Abstract
Physical inactivity, excess energy consumption, and obesity are associated with elevated systemic oxidative stress and the sustained activation of redox-sensitive stress-activated protein kinase (SAPK) and mitogen-activated protein kinase signaling pathways. Sustained SAPK activation leads to aberrant insulin signaling, impaired glycemic control, and the development and progression of cardiometabolic disease. Paradoxically, acute exercise transiently increases oxidative stress and SAPK signaling, yet postexercise glycemic control and skeletal muscle function are enhanced. Furthermore, regular exercise leads to the upregulation of antioxidant defense, which likely assists in the mitigation of chronic oxidative stress-associated disease. In this review, we explore the complex spatiotemporal interplay between exercise, oxidative stress, and glycemic control, and highlight exercise-induced reactive oxygen species and redox-sensitive protein signaling as important regulators of glucose homeostasis.
Highlights
Physical inactivity and excess adipose tissue are associated with the development of insulin resistance and type 2 diabetes mellitus (T2DM), which has reached epidemic proportions [1]
NC, no change compared to baseline or control; ↑, significant increase compared to baseline or control; ↓, significant decrease compared to baseline or control; iNOS, inducible nitric oxide synthase; eNOS, endothelial nitric oxide synthase; CS, citrate synthase; mtTFA, mitochondrial transcription factor A; NRF-1/2, nuclear respiratory factor-1 and 2; MyoD, myogenic determination factor; PGC-1 α, peroxisome proliferator-activated receptor gamma coactivator 1 α; young, participants 18–40 years old; middle aged, 40–65 years old; older, >65 years old; active, recreationally active; GPx, glutathione peroxidase; MnSOD, manganese superoxide dismutase; EcSOD, extracellular superoxide dismutase; MITOGEN-ACTIVATED PROTEIN KINASE (MAPK), mitogen-activated protein kinase; DEM, diethyl maleate; stressactivated protein kinase (SAPK), stress-activated protein kinase; IκBα, nuclear factor of kappa light polypeptide gene enhancer in β-cells inhibitor alpha
Ins., insulin stimulation; NC, no change compared to baseline or control; ↑, significant increase compared to baseline or control; ↓, significant decrease compared to baseline or control; Akt, protein kinase B; AS160, Akt substrate of 160 kDa; CMIE, continuous moderate-intensity exercise; glucose transporter 4 (GLUT4), glucose transporter type 4; GSK3, glycogen synthase kinase 3; HIIE, high-intensity interval exercise; HOMA-IR, homeostatic model assessment for insulin resistance; HXK2, hexokinase II; IRS-1/2, insulin receptor substrates 1 and 2; JNK, c-Jun N-terminal kinases; NAC, n-acetylcysteine; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; P38 MAPK, p38 mitogen-activated protein kinases; PI3K, phosphatidylinositol-3 kinase; PPARγ/α/β, peroxisome-proliferator-activated receptor gamma/alpha/beta; PTP1B, protein tyrosine phosphatase 1B; SIE, sprint interval exercise; SAPK, stress-activated protein kinase
Summary
Physical inactivity and excess adipose tissue are associated with the development of insulin resistance and type 2 diabetes mellitus (T2DM), which has reached epidemic proportions [1]. Improved glycemic control following acute and regular exercise occurs in part through improved insulin action and substrate metabolism in skeletal muscle [6, 7] by mechanisms that remain largely unknown. One potential mechanism may involve reactive oxygen species (ROS) and their paradoxical dual role in the pathophysiology of glucose homeostasis [8, 9]. Considering that acute and chronic exercise training lead to alterations in oxidation–reduction (redox) homeostasis [10, 11], it is not surprising that redox biology has been proposed as a possible modulator of glycemic control and skeletal muscle adaptation to exercise [12,13,14]. This review explores current evidence supporting exerciseinduced ROS and skeletal muscle redox-sensitive protein signaling as important regulators of glucose homeostasis
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