Reactive oxygen/nitrogen species and contractile function in skeletal muscle during fatigue and recovery

Abstract

The production of reactive oxygen/nitrogen species (ROS/RNS) is generally considered to increase during physical exercise. Nevertheless, direct measurements of ROS/RNS often show modest increases in ROS/RNS in muscle fibres even during intensive fatiguing stimulation, and the major source(s) of ROS/RNS during exercise is still being debated. In rested muscle fibres, mild and acute exposure to exogenous ROS/RNS generally increases myofibrillar submaximal force, whereas stronger or prolonged exposure has the opposite effect. Endogenous production of ROS/RNS seems to preferentially decrease submaximal force and positive effects of antioxidants are mainly observed during fatigue induced by submaximal contractions. Fatigued muscle fibres frequently enter a prolonged state of reduced submaximal force, which is caused by a ROS/RNS-dependent decrease in sarcoplasmic reticulum Ca(2+) release and/or myofibrillar Ca(2+) sensitivity. Increased ROS/RNS production during exercise can also be beneficial and recent human and animal studies show that antioxidant supplementation can hamper the beneficial effects of endurance training. In conclusion, increased ROS/RNS production have both beneficial and detrimental effects on skeletal muscle function and the outcome depends on a combination of factors: the type of ROS/RNS; the magnitude, duration and location of ROS/RNS production; and the defence systems, including both endogenous and exogenous antioxidants.

Living in flowing water increases resistance to ultraviolet B radiation

“…Increased rates of resequestration of calcium into the sarcoplasmic reticulum by the sarco(endo)plasmic reticulum ATPase (SERCA) improves both sprint and sustained locomotion (Seebacher and Walter, 2012). ROS can interfere with calcium release dynamics from the sarcoplasmic reticulum and the calcium sensitivity of troponin (Cheng et al, 2016). Hence, UV-B-induced ROS may reduce swimming performance by interfering with calcium cycling dynamics, although we have shown previously that UV-B did not affect SERCA activity in mosquitofish (Ghanizadeh Kazerouni et al, 2015).…”

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

“…4A-D) (Reid et al 1992;Matuszczak et al 2005;Powers et al 2011;Cheng et al 2015), because in this case the above-discussed "classical" fatigue mechanisms probably dominate (Allen et al 2008). The positive effects of reducing ROS/RNS during repeated submaximal contractions fit with the fact that acute effects of exogenously applied ROS/RNS are most marked on the steep part of the force-Ca 2þ relationship, where small changes in myofibrillar Ca 2þ sensitivity or SR Ca 2þ release have large effects on force production (Lamb and Westerblad 2011;Cheng et al 2016). However, the effects of ROS/RNS are highly complex and the results of some studies even imply that reducing ROS/RNS during fatigue would impair rather than improve performance.…”

“…Their effects are complex and depend on several factors: the type of ROS/RNS; the magnitude, duration, and location of production; and the defense systems consisting of both endogenous and exogenous antioxidants. It is generally accepted that the production of ROS/RNS increases during most types of physical activities (Powers and Jackson 2008), although exercise-induced increases in ROS/RNS are generally difficult to measure largely because of methodological limitations (Cheng et al 2016 …”

“…On the other hand, decreased myofibrillar Ca 2þ sensitivity is the major problem when O 2 †2 is more effectively metabolized to H 2 O 2 , or its downstream products. Thus, antioxidants do not prevent PLFFD, but they can change the underlying mechanism from impaired SR Ca 2þ release to reduced myofibrillar Ca 2þ sensitivity (Cheng et al 2016). …”

“…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).…”