Absence of cardiac damage induced by long-term intensive endurance exercise training: A cardiac magnetic resonance and exercise echocardiography analysis in masters athletes.

OBJECTIVES: It is under debate whether the long-term practice of intensive endurance exercise induces chronic cardiac damage such as myocardial fibrosis and ventricle contractile dysfunction. Multimodality analysis was performed to evaluate myocardial damage induced by long term intensive endurance training in master athletes. METHODS: Thirty-three asymptomatic endurance master athletes (47 ± 6 year-old, 9,6 ± 1,7 h training/week for 26 ± 6 years), were compared to 18 sedentary controls (49 ± 7 year-old). They underwent a CMR protocol including 4 chambers morphological and late gadolinium-enhancement (LGE) analysis, left (LV) and right ventricular (RV) T1 mapping and calculation of cardiac extracellular volume (ECV). A maximal exercise echocardiography with left and right ventricular longitudinal global strain (LGS) analysis was performed. Cardiac biomarkers of fibrosis (high sensitive cardiac Troponin T, N-Terminal pro brain natriuretic peptide, N-terminal propeptide of procollagen type I and N-terminal propeptide of procollagen type III) were analysed. RESULTS: Athletes had larger left and right atrial volume, LV and RV end diastolic volume and increased LV and RV mass compared to controls. LGE was not found in athletes. Native T1 values of LV and RV were not significantly different in athletes compared with controls. ECV was normal in both groups (21,5%± 1,6% [18.3 - 23%] in athletes, 22%± 2,2% [18.5 - 27%] in controls). LV and RV peak exercise LGS values were higher in athletes. Cardiac biomarkers levels were normal. CONCLUSION: Despite significant physiological cardiac remodelling, consistent with previous descriptions of athlete's heart, there was no evidence of myocardial fibrosis or exercise left or right ventricular dysfunction or cardiac fibrosis in endurance athletes. Our results are not supporting the hypothesis of deleterious cardiac effects induced by long term and intensive endurance exercise training.

Wearable cardioverter defibrillator: Bridge or alternative to implantation?

The implantable cardioverter-defibrillator (ICD) is effective to prevent sudden cardiac death (SCD) in selected patients with heart disease known to be at high risk for ventricular arrhythmia. Nevertheless, this invasive and definitive therapy is not indicated in patients with potentially transient or reversible causes of sudden death, or in patients with temporary contra-indication for ICD placement. The wearable cardioverter defibrillator (WCD) is increasingly used for SCD prevention both in patients awaiting ICD implantation or with an estimated high risk of ventricular arrhythmia though to be transient. We conducted a review of current clinical uses and benefits of the WCD, and described its technical aspects, limitations and perspectives.

Neuromuscular adaptations after a rehabilitation program in patients with chronic low back pain: case series (uncontrolled longitudinal study).

BACKGROUND: To investigate the impact of a short-term multimodal rehabilitation program for patients with low back pain (LBP) on trunk muscle reflex responses and feedforward activation induced by postural perturbations. METHODS: Case series (uncontrolled longitudinal study). Thirty chronic patients with LBP (21 women and 19 men, mean age 42.6 ± 8.6 years, mean weight 73 ± 14 kg, mean height 174 ± 10 cm) were included. The intervention consisted in a 5-day program including therapeutic education sessions (360 min), supervised abdominal and back muscle strength exercises (240 min), general aerobic training (150 min), stretching (150 min), postural education (150 min) and aqua therapy (150 min). Feedforward activation level and reflex amplitude determined by surface electromyographic activity triggered by postural perturbations were recorded from abdominal and paraspinal muscles in unexpected and expected conditions. Subjects were tested before, just after and again one month after the rehabilitation program. RESULTS: No main intervention effect was found on feedforward activation levels and reflex amplitudes underlining the absence of changes in the way patients with LBP reacted across perturbation conditions. However, we observed a shift in the behavioral strategy between conditions, in fact feedforward activation (similar in both conditions before the program) decreased in the unexpected condition after the program, whereas reflex amplitudes became similar in both conditions. CONCLUSIONS: The results suggest that a short-term rehabilitation program modifies trunk behavioral strategies during postural perturbations. These results can be useful to clinicians for explaining to patients how to adapt to daily life activities before and after rehabilitation.

The education of attention as explanation of variability of practice effects: learning the final approach phase in a flight simulator.

The present study reports two experiments in which a total of 20 participants without prior flight experience practiced the final approach phase in a fixed-base simulator. All participants received self-controlled concurrent feedback during 180 practice trials. Experiment 1 shows that participants learn more quickly under variable practice conditions than under constant practice conditions. This finding is attributed to the education of attention to the more useful informational variables: Variability of practice reduces the usefulness of initially used informational variables, which leads to a quicker change in variable use, and hence to a larger improvement in performance. In the practice phase of Experiment 2 variability was selectively applied to some experimental factors but not to others. Participants tended to converge toward the variables that were useful in the specific conditions that they encountered during practice. This indicates that an explanation for variability of practice effects in terms of the education of attention is a useful alternative to traditional explanations based on the notion of the generalized motor program and to explanations based on the notions of noise and local minima.

Factors responsible for force steadiness impairment with fatigue.

In this study we investigated the contribution of muscle activation to the impairment of fine force control with fatigue. In three experiments, we manipulated muscle activation and measured force variability before and after a fatigue protocol. When muscle activation was left free (subjects had to match the same absolute force pre- and post-fatigue), fatigue increased muscle activation at moderate force levels only, and force variability increased regardless of the level of force. When muscle activation was controlled (subjects had to match the same electromyographic activity), fatigue no longer increased force variability, except at low force levels. When voluntary muscle activation was suppressed (muscles were electrically stimulated), force variability was unaffected by fatigue. We conclude that the impairment of force steadiness with fatigue is mainly due to the increase in muscle activation at moderate forces, but there are other central sources of force fluctuation present at low force levels.

Relationship between oxygen uptake slow component and surface EMG during heavy exercise in humans: influence of pedal rate.

The aim of this study was to test the hypothesis that extreme pedal rates contributed to the slow component of oxygen uptake (VO(2) SC) in association with changes in surface electromyographic (sEMG) during heavy-cycle exercise. Eight male trained cyclists performed two square-wave transitions at 50 and 110 rpm at a work rate that would elicit a VO(2) corresponding to 50% of the difference between peak VO(2) and the ventilatory threshold. Pulmonary gas exchange was measured breath-by-breath and sEMG was obtained from the vastus lateralis and medialis muscles. Integrated EMG flow (QiEMG) and mean power frequency (MPF) were computed. The relative amplitude of the VO(2) SC was significantly higher during the 110-rpm bout (556+/-186 ml min(-1), P<0.05) with compared to the 50-rpm bout (372+/-227 ml min(-1)). QiEMG values increased throughout exercise only during the 110-rpm bout and were associated with the greater amplitude of the VO(2) SC observed for this condition (P<0.05). MPF values remained relatively constant whatever the cycle bout. These findings indicated a VO(2) SC at the two pedal rates but the association with sEMG responses was observed only at high pedal rate. Possible changes in motor units recruitment pattern, muscle energy turnover and muscle temperature have been suggested to explain the different VO(2) SC to heavy pedal rate bouts.

Muscular fatigue increases signal-dependent noise during isometric force production.

This study was designed to characterize the effect of fatigue on the relationship between muscular force and its variability over a broad range of submaximal forces. Eight participants had to match 4 levels of isometric force from 7 to 53% of their maximal capabilities. This task was repeated before and after a fatigue protocol that induced a loss of maximal force of approximately 31%. We found that, despite an increase in force variability that was proportional to the force level, the linear scaling of force variability with mean force was preserved during fatigue. Because this linear scaling is a prerequisite for optimal sensorimotor control models, our results broaden the explanatory power of these models to the fatigue case, while at the same time offering new routes towards understanding how the central nervous system adapts to fatigue.

The role of cocontraction in the impairment of movement accuracy with fatigue.

The present experiment was designed to test the hypothesis that fatigue-induced impairment in movement accuracy is caused by a decrease in muscle cocontraction rather than a reduced ability to produce muscular force. Seven participants performed fast and accurate elbow extensions aimed at a target, before and after a fatigue protocol. The inertia of the manipulandum was decreased after the fatigue protocol so that the ratio of required to available force during movements was identical pre- and post-fatigue. After the fatigue protocol, movement endpoint accuracy decreased and movement endpoint variability increased. These alterations were associated with a decrease in cocontraction. We concluded that the impairment of movement accuracy during fatigue could not be explained by the lack of available force, but was likely to be due to a fatigue-induced decrease in muscular cocontraction. We then speculate that fatigue influences the relative weights of accuracy and energy economy in the optimisation of sensorimotor control.