Heat shock protein expression is increased in cardiac and skeletal muscles of Fischer 344 rats after endurance training

Samelman, T. R.

doi:10.1017/s0958067000018947

Cited by 23 publications

(14 citation statements)

References 25 publications

(54 reference statements)

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“…1998, Noble et al. 1999, Samelman 2000, Harris & Starnes 2001). The great increase in HSP72 content found in our 24‐week animals suggests that the long‐term exercise training might have induced some type of stress over the rats’ myocardium.…”

Section: Discussionmentioning

confidence: 99%

Responses of rat myocardial antioxidant defences and heat shock protein HSP72 induced by 12 and 24‐week treadmill training

Morán

Delgado

González

et al. 2004

Acta Physiologica Scandinavica

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Section: Discussionmentioning

confidence: 99%

Responses of rat myocardial antioxidant defences and heat shock protein HSP72 induced by 12 and 24‐week treadmill training

Morán

Delgado

González

et al. 2004

Acta Physiologica Scandinavica

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“…Samelman (2000) demonstrated that endurance treadmill training for 16-20 weeks increased the HSP70, HSC70, and HSP60 protein content of the soleus muscle of rats, although the content of these HSPs remained unchanged in the anterior tibialis and gastrocnemius muscles after training. Mattson et al (2000) demonstrated an increase in the HSP60 content of the plantaris muscle of female Wistar rats after 8 weeks of treadmill running for 6 days a week at a 10% incline.…”

Section: Effect Of Training On Hsp Content Of Skeletal Musclementioning

confidence: 94%

The exercise-induced stress response in skeletal muscle: failure during aging

Kayani

Morton

McArdle

2008

Appl. Physiol. Nutr. Metab.

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Mammalian adult skeletal muscle adapts to the stress of contractile activity with increased gene expression by yielding a family of highly conserved cytoprotective proteins known as heat shock proteins (HSPs). Although the exercise-induced stress response of both animal and human skeletal muscle is now well documented, the precise mechanisms underlying this adaptation remain unclear. The induction of HSPs after exercise is severely blunted in the muscle of older individuals. This review focuses on the effects of different forms of exercise and training on the induction of HSPs in the muscles of adult individuals, and examines the proposed mechanisms underlying this adaptation. Furthermore, the functional effect of the inability of the muscles of older individuals to adapt in this way is discussed, together with the proposed mechanisms underlying this maladaptation.

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“…Thus it is not surprising that levels of many proteins involved in protection against stressors are increased either acutely or as an adaptation to repeated or habitual bouts of exercise in skeletal muscle and the heart (Locke et al . ; Samelman, ; Khassaf et al . ; Kim et al .…”

Section: Introductionmentioning

confidence: 99%

Mitochondria in the middle: exercise preconditioning protection of striated muscle

Lawler¹,

Rodriguez²,

Hord³

2016

The Journal of Physiology

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Cellular and physiological adaptations to an atmosphere which became enriched in molecular oxygen spurred the development of a layered system of stress protection, including antioxidant and stress response proteins. At physiological levels reactive oxygen and nitrogen species regulate cell signalling as well as intracellular and intercellular communication. Exercise and physical activity confer a variety of stressors on skeletal muscle and the cardiovascular system: mechanical, metabolic, oxidative. Transient increases of stressors during acute bouts of exercise or exercise training stimulate enhancement of cellular stress protection against future insults of oxidative, metabolic and mechanical stressors that could induce injury or disease. This phenomenon has been termed both hormesis and exercise preconditioning (EPC). EPC stimulates transcription factors such as Nrf‐1 and heat shock factor‐1 and up‐regulates gene expression of a cadre of cytosolic (e.g. glutathione peroxidase and heat shock proteins) and mitochondrial adaptive or stress proteins (e.g. manganese superoxide dismutase, mitochondrial KATP channels and peroxisome proliferator activated receptor γ coactivator‐1 (PGC‐1)). Stress response and antioxidant enzyme inducibility with exercise lead to protection against striated muscle damage, oxidative stress and injury. EPC may indeed provide significant clinical protection against ischaemia–reperfusion injury, Type II diabetes and ageing. New molecular mechanisms of protection, such as δ‐opioid receptor regulation and mitophagy, reinforce the notion that mitochondrial adaptations (e.g. heat shock proteins, antioxidant enzymes and sirtuin‐1/PGC‐1 signalling) are central to the protective effects of exercise preconditioning.

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Heat shock protein expression is increased in cardiac and skeletal muscles of Fischer 344 rats after endurance training

Cited by 23 publications

References 25 publications

Responses of rat myocardial antioxidant defences and heat shock protein HSP72 induced by 12 and 24‐week treadmill training

Responses of rat myocardial antioxidant defences and heat shock protein HSP72 induced by 12 and 24‐week treadmill training

The exercise-induced stress response in skeletal muscle: failure during aging

Mitochondria in the middle: exercise preconditioning protection of striated muscle

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