Redox reactions control fundamental processes of human biology. Therefore, it is safe to assume that the responses and adaptations to exercise are, at least in part, mediated by redox reactions. In this review, we are trying to show that redox reactions are the basis of exercise physiology by outlining the redox signaling pathways that regulate four characteristic acute exercise-induced responses (muscle contractile function, glucose uptake, blood flow and bioenergetics) and four chronic exercise-induced adaptations (mitochondrial biogenesis, muscle hypertrophy, angiogenesis and redox homeostasis). Based on our analysis, we argue that redox regulation should be acknowledged as central to exercise physiology.

Redox basis of exercise physiology.

Regular exercise with the appropriate intensity and duration may improve an athlete’s physical capacities by targeting different performance determinants across the endurance–strength spectrum aiming to delay fatigue. The mechanisms of muscle fatigue depend on exercise intensity and duration and may range from substrate depletion to acidosis and product inhibition of adenosinetriphosphatase (ATPase) and glycolysis. Fatigue mechanisms have been studied in isolated muscles; single muscle fibers (intact or skinned) or at the level of filamentous or isolated motor proteins; with each approach contributing to our understanding of the fatigue phenomenon. In vivo methods for monitoring fatigue include the assessment of various functional indices supported by the use of biochemical markers including blood lactate levels and more recently redox markers. Blood lactate measurements; as an accompaniment of functional assessment; are extensively used for estimating the contribution of the anaerobic metabolism to energy expenditure and to help interpret an athlete’s resistance to fatigue during high intensity exercise. Monitoring of redox indices is gaining popularity in the applied sports performance setting; as oxidative stress is not only a fatigue agent which may play a role in the pathophysiology of overtraining syndrome; but also constitutes an important signaling pathway for training adaptations; thus reflecting training status. Careful planning of sampling and interpretation of blood biomarkers should be applied; especially given that their levels can fluctuate according to an athlete’s lifestyle and training histories.

Monitoring Exercise-Induced Muscle Fatigue and Adaptations: Making Sense of Popular or Emerging Indices and Biomarkers.

Regulated methionine oxidation by monooxygenases

Going retro: Oxidative stress biomarkers in modern redox biology.

Renal failure is accompanied by progressive muscle weakness and premature fatigue, in part linked to hypokinesis and in part to uremic toxicity. These changes are associated with various detrimental biochemical and morphological alterations. All of these pathological parameters are collectively termed uremic myopathy. Various interventions while helpful can't fully remedy the pathological phenotype. Complex mechanisms that stimulate muscle dysfunction in uremia have been proposed, and oxidative stress could be implicated. Skeletal muscles continuously produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) at rest and more so during contraction. The aim of this mini review is to provide an update on recent advances in our understanding of how ROS and RNS generation might contribute to muscle dysfunction in uremia. Thus, a systematic review was conducted searching PubMed and Scopus by using the Cochrane and PRISMA guidelines. While few studies met our criteria their findings are discussed making reference to other available literature data. Oxidative stress can direct muscle cells into a catabolic state and chronic exposure to it leads to wasting. Moreover, redox disturbances can significantly affect force production per se. We conclude that oxidative stress can be in part responsible for some aspects of uremic myopathy. Further research is needed to discern clear mechanisms and to help efforts to counteract muscle weakness and exercise intolerance in uremic patients.

/pdf/uremic-myopathy-is-oxidative-stress-implicated-in-muscle-23w73hmxww.pdf

Uremic myopathy: is oxidative stress implicated in muscle dysfunction in uremia?

We have examined the structural and functional effects of site-directed methionine oxidation in Dictyostelium (Dicty) myosin II using mutagenesis, in vitro oxidation, and site-directed spin-labeling for electron paramagnetic resonance (EPR). Protein oxidation by reactive oxygen and nitrogen species is critical for normal cellular function, but oxidative stress has been implicated in disease progression and biological aging. Our goal is to bridge understanding of protein oxidation and muscle dysfunction with molecular-level insights into actomyosin interaction. In order to focus on methionine oxidation and to facilitate site-directed spectroscopy, we started with a Cys-lite version of Dicty myosin II. For Dicty myosin containing native methionines, peroxide treatment decreased actin-activated myosin ATPase activity, consistent with the decline in actomyosin function previously observed in biologically aged or peroxide-treated muscle. Methionine-to-leucine mutations, used to protect specific sites from oxidation, identified a single methionine that is functionally sensitive to oxidation: M394, near the myosin cardiomyopathy loop in the actin-binding interface. Previously characterized myosin labeling sites for spectroscopy in the force-producing region and actin-binding cleft were examined; spin-label mobility and distance measurements in the actin-binding cleft were sensitive to oxidation, but particularly in the presence of actin. Overall secondary structure and thermal stability were unaffected by oxidation. We conclude that the oxidation-induced structural change in myosin includes a redistribution of existing structural states of the actin-binding cleft. These results will be applicable to the many biological and therapeutic contexts in which a detailed understanding of protein oxidation as well as function and structure relationships is sought.

Structural and functional impact of site-directed methionine oxidation in myosin.

In the dynamic-shell (DS) concept [V. N. Goncharov et al., Novel Hot-Spot Ignition Designs for Inertial Confinement Fusion with Liquid-Deuterium-Tritium Spheres, Phys. Rev. Lett. 125, 065001 (2020).PRLTAO0031-900710.1103/PhysRevLett.125.065001] for laser-driven inertial confinement fusion the deuterium-tritium fuel is initially in the form of a homogeneous liquid inside a wetted-foam spherical shell. This fuel is ignited using a conventional implosion, which is preceded by a initial compression of the fuel followed by its expansion and dynamic formation of a high-density fuel shell with a low-density interior. This Letter reports on a scaled-down, proof-of-principle experiment on the OMEGA laser demonstrating, for the first time, the feasibility of DS formation. A shell is formed by convergent shocks launched by laser pulses at the edge of a plasma sphere, with the plasma itself formed as a result of laser-driven compression and relaxation of a surrogate plastic-foam ball target. Three x-ray diagnostics, namely, 1D spatially resolved self-emission streaked imaging, 2D self-emission framed imaging, and backlighting radiography, have shown good agreement with the predicted evolution of the DS and its stability to low Legendre mode perturbations introduced by laser irradiation and target asymmetries.

Proof-of-Principle Experiment on the Dynamic Shell Formation for Inertial Confinement Fusion.

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Structural and functional impact of site-directed methionine oxidation in myosin.

Proof-of-Principle Experiment on the Dynamic Shell Formation for Inertial Confinement Fusion.