Physical activity is central in prevention and treatment of metabolic syndrome. High‐intensity aerobic exercise can induce larger energy expenditure per unit of time compared with moderate‐intensity exercise. Furthermore, it may induce larger energy expenditure at post‐exercise recovery. The aim of this study is to compare the excess post‐exercise oxygen consumption (EPOC) in three different aerobic exercise sessions in men with metabolic syndrome. Seven men (age: 56.7 ± 10.8) with metabolic syndrome participated in this crossover study. The sessions consisted of one aerobic interval (1‐AIT), four aerobic intervals (4‐AIT), and 47‐min continuous moderate exercise (CME) on separate days, with at least 48 h between each test day. Resting metabolic rate (RMR) was measured pre‐exercise and used as baseline value. EPOC was measured until baseline metabolic rate was re‐established. An increase in O2 uptake lasting for 70.4 ± 24.8 min (4‐AIT), 35.9 ± 17.3 min (1‐AIT), and 45.6 ± 17.3 min (CME) was observed. EPOC were 2.9 ± 1.7 L O2 (4‐AIT), 1.3 ± 1.1 L O2 (1‐AIT), and 1.4 ± 1.1 L O2 (CME). There were significant differences (P < 0.001) between 4‐AIT, CME, and 1‐AIT. Total EPOC was highest after 4‐AIT. These data suggest that exercise intensity has a significant positive effect on EPOC in men with metabolic syndrome.

Background: Type 2 diabetes mellitus (T2DM) is associated with diastolic dysfunction (DD), which could ultimately lead to heart failure. Purpose: To compare the effect of high-intensity exercise (HIE) and moderate-intensity exercise (MIE) in accordance to present recommendations in patients with T2DM (duration <10 years) and DD. Methods: 47 subjects (mean age 56,6 years, 31 male) with DD defined as early diastolic tissue velocity (E') < 8 m/s were included and randomized to HIE (4x4minutes) at 90-95% of HRmax 3 times/week (n=24) or MIE for 210 minutes/week (n=23), both for 12 weeks. Subjects were examined with echocardiography including tissue Doppler, VO2peak-test and biochemical measurements pre- and post exercise. Results: There were no difference between groups at baseline and 38 completed the intervention (MIE n=17 and HIE n=21). HIE significantly improved DD; E' by 21%, early mitral filling velocity (E) by 16% and shortened isovolumic relaxation time (IVRT) by 11% (Table). Systolic tissue Doppler velocity (S') increased with 15% and stroke volume with 11%, waist circumference (WC) reduced with 2 cm, VO2peak increased with 4.1 ml/kg/min, HbA1c reduced with 6% (Table). The MIE group reduced WC with 2,1 cm and reduced insulin resistance (IR) with 8% (Table). There were no changes in resting heart rate or blood pressure (BP) after intervention. Baseline- and post exercise results Data are presented as mean ± SD. ap<0.001, bp<0.01, cp<0.05. Conclusions: In patients with T2DM with duration <10years, HIE improved DD and decreased HbA1c, in contrast to present recommendations of MIE. This could have future implications on today's exercise recommendations.

Effect of high and moderate frequency aerobic interval training on the oxygen transport chain.

The perilipin proteins enclose intracellular lipid droplets. We describe the mRNA expression of the five perilipins in human skeletal muscle in relation to fatty acid supply, exercise and energy balance. We observed that all perilipins were expressed in skeletal muscle biopsies with the highest mRNA levels of perilipin 2, 4 and 5. Cultured myotubes predominantly expressed perilipin 2 and 3. In vitro, incubation of myotubes with fatty acids enhanced mRNA expression of perilipin 1, 2 and 4. In vivo, low fat diet increased mRNA levels of perilipin 3 and 4. Endurance training, but not strength training, enhanced the expression of perilipin 2 and 3. Perilipin 1 mRNA correlated positively with body fat mass, whereas none of the perilipins were associated with insulin sensitivity. In conclusion, all perilipins mRNAs were expressed in human skeletal muscle. Diet as well as endurance exercise modulated the expression of perilipins.

Objective To study if young adults with low birth weight (LBW) had increased body fat or blood pressure (BP), poorer lung- or endothelial function, or lower maximal oxygen uptake than young adults with normal birth weight (controls). Methods Anthropometric measurements, BP, endothelial function, lung function and maximal oxygen uptake were recorded at age 18 in 37 subjects born prematurely with birth weight Results Both LBW groups were shorter, lighter, had smaller head circumference and higher subscapular-to-triceps skinfold-ratio than controls. Systolic and mean arterial BP was higher in the VLBW compared with the control group, whereas there were no differences between the groups in endothelial function. The VLBW group had reduced dynamic lung volumes and lower maximal oxygen uptake and both LBW groups had lower total lung capacity and lower carbon monoxide transfer factor compared with controls. In particular young adults born VLBW who were also growth retarded in utero had higher indices of central body fat, higher blood pressure and lower maximal oxygen uptake. Conclusions Consistent with the early origin of adult disease hypothesis, we found that very preterm birth, in particular if associated with growth retardation, may increase the risk of high blood pressure and central obesity in adulthood. However, no such risk was found among adolescents born growth retarded at term.

PURPOSE: Management of the metabolic syndrome and its risk factors constitutes an enormous economic burden on the society. Exercise training is known to reduce several of the risk factors related to the syndrome, but there is no consensus of what is the most optimal training program. The present study determines the cardiovascular effects of exercise training with an intensity corresponding to the upper range of current guidelines for humans. METHODS: Twenty-eight patients with metabolic syndrome took part in the study. Patients were randomized into aerobic interval training (AIT, n=1 1; 4×4 min at 90–95% of Hfmax, with 3-min active recovery at 70% of Hfmax between each interval), continuous moderate exercise (CME, n=8; To equalize training volume between the two groups, CME had to perform 47-min at 70% of Hfmax each exercise session) or to a control group (n=9). Both exercise-groups were walking/running “uphill” on a treadmill 3 times per week for 16 weeks. RESULTS: At post-test 46% of the patients in AIT and 37% in CME were no longer classified as having the metabolic syndrome. Both exercise group significantly decreased body weight (p<0.05). HDL-cholesterol increased by 22%, and fasting glucose decreased in AIT-patients (p<0.05). Both AIT and CME decreased systolic blood pressure with ∼10 mmHg (p<0.05), whilst only AIT (p<0.05) decreased the diastolic blood pressure. VO2max increased 35% and 16% (p<0.01) in AIT and CME, respectively. Both AIT and CME increased flow mediated dilatation with 167% and 104%, respectively (p<0.001). Western blot analysis demonstrated that skeletal muscle PGC-1a levels increased by 138% in AIT and was not altered in the other groups. Furthermore, the maximal rate of SR Ca2+ uptake in skeletal muscle was 53% and 30% (p<0.01) higher in AIT compared to controls and CME, respectively. Insulin receptor activity in AIT was significantly increased (p<0.001) and the increase was 11 and 4 fold higher in AIT compared to CME and control respectively. In fat tissue, Western analysis revealed that AIT caused a more marked decrease in the protein content of the lipogenic enzyme FAS, by comparison to CME (6-fold versus 3-fold). CONCLUSIONS: This study demonstrates that high-intensity exercise training was superior to moderate-intensity training in reversing risk factors related to the metabolic syndrome.

Cigarette smoke contains hundreds of potentially toxic compounds and is an important risk factor for impaired aerobic fitness and cardiovascular disease. However, the key components responsible for endothelial and myocardial dysfunction have not been fully identified. PURPOSE: To determine the cardiovascular effects of long-term inhalation of carbon monoxide (CO) at concentrations similar to those observed in heavy smoking. METHODS: Female Wistar rats (n=1 2) were randomized to 2 groups exposed to CO or air (control group). The CO group was exposed to 200 ppm CO (20 hours per day, 5 days per week) for 18 months. Myocyte length, contractile properties, and intracellular Ca2+ concentrations were measured in dissociated left ventricular cells in response to electrical stimulation at 5Hz. Endothelial function was measured in aorta segments ex vivo as maximal acetylcholine-induced relaxation and the concentration that induced half-maximal relaxation (EC 50). RESULTS: Rats exposed to CO had 24 % lower maximal oxygen uptake (75 vs. 57 mL/kg/min), longer (145 vs. 123 μm) and wider (47 vs. 25 μm) left ventricular myocytes, reduced cardiomyocyte shortening (12 vs. 7 %), and time to 50% re-lengthening after contraction was 26% slower compared to control rats. The intracellular Ca2+ transient was 48% lower (reduced peak systolic and increased diastolic concentrations). Time to 50% decay of intracellular Ca2+ from systole was 22% slower and maximal capacity of the sarcoplasmic reticulum ATPase (SERCA-2a) was 34% lower compared to control. CO exposure did not influence endothelial function, or systolic and diastolic blood pressure. Phosphorylation levels of phospholamban at Ser16 and Thr17 were significantly reduced by CO, whereas total concentration of phospholamban and SERCA-2a were unchanged. ANF, VEGF, calcineurin, calmodulin, pERK, and pS6 increased whereas pAKT, pCaMKII&rhcv; and HIF1α remained unchanged by CO. CONCLUSIONS: This is the first study to demonstrate that long-term CO exposure induces concentric myocardial hypertrophy, including reduced contractile function caused by impaired Ca2+ handling, in face of unchanged blood pressure and HIF1α. Previous studies had indicated endothelin-1 as a significant mediator of the effect.