponded to a stronger signal of elevated DNL. CONCLUSION: The current data provide support for the use of the VLDL-triacylglycerol 16:1n-7 molar percentage as a biomarker for elevated liver fat when isotope use is not feasible; however, larger-scale confirmatory studies are needed.

Postexercise macronutrient intake and subsequent postprandial triglyceride metabolism.

UNLABELLED: Acute endurance exercise has been shown to lower postprandial plasma triglyceride (PPTG) concentrations; however, whether this is due to the negative energy and/or CHO deficit from the exercise bout is not well understood. PURPOSE: This study aimed to examine the effects of a postexercise meal consisting of either high or low CHO content on PPTG and postprandial fat oxidation the morning after an exercise bout. METHODS: Healthy young men (n = 6) performed each of four experimental treatments: 1) nonexercise control (CON), 2) 80 min of cycling with either no meal replacement (EX), 3) a high-CHO postexercise meal (EX+HCHO), or a 4) low-CHO postexercise meal (EX+LCHO). A standardized meal for PPTG determination was provided (16.0 kcal · kg(-1) body mass, 1.02 g fa t · kg(-1), 1.36 g CHO · kg(-1), 0.31 g protein · kg(-1)) 12 h after the exercise, and measurements of plasma triglyceride (TG) concentration and whole-body resting fat oxidation were made in the fasted condition and during the 4-h postprandial period. RESULTS: The total area under the curve for plasma TG was significantly lower in EX+LCHO (325 (63) mg · dL(-1) per 4 h) compared with that in EX+HCHO (449 (118) mg · dL(-1) per 4 h, P = 0.03). Postprandial fat oxidation during this period was significantly greater in EX+LCHO (257 (58) kcal per 4 h, P = 0.003) compared with that in EX+HCHO (209 (56) kcal per 4 h). The change in total postprandial fat oxidation (kcal per 4 h) relative to CON was significantly and inversely correlated with the change in the total TG area under the curve relative to CON (mg · dL(-1) per 4 h, ΔTG AUC, R2 = 0.37, P = 0.008). CONCLUSIONS: The low CHO composition of the postexercise meal contributes to lower PPTG and increased fat oxidation, with lower PPTG related to an increase in fat oxidation.

Effects of moderate- and intermittent low-intensity exercise on postprandial lipemia.

UNLABELLED: The elevation of postprandial plasma triglycerides (PPTG) in the blood is an independent risk factor for atherosclerosis. Although acute exercise typically attenuates PPTG, the effect of exercise intensity on PPTG is less well established, particularly in well-controlled conditions for physical activities and diet. PURPOSE: We sought to determine the efficacy of exercise at 65% V˙O2max with an extended sitting time and isoenergetic intermittent walking exercise at a self-selected walking speed (approximately 25% V˙O2max) on PPTG compared with that of a sitting control condition. In a randomized crossover design, nine healthy young men completed three trials with a >1-wk interval between trials. After 2 d of activity and diet normalization, participants performed prolonged sitting nonexercise control (CON), prolonged sitting with subsequent 1-h running at 65% V˙O2max (MOD), or isoenergetic intermittent walking at approximately 25% V˙O2max (LOW) on day 3. This was followed on day 4 by a 6-h high-fat tolerance test. RESULTS: MOD and LOW reduced incremental triglyceride (TG) area under the curve (TG AUCI) compared with that in CON by 33.6% (P < 0.005) and 19.8% (P < 0.05), respectively. MOD also reduced TG AUCI compared with that in LOW by 17.2% (P < 0.03). The reduced TG AUCI in MOD was accompanied by reduced plasma glucose response and enhanced fat oxidation compared with those in LOW and CON (for all, P < 0.05), respectively. CONCLUSIONS: Both MOD and LOW were effective in reducing PPTG compared with CON. However, MOD was more effective in reducing PPTG compared with LOW.

Impact of polyphenol antioxidants on cycling performance and cardiovascular function.

This investigation sought to determine if supplementation with polyphenol antioxidant (PA) improves exercise performance in the heat (31.5 °C, 55% RH) by altering the cardiovascular and thermoregulatory responses to exercise. Twelve endurance trained athletes ingested PA or placebo (PLAC) for 7 days. Consecutive days of exercise testing were performed at the end of the supplementation periods. Cardiovascular and thermoregulatory measures were made during exercise. Performance, as measured by a 10 min time trial (TT) following 50 min of moderate intensity cycling, was not different between treatments (PLAC: 292 ± 33 W and PA: 279 ± 38 W, p = 0.12). Gross efficiency, blood lactate, maximal neuromuscular power, and ratings of perceived exertion were also not different between treatments. Similarly, performance on the second day of testing, as assessed by time to fatigue at maximal oxygen consumption, was not different between treatments (PLAC; 377 ± 117 s vs. PA; 364 ± 128 s, p = 0.61). Cardiovascular and thermoregulatory responses to exercise were not different between treatments on either day of exercise testing. Polyphenol antioxidant supplementation had no impact on exercise performance and did not alter the cardiovascular or thermoregulatory responses to exercise in the heat.

Acute high-intensity endurance exercise is more effective than moderate-intensity exercise for attenuation of postprandial triglyceride elevation.

Acute exercise has been shown to attenuate postprandial plasma triglyceride elevation (PPTG). However, the direct contribution of exercise intensity is less well understood. The purpose of this study was to examine the effects of exercise intensity on PPTG and postprandial fat oxidation. One of three experimental treatments was performed in healthy young men (n = 6): nonexercise control (CON), moderate-intensity exercise (MIE; 50% Vo2peak for 60 min), or isoenergetic high-intensity exercise (HIE; alternating 2 min at 25% and 2 min at 90% Vo2peak). The morning after the exercise, a standardized meal was provided (16 kcal/kg BM, 1.02 g fat/kg, 1.36 g CHO/kg, 0.31 g PRO/kg), and measurements of plasma concentrations of triglyceride (TG), glucose, insulin, and ß-hydroxybutyrate were made in the fasted condition and hourly for 6 h postprandial. Indirect calorimetry was used to determine fat oxidation in the fasted condition and 2, 4, and 6 h postprandial. Compared with CON, both MIE and HIE significantly attenuated PPTG [incremental AUC; 75.2 (15.5%), P = 0.033, and 54.9 (13.5%), P = 0.001], with HIE also significantly lower than MIE (P = 0.03). Postprandial fat oxidation was significantly higher in MIE [83.3 (10.6%) of total energy expenditure] and HIE [89.1 (9.8) %total] compared with CON [69.0 (16.1) %total, P = 0.039, and P = 0.018, respectively], with HIE significantly greater than MIE (P = 0.012). We conclude that, despite similar energy expenditure, HIE was more effective than MIE for lowering PPTG and increasing postprandial fat oxidation.

The effect of pomegranate juice supplementation on strength and soreness after eccentric exercise.

The purpose of this study was to determine if pomegranate juice supplementation improved the recovery of skeletal muscle strength after eccentric exercise in subjects who routinely performed resistance training. Resistance trained men (n = 17) were randomized into a crossover design with either pomegranate juice or placebo. To produce delayed onset muscle soreness, the subjects performed 3 sets of 20 unilateral eccentric elbow flexion and 6 sets of 10 unilateral eccentric knee extension exercises. Maximal isometric elbow flexion and knee extension strength and muscle soreness measurements were made at baseline and 2, 24, 48, 72, 96, and 168 hours postexercise. Elbow flexion strength was significantly higher during the 2- to 168-hour period postexercise with pomegranate juice compared with that of placebo (main treatment effect; p = 0.031). Elbow flexor muscle soreness was also significantly reduced with pomegranate juice compared with that of placebo (main treatment effect; p = 0.006) and at 48 and 72 hours postexercise (p = 0.003 and p = 0.038, respectively). Isometric strength and muscle soreness in the knee extensors were not significantly different with pomegranate juice compared with those using placebo. Supplementation with pomegranate juice attenuates weakness and reduces soreness of the elbow flexor but not of knee extensor muscles. These results indicate a mild, acute ergogenic effect of pomegranate juice in the elbow flexor muscles of resistance trained individuals after eccentric exercise.

Arterial stiffening following eccentric exercise-induced muscle damage.

Acute inflammatory responses are linked to a transient increase in risk of a cardiovascular event, and this risk may be mediated by a concomitant reduction in vascular function. Humans experience an acute inflammatory response as a consequence of infection, injury, or muscle damage. We measured macrovascular function before and after eccentric exercise to determine whether muscle damage from unaccustomed exercise has an unfavorable effect on the large elastic arteries. A total of 27 healthy sedentary or recreationally active men (age 18-38 years) participated in either bilateral leg press eccentric exercise or unilateral elbow flexor eccentric exercise. Postexercise muscle damage was confirmed by significant reductions in isometric strength and increases in muscle soreness (P < 0.05). Carotid-femoral pulse-wave velocity was significantly elevated 48 h after leg exercise (808 ± 31 vs. 785 ± 30 cm/s; P < 0.05) and arm exercise (790 ± 28 vs. 755 ± 24 cm/s; P < 0.05). There were no changes in mean arterial pressure. C-reactive protein was elevated after leg exercise but not after arm exercise. The increase in carotid-femoral pulse wave velocity 48 h after arm exercise was associated with muscle strength (r = -0.47; P < 0.05) and creatine kinase concentrations (r = 0.70; P < 0.01). We concluded that eccentric exercise in both small and large muscle mass translates to transient, unfavorable changes in central macrovascular function and that the increase in central arterial stiffness after small muscle eccentric exercise is associated with indicators of muscle damage.

Ellagitannin consumption improves strength recovery 2-3 d after eccentric exercise.

PURPOSE: Dietary supplementation with polyphenols,particularly ellagitannins, may attenuate the muscular damage experienced after eccentric exercise, producing delayed-onset muscle soreness. The purpose of this study was to determine whether ellagitannin supplementation from Wonderful variety pomegranate extract (POMx) improved recovery of skeletal muscle strength after eccentric exercise. METHODS: Recreationally active males were randomized into a crossover design with either pomegranate extract (POMx) or placebo (PLA), each given during a period of 9 d.To produce delayed-onset muscle soreness, subjects performed two sets of 20 maximal eccentric elbow flexion exercises with one arm.Maximal isometric elbow flexion strength and muscle soreness as well as serum measures of creatine kinase, myoglobin, interleukin 6, and C-reactive protein were made at baseline and 2, 24, 48, 72, and 96 h after exercise. RESULTS: With both treatments, strength was similarly reduced 2 h after exercise (i.e., 72% of baseline), and recovery of strength was incomplete after 96 h (i.e., 91% of baseline).However, strength was significantly higher in POMx compared with that in PLA at 48 h (85.4% +/- 2.5% and 78.3% +/- 2.6%, P = 0.01) and 72 h (88.9% +/- 2.0% and 84.0% +/- 2.0%, P = 0.009) after exercise. Serum markers of inflammation and muscle damage did not provide insight regarding possible mechanisms. CONCLUSIONS: Supplementation with ellagitannins from pomegranate extract significantly improves recovery of isometric strength 2-3 d after a damaging eccentric exercise.