Sprint training normalizes Ca2+ transients and SR function in postinfarction rat myocytes

2000 ◽  
Vol 89 (1) ◽  
pp. 38-46 ◽  
Author(s):  
Lian-Qin Zhang ◽  
Xue-Qian Zhang ◽  
Yuk-Chow Ng ◽  
Lawrence I. Rothblum ◽  
Timothy I. Musch ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sarcoplasmic Reticulum ◽  
Contractile Function ◽  
Half Time ◽  
Sprint Training ◽  
Cardiac Contractile Function ◽  
Cardiac Contractile ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Rat Myocytes

Previous studies have shown that myocytes isolated from sedentary (Sed) rat hearts 3 wk after myocardial infarction (MI) undergo hypertrophy, exhibit altered intracellular Ca2+ concentration ([Ca2+]i) dynamics and abnormal contraction, and impaired sarcoplasmic reticulum (SR) function manifested as prolonged half-time of [Ca2+]idecline. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+ regulation, the present study examined whether 6–8 wk of high-intensity sprint training (HIST) would restore [Ca2+]i dynamics and SR function in MI myocytes toward normal. In MI rats, HIST ameliorated myocyte hypertrophy as indicated by significant ( P ≤ 0.05) decreases in whole cell capacitances [Sham-Sed 179 ±12 ( n = 20); MI-Sed 226 ± 7 ( n = 20); MI-HIST 183 ± 11 pF ( n = 19)]. HIST significantly ( P < 0.0001) restored both systolic [Ca2+]i [Sham-Sed 421 ± 9 ( n = 79); MI-Sed 350 ± 6 ( n = 70); MI-HIST 399 ± 9 nM ( n = 70)] and half-time of [Ca2+]i decline (Sham-Sed 0.197 ± 0.005; MI-Sed 0.247 ± 0.006; MI-HIST 0.195 ± 0.006 s) toward normal. Compared with Sham-Sed myocytes, SR Ca2+-ATPase expression significantly ( P < 0.001) decreased by 44% in MI-Sed myocytes. Surprisingly, expression of SR Ca2+-ATPase was further reduced in MI-HIST myocytes to 26% of that measured in Sham-Sed myocytes. There were no differences in calsequestrin expression among the three groups. Expression of phospholamban was not different between Sham-Sed and MI-Sed myocytes but was significantly ( P < 0.01) reduced in MI-HIST myocytes by 25%. Our results indicate that HIST instituted shortly after MI improves [Ca2+]idynamics in surviving myocytes. Improvement in SR function by HIST is mediated not by increased SR Ca2+-ATPase expression, but by modulating phospholamban regulation of SR Ca2+-ATPase activity.

scholarly journals Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes

1998 ◽  
Vol 84 (2) ◽  
pp. 544-552 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Yuk-Chow Ng ◽  
Timothy I. Musch ◽  
Russell L. Moore ◽  
R. Zelis ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Citrate Synthase ◽  
Contractile Function ◽  
Sprint Training ◽  
Cardiac Contractile Function ◽  
Myocyte Hypertrophy ◽  
Cellular Hypertrophy ◽  
Cardiac Contractile ◽  
Rat Hearts ◽  
Exercise Activity

Zhang, Xue-Qian, Yuk-Chow Ng, Timothy I. Musch, Russell L. Moore, R. Zelis, and Joseph Y. Cheung. Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes. J. Appl. Physiol. 84(2): 544–552, 1998.—Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had decreased Na+/Ca2+exchange currents ( I Na/Ca; 3 Na+ out:1 Ca2+ in) and sarcoplasmic reticulum (SR)-releasable Ca2+contents. These defects in Ca2+regulation may contribute to abnormal contractility in MI myocytes. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+ regulation, the present study examined whether 6–8 wk of high-intensity sprint training (HIST) would ameliorate some of the cellular maladaptations observed in post-MI rats with limited exercise activity (Sed). In MI rats, HIST did not affect citrate synthase activities of plantaris muscles but significantly increased the percentage of cardiac α-myosin heavy chain (MHC) isoforms (57.2 ± 1.9 vs. 49.3 ± 3.5 in MI-HIST vs. MI-Sed, respectively; P ≤ 0.05). At the single myocyte level, HIST attenuated cellular hypertrophy observed post-MI, as evidenced by reductions in cell lengths (112 ± 4 vs. 130 ± 5 μm in MI-HIST vs. MI-Sed, respectively; P ≤ 0.005) and cell capacitances (212 ± 8 vs. 242 ± 9 pF in MI-HIST vs. MI-Sed, respectively; P ≤ 0.015). Reverse I Na/Ca was significantly lower ( P ≤ 0.0001) in myocytes from MI-Sed rats compared with those from rats that were sham operated and sedentary. HIST significantly increased reverse I Na/Ca( P ≤ 0.05) without affecting the amount of Na+/Ca2+exchangers (detected by immunoblotting) in MI myocytes. SR-releasable Ca2+ content, as estimated by integrating forward I Na/Ca during caffeine-induced SR Ca2+ release, was also significantly increased ( P ≤ 0.02) by HIST in MI myocytes. We conclude that the enhanced cardiac output and stroke volume in post-MI rats subjected to HIST are mediated, at least in part, by reversal of cellular maladaptations post-MI.

In situ SR function in postinfarction myocytes

1999 ◽  
Vol 87 (6) ◽  
pp. 2143-2150 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Yuk-Chow Ng ◽  
Russell L. Moore ◽  
Timothy I. Musch ◽  
Joseph Y. Cheung
Keyword(s):  
Myocardial Infarction ◽  
Sarcoplasmic Reticulum ◽  
Half Time ◽  
Time Constants ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Rat Myocytes ◽  
Electrophysiological Technique ◽  
Empirical Constants

Previous studies have shown lower systolic intracellular Ca2+ concentrations ([Ca2+]i) and reduced sarcoplasmic reticulum (SR)-releasable Ca2+ contents in myocytes isolated from rat hearts 3 wk after moderate myocardial infarction (MI). Ca2+ entry via L-type Ca2+ channels was normal, but that via reverse Na+/Ca2+exchange was depressed in 3-wk MI myocytes. To elucidate mechanisms of reduced SR Ca2+ contents in MI myocytes, we measured SR Ca2+uptake and SR Ca2+ leak in situ, i.e., in intact cardiac myocytes. For sham and MI myocytes, we first demonstrated that caffeine application to release SR Ca2+ and inhibit SR Ca2+ uptake resulted in a 10-fold prolongation of half-time ( t ½) of [Ca2+]itransient decline compared with that measured during a normal twitch. These observations indicate that early decline of the [Ca2+]itransient during a twitch in rat myocytes was primarily mediated by SR Ca2+-ATPase and that the t ½ of [Ca2+]idecline is a measure of SR Ca2+uptake in situ. At 5.0 mM extracellular Ca2+, systolic [Ca2+]iwas significantly ( P ≤ 0.05) lower (337 ± 11 and 416 ± 18 nM in MI and sham, respectively) and t ½ of [Ca2+]idecline was significantly longer (0.306 ± 0.014 and 0.258 ± 0.014 s in MI and sham, respectively) in MI myocytes. The 19% prolongation of t ½ of [Ca2+]i decline was associated with a 23% reduction in SR Ca2+-ATPase expression (detected by immunoblotting) in MI myocytes. SR Ca2+ leak was measured by a novel electrophysiological technique that did not require assigning empirical constants for intracellular Ca2+buffering. SR Ca2+ leak rate was not different between sham and MI myocytes: the time constants of SR Ca2+ loss after thapsigargin were 290 and 268 s, respectively. We conclude that, independent of decreased SR filling by Ca2+ influx, the lower SR Ca2+ content in MI myocytes was due to reduced SR Ca2+ uptake and SR Ca2+-ATPase expression, but not to enhanced SR Ca2+ leak.

scholarly journals Sprint training restores normal contractility in postinfarction rat myocytes

2000 ◽  
Vol 89 (3) ◽  
pp. 1099-1105 ◽  
Author(s):  
Lian-Qin Zhang ◽  
Xue-Qian Zhang ◽  
Timothy I. Musch ◽  
Russell L. Moore ◽  
Joseph Y. Cheung
Keyword(s):  
Contractile Function ◽  
Sprint Training ◽  
Maximal Contraction ◽  
Contraction Amplitude ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Rat Myocytes ◽  
Time Required ◽  
Cellular Ca ◽  
Homeostatic Mechanisms

The significance of 6–8 wk of high-intensity sprint training (HIST) on contractile abnormalities of myocytes isolated from rat hearts with prior myocardial infarction (MI) was investigated. Compared with the sedentary (Sed) condition, HIST attenuated myocyte hypertrophy observed post-MI primarily by reducing cell lengths but not cell widths. At high extracellular Ca2+ concentration (5 mM) and low pacing frequency (0.1 Hz), conditions that preferentially favored Ca2+ influx over efflux, MI-Sed myocytes shortened less than Sham-Sed myocytes did. HIST significantly improved contraction amplitudes in MI myocytes. Under conditions that favored Ca2+ efflux, i.e., low extracellular Ca2+ concentration (0.6 mM) and high pacing frequency (2 Hz), MI-Sed myocytes contracted more than Sham-Sed myocytes. HIST did not appreciably affect contraction amplitudes of MI myocytes under these conditions. Compared with MI-Sed myocytes, HIST myocytes showed significant improvement in time required to reach one-half maximal contraction amplitude shortening, maximal myocyte shortening and relengthening velocities, and half time of relaxation. Our results indicate that HIST instituted shortly after MI improved cellular contraction in surviving myocytes. Because our previous studies demonstrated that, in post-MI myocytes, HIST improved intracellular Ca2+ dynamics, enhanced sarcoplasmic reticulum Ca2+ uptake and Ca2+ content, and restored Na+/Ca2+ exchange current toward normal, we hypothesized that improvement in MI myocyte contractile function by HIST was likely mediated by normalization of cellular Ca2+ homeostatic mechanisms.

Isolated ventricular myocytes from copper-deficient rat hearts exhibit enhanced contractile function

2001 ◽  
Vol 281 (2) ◽  
pp. H476-H481 ◽  
Author(s):  
Loren E. Wold ◽  
Jack T. Saari ◽  
Jun Ren
Keyword(s):  
Cardiac Fibrosis ◽  
Copper Deficiency ◽  
Ventricular Myocytes ◽  
Contractile Function ◽  
Detection System ◽  
Cardiac Contractile Function ◽  
Acetoxymethyl Ester ◽  
Cardiac Contractile ◽  
Rat Hearts ◽  
Intracellular Ca

Dietary copper deficiency leads to cardiac hypertrophy, cardiac fibrosis, derangement of myofibrils, and impaired cardiac contractile and electrophysiological function. The purpose of this study was to determine whether impaired cardiac function from copper deficiency is due to depressed contractile function at the single myocyte level. Male Sprague-Dawley rats were fed diets that were either copper adequate (5.59–6.05 μg copper/g body wt; n = 11) or copper deficient (0.29–0.34 μg copper/g body wt; n = 11) for 5 wk. Ventricular myocytes were dispersed and mechanical properties were evaluated using the SoftEdge video-based edge-detection system. Intracellular Ca2+ transients were examined using fura 2-acetoxymethyl ester. Myocytes were electrically stimulated to contract at 0.5 Hz. Properties evaluated included peak shortening (PS), time to peak shortening (TPS), time to 90% relengthening (TR90), and maximal velocities of shortening and relengthening (±d L/d t). Myocytes from the copper-deficient rat hearts exhibited significantly enhanced PS values associated with shortened TR90 measurements compared with those from copper-adequate rat hearts. The ±d L/d t values were enhanced and the intracellular Ca2+ transient decay rate was depressed in myocytes from copper-deficient rats. These data indicate that impaired cardiac contractile function that is seen in copper-deficient whole hearts might not be due to depressed cardiac contractile function at the single cell level but rather to other mechanisms such as cardiac fibrosis.

scholarly journals Effects of sarcoplasmic reticulum Ca2+-ATPase overexpression in postinfarction rat myocytes

2005 ◽  
Vol 98 (6) ◽  
pp. 2169-2176 ◽  
Author(s):  
Belinda A. Ahlers ◽  
Jianliang Song ◽  
JuFang Wang ◽  
Xue-Qian Zhang ◽  
Lois L. Carl ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sarcoplasmic Reticulum ◽  
Ischemic Cardiomyopathy ◽  
Left Ventricular ◽  
Transport Pathways ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Rat Myocytes ◽  
Fractional Shortening ◽  
Expression And Activity

Previous studies in adult myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) demonstrated abnormal contractility and intracellular Ca2+ concentration ([Ca2+]i) homeostasis and decreased sarcoplasmic reticulum Ca2+-ATPase (SERCA2) expression and activity, but sarcoplasmic reticulum Ca2+ leak was unchanged. In the present study, we investigated whether SERCA2 overexpression in MI myocytes would restore contraction and [Ca2+]i transients to normal. Compared with sham-operated hearts, 3-wk MI hearts exhibited significantly higher left ventricular end-diastolic and end-systolic volumes but lower fractional shortening and ejection fraction, as measured by M-mode echocardiography. Seventy-two hours after adenovirus-mediated gene transfer, SERCA2 overexpression in 3-wk MI myocytes did not affect Na+-Ca2+ exchanger expression but restored the depressed SERCA2 levels toward those measured in sham myocytes. In addition, the reduced sarcoplasmic reticulum Ca2+ uptake in MI myocytes was improved to normal levels by SERCA2 overexpression. At extracellular Ca2+ concentration of 5 mM, the subnormal contraction and [Ca2+]i transient amplitudes in MI myocytes (compared with sham myocytes) were restored to normal by SERCA2 overexpression. However, at 0.6 mM extracellular Ca2+ concentration, the supernormal contraction and [Ca2+]i transient amplitudes in MI myocytes (compared with sham myocytes) were exacerbated by SERCA2 overexpression. We conclude that SERCA2 overexpression was only partially effective in ameliorating contraction and [Ca2+]i transient abnormalities in our rat model of ischemic cardiomyopathy. We suggest that other Ca2+ transport pathways, e.g., Na+-Ca2+ exchanger, may also play an important role in contractile and [Ca2+]i homeostatic abnormalities in MI myocytes.

scholarly journals Effects of impaired Ca2+homeostasis on contraction in postinfarction myocytes

1999 ◽  
Vol 86 (3) ◽  
pp. 943-950 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Timothy I. Musch ◽  
Robert Zelis ◽  
Joseph Y. Cheung
Keyword(s):  
Myocardial Infarction ◽  
Steady State ◽  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Mechanical Activity ◽  
Half Time ◽  
Rat Hearts ◽  
Rat Myocytes ◽  
State Contraction ◽  
Exchange Activity

The significance of altered Ca2+ influx and efflux pathways on contractile abnormalities of myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) was investigated by varying extracellular Ca2+concentration ([Ca2+]o, 0.6–5.0 mM) and pacing frequency (0.1–5.0 Hz). Myocytes isolated from 3-wk MI hearts were significantly longer than those from sham-treated (Sham) hearts (125 ± 1 vs. 114 ± 1 μm, P < 0.0001). At high [Ca2+]oand low pacing frequency, conditions that preferentially favored Ca2+ influx over efflux, Sham myocytes shortened to a greater extent than 3-wk MI myocytes. Conversely, under conditions that favored Ca2+ efflux (low [Ca2+]oand high pacing frequency), MI myocytes shortened more than Sham myocytes. At intermediate [Ca2+]oand pacing frequencies, differences in steady-state contraction amplitudes between Sham and MI myocytes were no longer significant. Collectively, the interpretation of these data was that Ca2+ influx and efflux pathways were subnormal in MI myocytes and that they contributed to abnormal cellular contractile behavior. Because Na+/Ca2+exchange activity, but not whole cell Ca2+ current, was depressed in 3-wk MI rat myocytes, our results on steady-state contraction are consistent with, but not proof of, the hypothesis that depressed Na+/Ca2+exchange accounted for abnormal contractility in MI myocytes. The effects of depressed Na+/Ca2+exchange on MI myocyte mechanical activity were further evaluated in relaxation from caffeine-induced contractures. Because Ca2+ uptake by sarcoplasmic reticulum was inhibited by caffeine and with the assumption that intracellular Na+ and membrane potential were similar between Sham and MI myocytes, myocyte relaxation from caffeine-induced contracture can be taken as an estimate of Ca2+ extrusion by Na+/Ca2+exchange. In MI myocytes, in which Na+/Ca2+exchange activity was depressed, the half time of relaxation (1.54 ± 0.14 s) was significantly ( P < 0.02) prolonged compared with that measured in Sham myocytes (1.10 ± 0.10 s).

scholarly journals ALTERED CONTRACTILE FUNCTION IN DOGS AFTER CLINICAL DEATH FOLLOWING ACUTE MIOCARDIAL INFARCTION AND INTACT HEART

2018 ◽  
Vol 7 (2) ◽  
pp. 121-128 ◽  
Author(s):  
G. V. Lisachenko ◽  
A. V. Budaev ◽  
S. V. Bannih
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Contractile Function ◽  
Clinical Death ◽  
Postresuscitation Period ◽  
Systemic Hemodynamics ◽  
Cardiac Contractile Function ◽  
Cardiac Contractile ◽  
Circulatory Insufficiency ◽  
Myocardial Contractile

Aim. To assess myocardial contractile function in dogs after clinical death following acute myocardial infarction and to determine its role in the development of hemodynamic derangements after cardiopulmonary resuscitation. Methods. 180 dogs included in the experiment received pentobarbital anesthesia to assess contractile function and systemic hemodynamics after a 5-min clinical death caused by myocardial infarction. Results Dogs had phase changes in the myocardial contractile function with its initial increase, subsequent depression and normalization in the early postresuscitation period after myocardial infarction. Depressed cardiac contractile function was accompanied by a decrease in the myocardial functional reserve. A similar tendency was found in the restoration of systemic hemocirculation. Conclusion. Similar phase alterations in the myocardial contractile function and systemic hemodynamics developed in the postresuscitation period of acute myocardial infarction. Immediately after recovery, the parameters of systemic hemoperfusion increased due to the activation of the cardiac contractile function. The subsequent initial (3 – 60 min) decrease in the volumetric perfusion parameters was mainly caused by the depressed cardiac contractile function. Rhythm disturbances affected on-going circulatory insufficiency 4 - 5 hours after the recovery. The subsequent progressive decrease in the volumetric perfusion was caused by the extracardiac factors.

scholarly journals Effects of sprint training on contractility and [Ca2+]i transients in adult rat myocytes

2002 ◽  
Vol 93 (4) ◽  
pp. 1310-1317 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Jianliang Song ◽  
Lois L. Carl ◽  
Weixing Shi ◽  
Anwer Qureshi ◽  
...  
Keyword(s):  
Contractile Function ◽  
Sprint Training ◽  
Cell Width ◽  
Western Blots ◽  
Adult Rat ◽  
Protein Levels ◽  
Intracellular Ca ◽  
Uptake Activity ◽  
Rat Myocytes ◽  
Myocyte Contractility

The effects of 6–8 wk of high-intensity sprint training (HIST) on rat myocyte contractility and intracellular Ca2+ concentration ([Ca2+]i) transients were investigated. Compared with sedentary (Sed) myocytes, HIST induced a modest (5%) but significant ( P < 0.0005) increase in cell length with no changes in cell width. In addition, the percentage of myosin heavy chain α-isoenzyme increased significantly ( P < 0.02) from 0.566 ± 0.077% in Sed rats to 0.871 ± 0.006% in HIST rats. At all three (0.6, 1.8, and 5 mM) extracellular Ca2+concentrations ([Ca2+]o) examined, maximal shortening amplitudes and maximal shortening velocities were significantly ( P < 0.0001) lower and half-times of relaxation were significantly ( P < 0.005) longer in HIST myocytes. HIST myocytes had significantly ( P < 0.0001) higher diastolic [Ca2+]i levels. Compared with Sed myocytes, systolic [Ca2+]ilevels in HIST myocytes were higher at 0.6 mM [Ca2+]o, similar at 1.8 mM [Ca2+]o, and lower at 5 mM [Ca2+]o. The amplitudes of [Ca2+]i transients were significantly ( P < 0.0001) lower in HIST myocytes. Half-times of [Ca2+]i transient decline, an estimate of sarcoplasmic reticulum (SR) Ca2+ uptake activity, were not different between Sed and HIST myocytes. Compared with Sed hearts, Western blots demonstrated a significant ( P < 0.03) threefold decrease in Na+/Ca2+ exchanger, but SR Ca2+-ATPase and calsequestrin protein levels were unchanged in HIST hearts. We conclude that HIST effected diminished myocyte contractile function and [Ca2+]itransient amplitudes under the conditions studied. We speculate that downregulation of Na+/Ca2+ exchanger may partly account for the decreased contractility in HIST myocytes.

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