Heart, liver, and skeletal muscle myeloperoxidase activity during exercise

Abstract

The purpose of this study was to determine whether contractile activity associated with running exercise was a prerequisite for neutrophil infiltration into rat tissues. H2O2-dependent myeloperoxidase (MPO) activity for rat (n = 8) liver, heart, and gastrocnemius muscles was assayed after 58 +/- 11 min of running to voluntary exhaustion (25 m/min; 0% grade). MPO activity values measured with 0.6 mM H2O2 were 0.988 +/- 0.331 (SD) U/g (skeletal muscle), 1.563 +/- 0.303 U/g (heart), and 1.652 +/- 0.510 U/g (liver) for control samples, compared with 1.690 +/- 0.321, 3.128 +/- 1.221, and 2.752 +/- 0.437 U/g, respectively, for the exercise group (P < or = 0.05). Kinetic analysis revealed that maximum velocity for all tissues increased as a result of the exercise (P < 0.05). The Michaelis constant (Km) values at rest for all tissues were similar (range 0.53-0.57 mM H2O2; P > or = 0.05). Exercise did not alter the Km values for cardiac and liver samples; however, for skeletal muscle, the Km was 28% lower than control (P < or = 0.05). The results of this study show that, with prolonged running, MPO activity is elevated in most rat tissues and not exclusively in skeletal muscle. Moreover, the metabolic status of the tissues may be an important factor for neutrophil infiltration with exercise and not exclusively the type of muscle contraction, as previously hypothesized.

Degenerative and regenerative features of myofibers differ among skeletal muscles in a murine model of muscular dystrophy

“…The present study demonstrated that Iba1-positive macrophages are the major inflammatory cells in skeletal muscle lesions that positively correlate with the number of regenerating myofibers, whereas Gr1-positive granulocytes, mainly neutrophils, negatively correlate with regenerated myofibers in mdx mice. After muscle injury caused by trauma such as extensive physical activity, or by innate genetic defects, inflammatory cells such as neutrophils and macrophages infiltrate into the lesions (Belcastro et al 1996). Necrosis of myofibers is the initial event in skeletal muscle degeneration, accompanied by the activation of mononucleated cells, principally inflammatory and myogenic cells.…”

Estrogen supplementation failed to attenuate biochemical indices of neutrophil infiltration or damage in rat skeletal muscles following ischemia

“…The presence of CD43 has been used as an indicator on neutrophil infiltration of skeletal muscle following damage (Tidball et al, 1999). Muscle MPO activity also has been commonly used as a quantitative marker of muscle neutrophil infiltration following exercise or ischemia induced damage (i.e., Squadrito et al, 1997;Belcastro et al, 1996;Tiidus et al, 2001). Our previous study found no elevation in MPO activities in soleus muscle at two hours after a two-hour ischemic period in ovariectomized or gonad-intact female rats (Stupka and Tiidus, 2001).…”

“…All muscle samples (PL, WG, RG) were analyzed for myeloperoxidase (MPO), glucose-6-phosphate dehydrogenase (G6PD) and bglucuronidase (bGLU) activites. Muscle MPO activity is a marker of leukocyte (primarily neutrophil) infiltration (Belcastro et al, 1996). Muscle MPO activity was determined spectrophotometrically from homogenates using the method of Smith and colleagues (1989).…”

“…Muscle MPO activity was determined spectrophotometrically from homogenates using the method of Smith and colleagues (1989). One unit of MPO activity was defined as a change in one unit of abs at 480 nm min -1 and expressed per g muscle wet weight (Belcastro et al, 1996). Muscle G6PD activity is a semi-quantitative marker of muscle damage (Armstrong et al, 1983).…”

The contribution of paraoxonase 1 and myeloperoxidase to HDL-cholesterol functionality

“…It has also been well documented that the MPO activity becomes elevated in response to intensive exercise both in humans and animals [11,52,53]. However, it should be stressed that the main source of the circulating MPO is its release from the neutrophils, whose count in the blood is stimulated in response to exercise [54,56].…”