No Effect of Calanus Oil on Maximal Oxygen Uptake in Healthy Participants: A Randomized Controlled Study

We aimed to investigate the long-term effect of daily Calanus oil supplementation on maximal oxygen uptake (VO2max) in healthy 30- to 50-year-old participants. The study was motivated by preclinical studies reporting increased VO2max and metabolic health with omega-3 rich Calanus oil. In a double-blinded study, 71 participants were randomized to receive 2 g/day of Calanus or placebo supplementation for a total of 6 months. The participants underwent exercise testing and clinical investigations at baseline, 3 months, and 6 months. Main study endpoint was change in VO2max from baseline to 6 months. Fifty-eight participants completed the 6-month test and were included in the final data analysis (age: Calanus, 39.7 [38.0, 41.4] and placebo, 38.8 [36.8, 40.9] years; body mass index: Calanus, 24.8 [24.0, 25.6] and placebo, 24.8 [23.7, 25.8] kg/m2; and VO2max: Calanus, 50.4 [47.1, 53.8] and placebo, 50.2 [47.2, 53.1] ml·kg−1·min−1). There were no between-group differences at baseline, nor were there any between-group differences in absolute (Calanus, 3.74 [3.44, 4.04] and placebo, 3.79 [3.44, 4.14] L/min) or relative VO2max (Calanus, 49.7 [46.2, 53.2] and placebo, 49.5 [46.0, 53.1] ml·kg−1·min−1) at 6 months (mean [95% confidence interval]). There were no between-groups change in clinical measures from baseline to 3 and 6 months. In conclusion, VO2max was unaffected by 6 months of daily Calanus oil supplementation in healthy, physically fit, normal to overweight men and women between 30 and 50 years old

Aerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failure

Background: There is limited knowledge about atrial myocyte Ca2+ handling in the failing hearts. The aim of this study was to examine atrial myocyte contractile function and Ca2+ handling in rats with post-infarction heart failure (HF) and to examine whether aerobic interval training could reverse a potential dysfunction. Methods and results: Post-infarction HF was induced in Sprague Dawley rats by ligation of the left descending coronary artery. Atrial myocyte shortening was depressed (p<0.01) and time to relaxation was prolonged (p<0.01) in sedentary HF-rats compared to healthy controls. This was associated with decreased Ca2+ amplitude, decreased SR Ca2+ content, and slower Ca2+ transient decay. Atrial myocytes from HF-rats had reduced sarcoplasmic reticulum Ca2+ ATPase activity, increased Na+/Ca2+-exchanger activity and increased diastolic Ca2+ leak through ryanodine receptors. High intensity aerobic interval training in HF-rats restored atrial myocyte contractile function and reversed changes in atrial Ca2+ handling in HF. Conclusion: Post infarction HF in rats causes profound impairment in atrial myocyte contractile function and Ca2+ handling. The observed dysfunction in atrial myocytes was partly reversed after aerobic interval training.© 2013 Johnsen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Aerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failure.

BACKGROUND: There is limited knowledge about atrial myocyte Ca(2+) handling in the failing hearts. The aim of this study was to examine atrial myocyte contractile function and Ca(2+) handling in rats with post-infarction heart failure (HF) and to examine whether aerobic interval training could reverse a potential dysfunction. METHODS AND RESULTS: Post-infarction HF was induced in Sprague Dawley rats by ligation of the left descending coronary artery. Atrial myocyte shortening was depressed (p<0.01) and time to relaxation was prolonged (p<0.01) in sedentary HF-rats compared to healthy controls. This was associated with decreased Ca(2+) amplitude, decreased SR Ca(2+) content, and slower Ca(2+) transient decay. Atrial myocytes from HF-rats had reduced sarcoplasmic reticulum Ca(2+) ATPase activity, increased Na(+)/Ca(2+)-exchanger activity and increased diastolic Ca(2+) leak through ryanodine receptors. High intensity aerobic interval training in HF-rats restored atrial myocyte contractile function and reversed changes in atrial Ca(2+) handling in HF. CONCLUSION: Post infarction HF in rats causes profound impairment in atrial myocyte contractile function and Ca(2+) handling. The observed dysfunction in atrial myocytes was partly reversed after aerobic interval training

Absent exercise-induced improvements in fat oxidation in women with polycystic ovary syndrome after high-intensity interval training

Background: Polycystic ovary syndrome (PCOS) and metabolic inflexibility are linked to insulin resistance, and women with PCOS appear to be metabolic inflexible in the rested, insulin-stimulated state. Exercise training is a primary lifestyle intervention in PCOS. Exercise training improves whole-body fat oxidation during submaximal exercise in healthy women, yet little is known about the effect on this outcome in women with PCOS. Methods: We measured whole-body fat oxidation rates during sub maximal exercise before and after 16 weeks of high-intensity interval training (HIT) in women with PCOS randomly allocated to either: low- or high-volume HIT (n = 41; low-volume HIT, 10 × 1 min work bouts at maximal, sustainable intensity and high-volume HIT, 4 × 4 min work bouts at 90–95% of maximal heart rate) or non-exercise control (n = 23), and in women without PCOS (Non-PCOS) allocated to low- or high volume HIT (n = 15). HIT was undertaken three times weekly. In a subset of women with and without PCOS, we measured mitochondrial respiration in abdominal and gluteal subcutaneous adipose tissue using high-resolution respirometry, as well as fat cell sizes in these tissues. Results: At baseline, women with PCOS had lower whole-body fat oxidation and mitochondrial respiration rates in abdominal adipose tissue compared to Non-PCOS. Peak oxygen uptake (mL/min/kg) increased in women with PCOS (∼4%, p = 0.006) and Non-PCOS (∼6%, p = 0.003) after 16 weeks of HIT. Whole-body fat oxidation only improved in Non-PCOS after HIT. No changes were observed in mitochondrial respiration and cell size in abdominal and gluteal adipose tissue after HIT in either group of women. Conclusion: We observed exercise-induced improvements in whole-body fat oxidation Lionett et al. Metabolic Inflexibility in PCOS during submaximal exercise in Non-PCOS, but not in women with PCOS, after 16 weeks of HIT, suggesting metabolic inflexibility in women with PCOS

Averaged data of rates of decay of the twitch- and Caffeine induced Ca²⁺ transient indicating the SERCA2a function (A) and NCX function (B).

<p>All data presented as mean values ± SD. * <i>p<0.05</i> versus sham sedentary, <i># p<0.001</i> versus sham sedentary.</p

Illustration of the SR Ca²⁺ leak protocol (A), mean data of SR Ca²⁺ leak normalized to SR Ca²⁺ content (B), and mean data of SR Ca²⁺ leak after CaMKII inhibition (AIP) (C) and PKA inhibition (H89) (D).

<p>* <i>p<0.05</i> versus sham sedentary, <i># p<0.001</i> versus sham sedentary.</p

Representative sample traces of cardiomyocyte fractional shortening (A) and Fura-2 ratio (D) from sham, HF-inactive and HF-trained rats.

<p>Averaged data of myocyte fractional shortening (B), time to 50% diastolic relaxation (C), Ca²⁺ amplitude (E), SR Ca²⁺ content (F), time to 50% Ca²⁺ decay (G) and diastolic Ca²⁺ (H). All averaged data presented as mean values ± SD. * <i>p<0.05</i> versus sham sedentary, <i># p<0.001</i> versus sham sedentary.</p

Lipoprotein subfraction profiling in the search of new risk markers for myocardial infarction: The HUNT study.

BackgroundTraditional biomarkers used to measure risk of myocardial infarction (MI) only explain a modest proportion of the incidence. Lipoprotein subfractions have the potential to improve risk prediction of MI.AimWe aimed to identify lipoprotein subfractions that were associated with imminent MI risk.MethodsWe identified apparently healthy participants with a predicted low 10-year risk of MI from The Trøndelag Health Survey 3 (HUNT3) that developed MI within 5 years after inclusion (cases, n = 50) and 100 matched controls. Lipoprotein subfractions were analyzed in serum by nuclear magnetic resonance spectroscopy at time of inclusion in HUNT3. Lipoprotein subfractions were compared between cases and controls in the full population (N = 150), and in subgroups of males (n = 90) and females (n = 60). In addition, a sub analysis was performed in participants that experienced MI within two years and their matched controls (n = 56).ResultsNone of the lipoprotein subfractions were significantly associated with future MI when adjusting for multiple testing (pConclusionNone of the investigated lipoprotein subfractions were associated with future MI after adjustment for multiple testing. However, our findings suggests that HDL subfractions may be of interest in relation to risk prediction for MI, especially in males. This need to be further investigated in future studies