Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca
            <sup>2+</sup>
            leak after one session of high-intensity interval exercise

Place, Nicolas; Ivarsson, Niklas; Venckūnas, Tomas; Neyroud, Daria; Brazaitis, Marius; Cheng, Arthur J.; Ochala, Julien; Kamandulis, Sigitas; Girard, Sébastien; Volungevičius, Gintautas; Paužas, Henrikas; Mekideche, Abdelhafid; Kayser, Bengt; Martínez-Redondo, Vicente; Ruas, Jorge L.; Bruton, Joseph D.; Truffert, André; Lanner, Johanna T.; Skurvydas, Albertas; Westerblad, Håkan

doi:10.1073/pnas.1507176112

Cited by 149 publications

(257 citation statements)

References 48 publications

(76 reference statements)

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“…Exercise can also increase locomotor performance by improving muscle efficiency -that is, the amount of oxygen used for a given amount of force produced (Joyner and Coyle, 2007;Lichtwark and Wilson, 2005;Salin et al, 2015). Additionally, exercise can alter contractile properties and fatigue resistance by modulating calcium cycling dynamics and fibre-type composition (Anttila et al, 2008;Gundersen, 2011;Place et al, 2015). Calcium cycling dynamics, in particular, are important in determining force production and fatigue resistance, and hence swimming performance (Gundersen, 2011).…”

Section: Discussionmentioning

confidence: 99%

Living in flowing water increases resistance to ultraviolet B radiation

Ghanizadeh-Kazerouni

Franklin

Seebacher

2017

Journal of Experimental Biology

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Ultraviolet B radiation (UV-B) is an important environmental driver that can affect locomotor performance negatively by inducing production of reactive oxygen species (ROS). Prolonged regular exercise increases antioxidant activities, which may alleviate the negative effects of UV-B-induced ROS. Animals naturally performing exercise, such as humans performing regular exercise or fish living in flowing water, may therefore be more resilient to the negative effects of UV-B. We tested this hypothesis in a fully factorial experiment, where we exposed mosquitofish (Gambusia holbrooki) to UV-B and control (no UV-B) conditions in flowing and still water. We show that fish exposed to UV-B and kept in flowing water had increased sustained swimming performance (U crit ), increased antioxidant defences (catalase activity and glutathione concentrations) and reduced cellular damage (lipid peroxidation and protein carbonyl concentrations) compared with fish in still water. There was no effect of UV-B or water flow on resting or maximal rates of oxygen consumption. Our results show that environmental water flow can alleviate the negative effects of UV-Binduced ROS by increasing defence mechanisms. The resultant reduction in ROS-induced damage may contribute to maintain locomotor performance. Hence, the benefits of regular exercise are 'transferred' to improve resilience to the negative impacts of UV-B. Ecologically, the mechanistic link between responses to different habitat characteristics can determine the success of animals. These dynamics have important ecological connotations when river or stream flow changes as a result of weather patterns, climate or human modifications.

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Section: Discussionmentioning

confidence: 99%

Living in flowing water increases resistance to ultraviolet B radiation

Ghanizadeh-Kazerouni

Franklin

Seebacher

2017

Journal of Experimental Biology

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“…The elite endurance athletes had higher levels of the antioxidant enzymes SOD2 and catalase in their muscles than recreationally active subjects. Furthermore, RyR1 fragmentation was induced by high-intensity stimulation of isolated mouse muscles and this fragmentation was blocked by the antioxidant N-acetyl cysteine (Place et al 2015). To sum up, accumulation of O 2 †2…”

Section: The Primary Ros In Cells Are the Superoxide Anion (O 2 †2mentioning

confidence: 98%

“…4E,F) . We recently exposed human subjects to one session of high-intensity interval training (six Wingate tests, i.e., 6 Â 30 sec allout cycling with 4 min rest in between) (Place et al 2015). This exhaustive exercise caused a marked PLFFD accompanied by an unexpected RyR1 fragmentation in vastus lateralis muscles of recreationally active subjects.…”

Section: The Primary Ros In Cells Are the Superoxide Anion (O 2 †2mentioning

confidence: 99%

“…In addition, force recovery after fatiguing exercise can be very slow and even take days to be completed and ROS/RNS appear to have key roles in the induction of this severely delayed recovery Cheng et al 2016). Intriguingly, an extra intake of antioxidants has been shown to hamper beneficial effects of endurance training (Gomez-Cabrera et al 2008;Ristow et al 2009;Paulsen et al 2014) and there might be common Ca 2þ -dependent mechanisms underlying the ROS/RNS-related delayed recovery and the triggering of adaptive responses to endurance training (Place et al 2015;Cheng et al 2016).…”

mentioning

confidence: 99%

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Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular Ca²⁺Handling

Cheng

Place

Westerblad

2017

Cold Spring Harb Perspect Med

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118

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The contractile function of skeletal muscle declines during intense or prolonged physical exercise, that is, fatigue develops. Skeletal muscle fibers fatigue acutely during highly intense exercise when they have to rely on anaerobic metabolism. Early stages of fatigue involve impaired myofibrillar function, whereas decreased Ca 2þ release from the sarcoplasmic reticulum (SR) becomes more important in later stages. SR Ca 2þ release can also become reduced with more prolonged, lower intensity exercise, and it is then related to glycogen depletion. Increased reactive oxygen/nitrogen species can cause long-lasting impairments in SR Ca 2þ release resulting in a prolonged force depression after exercise. In this article, we discuss molecular and cellular mechanisms of the above fatigue-induced changes, with special focus on multiple mechanisms to decrease SR Ca 2þ release to avoid energy depletion and preserve muscle fiber integrity. We also discuss fatigue-related effects of exerciseinduced Ca 2þ fluxes over the sarcolemma and between the cytoplasm and mitochondria.T he contractile function of skeletal muscle fibers declines during intense or prolonged physical exercise, that is, fatigue develops. Within the muscle fibers, fatigue is generally related to increased energy demands, in which effective ATP resynthesis is needed to match the dramatically increased ATP consumption during contractions. In contracting muscle fibers, ATP is mainly consumed by the molecular motorsthe actomyosin cross-bridges; ion pumps-the sarcoplasmic reticulum (SR) Ca 2þ -pumps (SERCA); and, to a minor degree, the sarcolemmal Na þ -K þ -pumps. Adequate ATP delivery to these ATP-consuming proteins is essential for normal cell function and integrity, because depletion of ATP would have devastating consequences: constantly attached, noncycling crossbridges and rigor development; insufficient SR Ca 2þ pumping leading to an uncontrolled increase in the free cystolic [Ca 2þ ] ([Ca 2þ ] i ); and inadequate maintenance of Na þ and K þ gradients over the sarcolemma resulting in impaired action potential propagation and muscle fibers eventually becoming inexcitable. Obviously, mechanisms to prevent these catastrophic consequences of ATP depletion exist within the

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“…likely correspond to degraded RyR [10] [24]. ECC-induced reductions in the ratio of full-length to total RyR (i.e., increases in degraded RyR) were observed only in non-treated rats (Figure 4(c)).…”

Section: Amounts Of Serca and Ryrmentioning

confidence: 99%

The Efficacy of Microcurrent Therapy on Eccentric Contraction-Induced Muscle Damage in Rat Fast-Twitch Skeletal Muscle

Hiroshige¹,

Watanabe²,

Aibara³

et al. 2018

OJAppS

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Microcurrent (MC) therapy, in which a very small electric current is applied to the body, has widely been used to promote tissue healing and relieve symptoms. The aim of this study was to examine the effect of MC treatment on eccentric contraction (ECC)-induced muscle damage in rat fast-twitch skeletal muscles. Tibialis anterior muscles underwent 200 repeated ECCs in situ and were then stimulated (25 μA, 0.3 Hz) for 20 min (MC treatment). MC treatment was performed immediately after ECC and during a recovery period of 3 days (a total of 4 times). Three days after ECC, the muscles were excised and used for measure of force output and for biochemical analyses. In MC-treated muscles, tetanic forces at 20 Hz and 100 Hz were partially and fully restored, respectively, whereas in non-treated muscles, both forces remained depressed. Biochemical analyses revealed that MC treatment partially or completely inhibited ECC-induced reductions: in 1) the Ca 2+ -release function of sarcoplasmic reticulum (SR), 2) proteolysis of ryanodine receptor, a Ca 2+ release channel of SR, and 3) myosin ATPase activity. On the other hand, MC treatment was unable to lessen increases in the activity of calpain, a cytosolic, Ca 2+ -activated neutral protease. These results indicate that MC treatment results in beneficial effects, such as restoration of muscle performance following ECC, although the precise mechanisms are still unknown at this time.

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Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca ²⁺ leak after one session of high-intensity interval exercise

Cited by 149 publications

References 48 publications

Living in flowing water increases resistance to ultraviolet B radiation

Living in flowing water increases resistance to ultraviolet B radiation

Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular Ca²⁺Handling

The Efficacy of Microcurrent Therapy on Eccentric Contraction-Induced Muscle Damage in Rat Fast-Twitch Skeletal Muscle

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Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca 2+ leak after one session of high-intensity interval exercise

Cited by 149 publications

References 48 publications

Living in flowing water increases resistance to ultraviolet B radiation

Living in flowing water increases resistance to ultraviolet B radiation

Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular Ca2+Handling

The Efficacy of Microcurrent Therapy on Eccentric Contraction-Induced Muscle Damage in Rat Fast-Twitch Skeletal Muscle

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Product

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Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca ²⁺ leak after one session of high-intensity interval exercise

Molecular Basis for Exercise-Induced Fatigue: The Importance of Strictly Controlled Cellular Ca²⁺Handling