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

Xue Qian Zhang, Yuk Chow Ng, Timothy I. Musch, Russell L. Moore, Robert Zelis, Joseph Y. Cheung

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)544-552
Number of pages9
JournalJournal of Applied Physiology
Volume84
Issue number2
StatePublished - Feb 1 1998

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Muscle Cells
Hypertrophy
Homeostasis
Myocardial Infarction
Sarcoplasmic Reticulum
Cardiac Myosins
Citrate (si)-Synthase
Cardiac Volume
Myosin Heavy Chains
Caffeine
Immunoblotting
Cardiac Output
Stroke Volume
Protein Isoforms
Skeletal Muscle

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Zhang, X. Q., Ng, Y. C., Musch, T. I., Moore, R. L., Zelis, R., & Cheung, J. Y. (1998). Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes. Journal of Applied Physiology, 84(2), 544-552.
Zhang, Xue Qian ; Ng, Yuk Chow ; Musch, Timothy I. ; Moore, Russell L. ; Zelis, Robert ; Cheung, Joseph Y. / Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes. In: Journal of Applied Physiology. 1998 ; Vol. 84, No. 2. pp. 544-552.
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Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes. / Zhang, Xue Qian; Ng, Yuk Chow; Musch, Timothy I.; Moore, Russell L.; Zelis, Robert; Cheung, Joseph Y.

In: Journal of Applied Physiology, Vol. 84, No. 2, 01.02.1998, p. 544-552.

Research output: Contribution to journalArticle

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T1 - Sprint training attenuates myocyte hypertrophy and improves Ca2+ homeostasis in postinfarction myocytes

AU - Zhang, Xue Qian

AU - Ng, Yuk Chow

AU - Musch, Timothy I.

AU - Moore, Russell L.

AU - Zelis, Robert

AU - Cheung, Joseph Y.

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N2 - 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.

AB - 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.

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