Abstract
BackgroundRegular exercises are commonly described as an important factor in health improvement, being directly related to contractile force development in cardiac cells.In order to evaluate the links between swimming exercise intensity and cardiac adaptation by using high molecular mass proteomics, isogenic Wistar rats were divided into four groups: one control (CG) and three training groups (TG’s), with low, moderate and high intensity of exercises.In order to evaluate the links between swimming exercise intensity and cardiac adaptation by using high molecular mass proteomics, isogenic Wistar rats were divided into four groups: one control (CG) and three training groups (TG’s), with low, moderate and high intensity of exercises.ResultsFindings here reported demonstrated clear morphologic alterations, significant cellular injury and increased energy supplies at high exercise intensities. α-MyHC, as well proteins associated with mitochondrial oxidative metabolism were shown to be improved. α-MyHC expression increase 1.2 fold in high intensity training group when compared with control group. α-MyHC was also evaluated by real-time PCR showing a clear expression correlation with protein synthesis data increase in 8.48 fold in high intensity training group. Other myofibrillar protein, troponin , appear only in high intensity group, corroborating the cellular injury data. High molecular masses proteins such as MRS2 and NADH dehydrogenase, involved in metabolic pathways also demonstrate increase expression, respectily 1.5 and 1.3 fold, in response to high intensity exercise.ConclusionsHigh intensity exercise demonstrated an increase expression in some high molecular masses myofibrilar proteins, α-MyHC and troponin. Furthermore this intensity also lead a significant increase of other high molecular masses proteins such as MRS2 and NADH dehydrogenase in comparison to low and moderate intensities. However, high intensity exercise also represented a significant degree of cellular injury, when compared with the individuals submitted to low and moderate intensities.
Highlights
Regular exercises are commonly described as an important factor in health improvement, being directly related to contractile force development in cardiac cells
Similar data were obtained from left ventricle histological sectioning of rats from TG2 and TG3 (TG1) (Additional file 1: Figure S1), demonstrating no structural alteration in the heart tissue, which indicated lower hypertrophy
This pigment is closely associated with oxygen-derived free radicals, which are an important component of muscle fatigue [7] indicating that TG2 are inducing heart tissue modifications to the detriment of improvement in metabolism
Summary
Regular exercises are commonly described as an important factor in health improvement, being directly related to contractile force development in cardiac cells. The cardiac cells of mammals are submitted to a growth phase after birth maturation period defied as cardiac hypertrophy which is characterized by n increase in individual size of the cardiomyocyties without cell division This pattern of hypertrophy development can be initiated in response to some intrinsic and extrinsic stimuli such mechanical stress, neurohumoral factor, cytokines, ischemia and endocrine disorders [1,2]. The mechanism proposed for this structural adaptation is hypertrophy by increase in functional load [3] This overload is followed by modifications in the gene expression pattern, activation of signaling pathways which included up regulation in the contractile protein synthesis and his organization into sarcomeric units [1,2,3]. It is not clear what role is played by the impact of differing training intensities on the physiological heart muscle’s adaptation, in terms of molecular changes
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