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Review
. 2017 Aug 1;123(2):460-472.
doi: 10.1152/japplphysiol.00418.2017. Epub 2017 Jun 1.

Exercise: Teaching myocytes new tricks

Scott K Powers  1
Affiliations
Review

Exercise: Teaching myocytes new tricks

Scott K Powers. J Appl Physiol (1985). .

Abstract

Endurance exercise training promotes numerous cellular adaptations in both cardiac myocytes and skeletal muscle fibers. For example, exercise training fosters changes in mitochondrial function due to increased mitochondrial protein expression and accelerated mitochondrial turnover. Additionally, endurance exercise training alters the abundance of numerous cytosolic and mitochondrial proteins in both cardiac and skeletal muscle myocytes, resulting in a protective phenotype in the active fibers; this exercise-induced protection of cardiac and skeletal muscle fibers is often referred to as "exercise preconditioning." As few as 3-5 consecutive days of endurance exercise training result in a preconditioned cardiac phenotype that is sheltered against ischemia-reperfusion-induced injury. Similarly, endurance exercise training results in preconditioned skeletal muscle fibers that are resistant to a variety of stresses (e.g., heat stress, exercise-induced oxidative stress, and inactivity-induced atrophy). Many studies have probed the mechanisms responsible for exercise-induced preconditioning of cardiac and skeletal muscle fibers; these studies are important, because they provide an improved understanding of the biochemical mechanisms responsible for exercise-induced preconditioning, which has the potential to lead to innovative pharmacological therapies aimed at minimizing stress-induced injury to cardiac and skeletal muscle. This review summarizes the development of exercise-induced protection of cardiac myocytes and skeletal muscle fibers and highlights the putative mechanisms responsible for exercise-induced protection in the heart and skeletal muscles.

Keywords: cardioprotection; diaphragm; endurance exercise; mechanical ventilation; skeletal muscle.

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Figures

Fig. 1.
Fig. 1.
Several of the major damaging events in the cardiac myocyte during ischemia and reperfusion. I-R, ischemia-reperfusion; ROS, reactive oxygen species.
Fig. 2.
Fig. 2.
As few as 3–5 consecutive days of endurance exercise training result in significant cardioprotection against IR-induced myocardial infarction. Sed, sedentary animals; Ex, exercise-trained animals. *Significantly different (P < 0.05) from Sed. [Data are from Quindry et al. (114).]
Fig. 3.
Fig. 3.
Time course of the loss of cardioprotection following cessation of exercise training. After an IR insult in an isolated working heart preparation, lactate dehydrogenase (LDH) release from the heart was measured before and after IR as a biomarker of myocardial injury. 1D, 3D, 9D, and 18D, endurance exercise training followed by 1, 3, 9, and 18 days of rest, respectively. *Significantly different (P < 0.05) from Sed. #Significantly different (P < 0.05) from 18D. [Data from Lennon et al. (77).]
Fig. 4.
Fig. 4.
Evidence that exercise-induced increases in superoxide dismutase 2 (SOD2) within the mitochondria are essential to achieve the full benefits of exercise-induced protection against IR-induced myocardial infarction. An antisense oligonucleotide (AS) directed against SOD2 was used to prevent the exercise-induced increase in SOD2 expression in the heart. Compared with exercise-trained animals with no experimental treatment, prevention of exercise-induced increases in SOD2 significantly impaired the level of exercise-induced cardioprotection. Ex-AS, endurance exercise-trained animals treated with an AS directed against SOD2. *Significantly different (P < 0.05) from Sed. #Significantly different (P < 0.05) from Ex-AS. [Data are from French et al. (41).]
Fig. 5.
Fig. 5.
Endurance exercise-induced changes in mitochondria that contribute to cardioprotection against IR injury. Exercise training increases both mitochondrial biogenesis and mitochondrial turnover; this results in a healthy population of mitochondria in cardiac myocytes. Exercise training also improves mitochondrial antioxidant capacity by increasing the abundance of SOD2 and the activity of glutathione reductase (GR).
Fig. 6.
Fig. 6.
Prolonged (18 h of full support) mechanical ventilation (MV) results in rapid atrophy of all diaphragmatic fiber types in rats. CSA, cross-sectional area. *Significantly different (P < 0.05) from control animals (CON). [Data are from Shanely et al. (127).]
Fig. 7.
Fig. 7.
Similar to rats, prolonged (18–69 h of full support) MV results in rapid atrophy of all diaphragmatic fiber types in humans. Type II fibers include types IIa and IIx. *Significantly different (P < 0.05) from control animals (CON). [Data are from Levine et al. (79).]
Fig. 8.
Fig. 8.
Endurance exercise training performed before MV protects the rat diaphragm against MV-induced atrophy of all diaphragmatic fiber types. *Significantly different (P < 0.05) from control animals (CON). [Data are from Smuder et al. (130).]
Fig. 9.
Fig. 9.
Endurance exercise-induced alterations in diaphragm fibers that could contribute to protection against MV-induced diaphragmatic atrophy. Exercise training increases the abundance of numerous cytoprotective cytosolic proteins, including heat shock protein 72 (HSP72), superoxide dismutase 1 (SOD1), and glutathione peroxidase 1 (GPX1). Furthermore, exercise training alters mitochondrial phenotype by altering mitochondrial protein abundance, including enhancements in mitochondrial antioxidant capacity, as evidenced by an increased abundance of both SOD2 and sirtuin 3 (SIRT3). mtHSP70, mitochondrial HSP70.
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References

    1. Abete P, Ferrara N, Cacciatore F, Sagnelli E, Manzi M, Carnovale V, Calabrese C, de Santis D, Testa G, Longobardi G, Napoli C, Rengo F. High level of physical activity preserves the cardioprotective effect of preinfarction angina in elderly patients. J Am Coll Cardiol 38: 1357–1365, 2001. doi:10.1016/S0735-1097(01)01560-1. - DOI - PubMed
    1. Adhikari NK, Fowler RA, Bhagwanjee S, Rubenfeld GD. Critical care and the global burden of critical illness in adults. Lancet 376: 1339–1346, 2010. doi:10.1016/S0140-6736(10)60446-1. - DOI - PMC - PubMed
    1. Adlam VJ, Harrison JC, Porteous CM, James AM, Smith RA, Murphy MP, Sammut IA. _targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury. FASEB J 19: 1088–1095, 2005. doi:10.1096/fj.05-3718com. - DOI - PubMed
    1. Agten A, Maes K, Smuder A, Powers SK, Decramer M, Gayan-Ramirez G. N-acetylcysteine protects the rat diaphragm from the decreased contractility associated with controlled mechanical ventilation. Crit Care Med 39: 777–782, 2011. doi:10.1097/CCM.0b013e318206cca9. - DOI - PubMed
    1. Agten A, Maes K, Thomas D, Cielen N, Van Hees HW, Dekhuijzen RP, Decramer M, Gayan-Ramirez G. Bortezomib partially protects the rat diaphragm from ventilator-induced diaphragm dysfunction. Crit Care Med 40: 2449–2455, 2012. doi:10.1097/CCM.0b013e3182553a88. - DOI - PubMed

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