Acute effects of swimming aerobic exercise on contractility and intracellular calcium handling in isolated right ventricular cardiomyocytes (original) (raw)
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Exercise capacity is related to calcium transients in ventricular cardiomyocytes
Journal of Applied Physiology, 2009
Prímola-Gomes TN, Campos LA, Lauton-Santos S, Balthazar CH, Guatimosim S, Capettini LS, Lemos VS, Coimbra CC, Soares DD, Carneiro-Jú nior MA, Quintão-Jú nior JF, Souza MO, Cruz JS, Natali AJ. Exercise capacity is related to calcium transients in ventricular cardiomyocytes. aim of the present study was to evaluate the Ca 2ϩ handling and contractility properties of cardiomyocytes isolated from rats with high intrinsic aerobic exercise capacity. Standard-performance (SP) and high-performance (HP) rats were categorized with a treadmill progressive exercise test according to the exercise time to fatigue (TTF). The SP group included rats with TTF between 16.63 and 46.57 min, and the HP group included rats with TTF Ͼ46.57 min. Isolated ventricular cardiomyocytes were dissociated from the hearts of SP and HP rats, and intracellular global Ca 2ϩ ([Ca 2ϩ ]i) transients were measured. The [Ca 2ϩ ]i transient peak was increased in the HP group relative to the SP group (5.54 Ϯ 0.31 vs. 4.18 Ϯ 0.12 F/F0; P Յ 0.05) and was positively correlated with the TTF attained during the progressive test (r ϭ 0.81). We also performed contractility measurements in isolated cardiomyocytes and found higher amplitude of contraction in the HP group compared with the SP group (6.7 Ϯ 0.2 vs. 6.0 Ϯ 0.3% resting cell length; P Յ 0.05). To reinforce the intrinsic differences between SP and HP rats, we performed Western blot experiments and observed increased expression of sarco-(endo)plasmic reticulum Ca 2ϩ -ATPase type 2a (1.30 Ϯ 0.07 vs. 1.74 Ϯ 0.18 arbitrary units; P Յ 0.05) and ryanodine receptor type 2 (1.86 Ϯ 0.13 vs. 3.57 Ϯ 0.12 arbitrary units; P Յ 0.05) in HP rats. In summary, our data showed important intrinsic differences in cardiomyocyte properties that could explain some of the divergence observed in rats with high intrinsic aerobic exercise capacity. intrinsic exercise aerobic capacity; confocal microscopy Address for reprint requests and other correspondence: A. J. Natali, Av.
Ca2+ regulatory systems in rat myocardium are altered by 24 weeks treadmill training
Pflügers Archiv : European journal of physiology, 2003
The present study was conducted to investigate the effects of long-term exercise training on the main components involved in excitation-contraction coupling and relaxation in rat myocardium. Twenty male Wistar rats were divided into sedentary (S) and treadmill-trained (T) groups. Group T was trained for 24 weeks, 5 days/week (25 m/min, 45-60 min, 0% slope). 48 h after the last exercise session, animals were killed and ventricular and soleus muscle homogenates were obtained. The citrate synthase activity in soleus muscle was significantly increased (163%) in T compared with S rats ( P<0.01), confirming the exercise training efficacy. Although heart weight and cardiac oxidative capacity were not modified by exercise training, the binding of [(3)H] ryanodine and the dihydropyridine [(3)H]PN200-110 to cardiac homogenates, and sarcoplasmic reticulum Ca(2+)-ATPase activity were increased significantly in the ventricular homogenates from T compared with S animals ( P<0.01). Western b...
Journal of Applied Physiology
The purpose of this investigation was to examine the effects of chronic and acute exercise on the main components involved in excitation-contraction coupling and relaxation in rat heart. Sixty male Wistar rats were divided into a sedentary (S) and three 12-wk treadmill-trained groups (T-1, moderate intensity; T-2, high intensity; T-3, interval running). After 12-wk, 15 rats from the S group and 15 rats from the T-2 group were subjected to a single treadmill-exercise session until exhaustion before being killed at 0, 24, or 48 h (acute exercise). The remaining animals were killed 48 h after the last standard exercise session (chronic exercise). The efficacy of the training programs was confirmed by an increase in treadmill endurance time and in skeletal muscle citrate synthase activity. None of the exercise programs modified heart weight or cardiac oxidative capacity. [3H]PN200–110 and [3H]ryanodine binding to cardiac homogenates indicated that the density of L-type and sarcoplasmic ...
Effects of an acute swimming session until exhaustion in myocytes isolated from Wistar rats
Research, Society and Development
The role of regular physical exercise is recognized for the prevention, control and treatment of cardiovascular diseases. However, studies show that after strenuous aerobic exercise sessions in healthy individuals can lead to cardiac damage, due to the high degree of stress imposed on myocardial structures. This study verifies the effects of swimming to exhaustion on contraction and relaxation velocities, as well as the velocity of calcium release and reuptake in cardiomyocytes isolated from the left ventricle. Wistar animals aged 16 weeks were submitted to a protocol of swimming until exhaustion with a load of 5% of body weight and later the cardiomyocytes were isolated. It was observed that an acute session of swimming until exhaustion promoted an increase in the velocity of contraction and relaxation and an increase in the velocity of calcium release. Exercise to exhaustion promotes adverse effects on the myocardium, however more studies are needed to explain these effects and de...
Scientific Reports, 2020
Sudden cardiac death among top athletes is very rare, however, it is 2–4 times more frequent than in the age-matched control population. In the present study, the electrophysiological consequences of long-term exercise training were investigated on Ca2+ homeostasis and ventricular repolarization, together with the underlying alterations of ion channel expression, in a rat athlete's heart model. 12-week swimming exercise-trained and control Wistar rats were used. Electrophysiological data were obtained by using ECG, patch clamp and fluorescent optical measurements. Protein and mRNA levels were determined by the Western immunoblot and qRT-PCR techniques. Animals in the trained group exhibited significantly lower resting heart rate, higher incidence of extrasystoles and spontaneous Ca2+ release events. The Ca2+ content of the sarcoplasmic reticulum (SR) and the Ca2+ transient amplitude were significantly larger in the trained group. Intensive physical training is associated with el...
Physical Exercise and Regulation of Intracellular Calcium in Cardiomyocytes of Hypertensive Rats
Arquivos brasileiros de cardiologia, 2018
Regulation of intracellular calcium (Ca2+) in cardiomyocytes is altered by hypertension; and aerobic exercise brings benefits to hypertensive individuals. To verify the effects of aerobic exercise training on contractility and intracellular calcium (Ca2+) transients of cardiomyocytes and on the expression of microRNA 214 (miR-214) in the left ventricle of spontaneously hypertensive rats (SHR). SHR and normotensive Wistar rats of 16 weeks were divided into 4 groups -sedentary hypertensive (SH); trained hypertensive (TH); sedentary normotensive (SN); and trained normotensive (TN). Animals of the TH and TN groups were subjected to treadmill running program, 5 days/week, 1 hour/day at 60-70% of maximum running velocity for 8 weeks. We adopted a p ≤ 0.05 as significance level for all comparisons. Exercise training reduced systolic arterial pressure in hypertensive rats. In normotensive rats, exercise training reduced the time to 50% cell relaxation and the time to peak contraction and in...
Journal of Molecular and Cellular Cardiology, 2007
Cardiac adaptation to aerobic exercise training includes improved cardiomyocyte contractility and calcium handling. Our objective was to determine whether cytosolic calcium/calmodulindependent kinase II and its downstream targets are modulated by exercise training. A six-week aerobic interval training program by treadmill running increased maximal oxygen uptake by 35% in adult mice, whereupon left ventricular cardiomyocyte function was studied and myocardial tissue samples were used for biochemical analysis. Cardiomyocytes from trained mice had enhanced contractility and faster relaxation rates, which coincided with larger amplitude and faster decay of the calcium transient, but not increased peak systolic calcium levels. These changes were associated with reduced phospholamban expression relative to sarcoplasmic reticulum calcium ATPase, and constitutively increased phosphorylation of phospholamban at the threonine 17, but not at the serine 16 site. Calcium-calmodulin-dependent kinase IIδ phosphorylation was increased at Threonine 287, indicating activation. To investigate the physiological role of calcium/ calmodulin-dependent kinase IIδ phosphorylation, this kinase was blocked specifically by autocamtide-2 related inhibitory peptide II. This maneuver completely abolished training-induced improvements of cardiomyocyte contractility and calcium handling, and blunted, but did not completely abolish the training-induced increase in Ca 2+ sensitivity. Also, inhibition of calcium/ calmodulin-dependent kinase II reduced the greater frequency-dependent acceleration of relaxation that was observed after aerobic interval training. These observations indicate that calcium/calmodulin-dependent kinase IIδ contributes significantly to the functional adaptation of the cardiomyocyte to regular exercise training.
Brazilian Journal of Medical and Biological Research, 2014
In cardiomyocytes, calcium (Ca 2+ +) release units comprise clusters of intracellular Ca 2+ + release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca 2+ + sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca 2+ + sparks (HC=7.61±0.26 vs NC=4.79±0.19 per 100 mm/s) and decreased its amplitude (HC=0.260±0.08 vs NC=0.324±0.10 DF/F 0), full width at half-maximum amplitude (HC=1.05±0.08 vs NC=1.26±0.01 mm), total duration (HC=11.51±0.12 vs NC=14.97±0.24 ms), time to peak (HC=4.84±0.06 vs NC=6.31±0.14 ms), and time constant of decay (HC=8.68±0.12 vs NC=10.21±0.22 ms). These changes were partially reversed in HT rats (frequency of Ca 2+ + sparks=6.26±0.19 mm/s, amplitude=0.282±0.10 DF/F 0 , full width at half-maximum amplitude=1.14±0.01 mm, total duration=13.34±0.17 ms, time to peak=5.43±0.08 ms, and time constant of decay=9.43±0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.
Effects of high-altitude exercise training on contractile function of rat skinned cardiomyocyte
Cardiovascular Research, 2006
Objective: Previous studies have questioned whether there is an improved cardiac function after high-altitude training. Accordingly, the present study was designed specifically to test whether this apparent blunted response of the whole heart to training can be accounted for by altered mechanical properties at the cellular level. Methods: Adult rats were trained for 5 weeks under normoxic (N, NT for sedentary and trained animals, respectively) or hypobaric hypoxic (H, HT) conditions. Cardiac morphology and function were evaluated by echocardiography. Calcium Ca 2+ sensitivity of the contractile machinery was estimated in skinned cardiomyocytes isolated from the left ventricular (LV) sub-epicardium (Epi) and sub-endocardium (Endo) at short and long sarcomere lengths (SL). Results: Cardiac remodelling was harmonious (increase in wall thickness with chamber dilatation) in NT rats and disharmonious (hypertrophy without chamber dilatation) in HT rats. Contrary to NT rats, HT rats did not exhibit enhancement in global cardiac performance evaluated by echocardiography. Stretch-dependent Ca 2+ sensitization of the myofilaments (cellular index of the Frank-Starling mechanism) increased from Epi to Endo in N rats. Training in normoxic conditions further increased this stretch-dependent Ca 2+ sensitization. Chronic hypoxia did not significantly affect myofibrilar Ca 2+ sensitivity. In contrast, high-altitude training decreased Ca 2+ sensitivity of the myofilaments at both SL, mostly in Endo cells, resulting in a loss of the transmural gradient of the stretch-dependent Ca 2+ sensitization. Expression of myosin heavy chain isoforms was affected both by training and chronic hypoxia but did not correlate with mechanical data. Conclusions: Training at sea level increased the transmural gradient of stretch-dependent Ca 2+ sensitization of the myofilaments, accounting for an improved Frank-Starling mechanism. High-altitude training depressed myofilament response to Ca 2+ , especially in the Endo layer. This led to a reduction in this transmural gradient that may contribute to the lack of improvement in LV function via the Frank-Starling mechanism.