542 Chronic Treadmill Training Does Not Influence Ryanodine Binding to Rat Myocardium

Chronic and acute exercise do not alter Ca2+regulatory systems and ectonucleotidase activities in rat heart

“…Similarly, RyR levels were unmodified by the training programs, although a small, nonsignificant decrease (P Ͻ 0.1) that paralleled that of DHPR levels was observed in heart homogenates of T-1 trained rats. In agreement with these results, no changes in both B max and K d of ryanodine binding have been observed in heart homogenates of female rats subjected to an intense running program for 16 wk (30). However, these data do not exclude the possibility that training elicits a modification of the properties of the SR channel, involving an improvement of the release of Ca 2ϩ necessary for cardiac contraction.…”

“…Similarly, methods allowing measurement of the concentration of [ 3 H]PN200-110 and [ 3 H]ryanodine binding sites in whole cardiac homogenates were developed, establishing the experimental conditions to minimize nonspecific binding. It must be pointed out that present values of DHPR and RyR densities for S and trained rats were obtained from experiments performed at a single, nonsaturating ligand concentration (2 and 10 nM, respectively) and that we assumed that K d values were not affected by exercise training, as it has been previously reported for these receptors (30,38).…”

“…Similarly, an increase in the SR Ca 2ϩ uptake (12,19) and SR Ca 2ϩ -ATPase mRNA levels (7) has also been observed in hearts of swim-trained rats. In contrast, endurance training has been reported to cause no modification in heart SR Ca 2ϩ uptake and Ca 2ϩ -ATPase activity (10,17,18,31), SL Na ϩ /Ca 2ϩ exchange activity (10), RyR density or modulation by Ca 2ϩ (30), or L-type Ca 2ϩ channel number or intrinsic function (13). The intensity, duration, and type of exercise training program used are factors that may contribute to these controversial results.…”

Exercise-induced changes in calcium handling in left ventricular cardiomyocytes

“…Exercise training-induced effects on isolated SR Ca 2+ release per se have not been studied, but could potentially be interesting as the RyR2 complex is responsive to different stimuli (75)(76)(77)(78). Faster [Ca 2+ ] i transient decay after exercise training seems to at least partly be explained by increased levels of SERCA2a and NCX (36,37,(79)(80)(81)(82), although other studies do not support this (83)(84)(85). The reason for this discrepancy is presently unclear, but may be due to different exercise intensities; studies of high exercise intensity report upregulated expression, whereas those of low exercise intensity do not report changes.…”

Exercício e restrição alimentar aumentam o RNAm de proteínas do trânsito de Ca2+ miocárdico em ratos

“…Molecular structures found in the sarcolemma, slow L-type calcium channel (L-channel) and sodium/potassium exchanger (NCX), also found in the sarcoplasmic reticulum, ryanodine channel, the calsequestrin (CQS), the sarcoplasmic reticulum calcium pump (SERCA2a) and phospholamban, are involved in the intracellular calcium handling and participate in the cardiac muscle contraction and relaxation 11 . Studies show that FR decreases the gene expression of ryanodine 12 , SERCA2 13 , L-channel 14 , while physical training (PT) increases the mRNA of SERCA2 [15][16][17] , ryanodine 18,19 and L-channel 20 . The transcription of the molecular structures involved in the intracellular calcium handling can be modulated by thyroid hormones (TH), via nuclear receptors of HT [21][22][23] .…”