Cardiac adaptation to training and decreased training loads in endurance athletes: a systematic review

Montero, Francisco; Peinado, Pedro José Benito; Salvo, Valter Di; Pigozzi, Fabio; Maffulli, Nicola

doi:10.1093/bmb/ldm027

Cited by 9 publications

(2 citation statements)

References 21 publications

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“…Lastly, regression of the trained heart back to normal dimensions with training cessation has been identified by various researchers to differentiate training cardiac adaptations from hypertrophic cardiomyopathy. A meta‐analysis that studied the aforementioned regression phenomenon concluded that due to the heterogeneity among studies, it is difficult to indicate how much do dilation and hypertrophy decline when athletes decrease or stop training (Calderon Montero et al ., ).…”

Section: Comparative Analysis Of the Ventricular Function Of An Athlementioning

confidence: 97%

Limits of ventricular function: from athlete's heart to a failing heart

Forteza-Albertí

Sanchís-Gomar

Lippi

et al. 2016

Clin Physio Funct Imaging

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The interest in the study of ventricular function has grown considerably in the last decades. In this review, we analyse the extreme values of ventricular function as obtained with Doppler echocardiography. We mainly focus on the parameters that have been used throughout the history of Doppler echocardiography to assess left ventricular (LV) systolic and diastolic function. The 'athlete's heart' would be the highest expression of ventricular function whereas its lowest expression is represented by the failing heart, independently from the original aetiology leading to this condition. There are, however, morphological similarities (dilation and hypertrophy) between the athlete's and the failing heart, which emerge as physiological and pathophysiological adaptations, respectively. The introduction of new assessment techniques, specifically speckle tracking, may provide new insight into the properties that determine ventricular filling, specifically left ventricular twisting. The concept of ventricular function must be always considered, although it may not be always possible to distinguish the normal heart of sedentary individuals from that of highly trained hearts based solely on echocardiographic or basic studies.

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Section: Comparative Analysis Of the Ventricular Function Of An Athlementioning

confidence: 97%

Limits of ventricular function: from athlete's heart to a failing heart

Forteza-Albertí

Sanchís-Gomar

Lippi

et al. 2016

Clin Physio Funct Imaging

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“…Potassium channels and mitochondrial biogenesis are among the cardiovascular adaptations affected by exercise [5,6]. ATP-sensitive potassium (KATP) channels are expressed in various tissues such as the heart [7].…”

Section: Introductionmentioning

confidence: 99%

The Effect of a Detraining After Resistance Training on the Histochemical Expression of Potassium Channels and Mitochondrial Biogenesis of Heart Tissue in Male Rats

احمدی¹,

کوهیان²,

میردار³

et al. 2021

Horizon Med Sci

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Aims: Detraining may affect cardiovascular adaptations. The present study aimed to investigate the effect of a detraining period followed by resistance training on immunohistochemical expression of ATP-sensitive potassium channels and mitochondrial biogenesis of heart tissue in male rats. Methods & Materials: The present study was experimental. Thirty male Wistar rats were randomly divided into four groups (control, control-detraining, resistance training, and resistance-detraining training). The control group was sacrificed at the beginning of the study, and the control-detraining group did not exercise for 11 weeks. The resistance training group performed eight weeks of training. The resistance-detraining group did not train for three weeks after training. One-way analysis of variance and Tukey’s post hoc test were used for statistical analysis. Findings: The expression of KIR6.2, SUR2a, PGC1α, and TFAM in the heart tissue of the control-detraining group was significantly lower than those in the resistance training group (P=0.001). Also, they were significantly higher in the resistance training group compared to those in the resistance-detraining group (P=0.001). PGC1α expression in the resistance-detraining group was higher than in the control-detraining group (P=0.001). Conclusion: Resistance training increases PGC1α and TFAM in the heart tissue of rats by increasing the expression of KIR6.2 and SUR2a. But lack of exercise reduces the expression of potassium channels and factors that increase mitochondrial biogenesis.

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