No abstract

A greater degree of LV hypertrabeculation is seen in healthy African athletes, combined with biventricular EF reduction at rest. Recognition of this phenomenon is necessary to avoid misdiagnosis of LVNC.

Physical training led to normalization of the stimulated plasma vWF release. Plasma levels of other endothelial markers were not affected by physical training either at rest or under stimulated (maximal exercise) conditions.

To determine the effect of training on insulin sensitivity (IS) and how this relates to peak V(.)O(2) (peak oxygen uptake) in CHF (chronic heart failure), 77 CHF patients (New York Heart Association class, II/III; men/women, 59/18; age, 60+/-9 years; body mass index, 26.7+/-3.9 kg/m(2); left ventricular ejection fraction, 26.9+/-8.1%; expressed as means+/-S.D.) participated in the study. Patients were randomly assigned to a training or control group (TrG or CG respectively). Sixty-one patients completed the study. Patients participated in training (combined strength and endurance exercises) four times per week, two times supervised and two times at home. Before and after intervention, anthropometry, IS (euglycaemic hyperinsulinaemic clamp) and peak V(.)O(2) (incremental cycle ergometry) were assessed. Intervention did not affect IS significantly, even though IS increased by 20% in TrG and 11% in CG (not significant). Peak V(.)O(2) increased as a result of training (6% increase in TrG; 2% decrease in CG; P <0.05). In both groups (TrG and CG), the change in IS correlated positively with the change in peak V(.)O(2) ( r =0.30, P <0.05). Training resulted in an increase in peak V(.)O(2), but not in IS. Whether physical training actually increases IS in CHF patients remains unclear.

Muscle strength and muscle endurance, combined with quadriceps muscle area are the main predictors of maximal exercise performance in patients with CHF.

Objective: To describe the determinants of insulin sensitivity (IS) in chronic heart failure (CHF), we created a model in which the influence of lifestyle factors and etiology of heart failure on IS were incorporated concomitantly with age, left ventricular ejection fraction (LVEF) and parameters of body composition. Design: Observational cohort study. Setting: Outpatient clinic for chronic heart failure. Patients: Fifty-seven male CHF patients wNYHA class II-III, age 61"9 years, body mass index (BMI) 26.9"3.3 kgym (mean"S.D.)x. Interventions: Euglycemic hyperinsulinemic clamp, cycle ergometry, anthropometric measure-2 ments, LVEF and a physical activity questionnaire. Main outcome measures: A model explaining the variance of IS in CHF. Results: IS was 18.2"8.6 mgØkg Ømin ØmU Øl , fasting insulin level was 15.9"11.0 mUyl and fasting glucose level was y1 y1 y1 y15.5"0.6 mmolyl. Peak was 19.1"4.9 mlØkg Ømin and LVEF 26.2"7.1%. IS was inversely associated with fasting y1 y1VO 2 insulin concentration (rsy0.50, P-0.001) and BMI (rsy0.54, P-0.001). After controlling for BMI, IS also revealed a correlation with age (rsy0.36, P-0.01). The model explained 60% of variance in IS: BMI contributed 20%, smoking 17%, age 17% and physical activity in daily life (DPA) 16% (all P-0.05) to the variance of IS, whereas LVEF (9%) and etiology of heart failure (8%) contributed moderately. Conclusions: In CHF patients, IS is for a major part predicted by BMI, smoking, age, daily physical activity, LVEF and etiology of heart failure.

No abstract

Left ventricular false tendons (LVFTs) are fibromuscular structures, connecting the left ventricular free wall or papillary muscle and the ventricular septum.There is some discussion about safety issues during intense exercise in athletes with LVFTs, as these bands have been associated with ventricular arrhythmias and abnormal cardiac remodelling. However, presence of LVFTs appears to be much more common than previously noted as imaging techniques have improved and the association between LVFTs and abnormal remodelling could very well be explained by better visibility in a dilated left ventricular lumen.Although LVFTs may result in electrocardiographic abnormalities and could form a substrate for ventricular arrhythmias, it should be considered as a normal anatomic variant. Persons with LVFTs do not appear to have increased risk for ventricular arrhythmias or sudden cardiac death.