D L Enns1, S Iqbal, P M Tiidus. 1. Department of Kinesiology & Physical Education, Wilfrid Laurier University, Waterloo, ON, Canada.
Abstract
AIM: Our laboratory recently demonstrated that increases in post-exercise muscle satellite cell numbers are augmented by oestrogen. We investigated whether muscle oestrogen receptors (ORs) mediate this effect through administration of an OR antagonist, ICI 182,780. METHODS: Ovariectomized female rats were divided into three groups: sham, oestrogen (0.25 mg pellet) and oestrogen plus OR blocker (ICI 182,780). Each group was divided into control and exercised groups. ICI 182,780 (5 mg kg(-1) sc) was administered 1 day prior to and 6 days following oestrogen pellet implantation. After 8 days of oestrogen exposure, animals ran downhill for 90 min (17 m min(-1), -13.5 degrees grade) on a treadmill. Soleus and white vastus muscles were removed 24 and 72 h post-exercise and immunostained for total (Pax7), activated (MyoD) and proliferating (BrdU) satellite cells. Muscle damage was indirectly assessed by measuring beta-glucuronidase activity. Two markers (His48 and ED1) of leucocyte infiltration were also examined. RESULTS: beta-Glucuronidase activities and His48+ and ED1+ leucocytes increased post-exercise, and these increases were attenuated with oestrogen. ICI 182,780 did not influence the attenuating effect of oestrogen on leucocyte infiltration or beta-glucuronidase activities in muscle. Total (Pax7+), activated (MyoD+) and proliferating (BrdU+) satellite cells increased post-exercise, and these increases were augmented with oestrogen. Interestingly, ICI 182,780 abolished both exercise- and oestrogen-mediated increases in these satellite cell markers. CONCLUSION: Oestrogen may augment increases in muscle satellite cells following exercise through OR-mediated mechanisms; furthermore, the attenuation of post-exercise muscle damage and leucocyte infiltration by oestrogen appears to be a non-OR-mediated process.
AIM: Our laboratory recently demonstrated that increases in post-exercise muscle satellite cell numbers are augmented by oestrogen. We investigated whether muscle oestrogen receptors (ORs) mediate this effect through administration of an OR antagonist, ICI 182,780. METHODS: Ovariectomized female rats were divided into three groups: sham, oestrogen (0.25 mg pellet) and oestrogen plus OR blocker (ICI 182,780). Each group was divided into control and exercised groups. ICI 182,780 (5 mg kg(-1) sc) was administered 1 day prior to and 6 days following oestrogen pellet implantation. After 8 days of oestrogen exposure, animals ran downhill for 90 min (17 m min(-1), -13.5 degrees grade) on a treadmill. Soleus and white vastus muscles were removed 24 and 72 h post-exercise and immunostained for total (Pax7), activated (MyoD) and proliferating (BrdU) satellite cells. Muscle damage was indirectly assessed by measuring beta-glucuronidase activity. Two markers (His48 and ED1) of leucocyte infiltration were also examined. RESULTS: beta-Glucuronidase activities and His48+ and ED1+ leucocytes increased post-exercise, and these increases were attenuated with oestrogen. ICI 182,780 did not influence the attenuating effect of oestrogen on leucocyte infiltration or beta-glucuronidase activities in muscle. Total (Pax7+), activated (MyoD+) and proliferating (BrdU+) satellite cells increased post-exercise, and these increases were augmented with oestrogen. Interestingly, ICI 182,780 abolished both exercise- and oestrogen-mediated increases in these satellite cell markers. CONCLUSION: Oestrogen may augment increases in muscle satellite cells following exercise through OR-mediated mechanisms; furthermore, the attenuation of post-exercise muscle damage and leucocyte infiltration by oestrogen appears to be a non-OR-mediated process.
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