Leg vascular and skeletal muscle mitochondrial adaptations to aerobic high-intensity exercise training are enhanced in the early postmenopausal phase

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Exercise training leads to favourable adaptations within skeletal muscle; however, this effect of exercise training may be blunted in postmenopausal women due to the loss of oestrogens. Furthermore, postmenopausal women may have an impaired vascular response to acute exercise. We examined the haemodynamic response to acute exercise in matched pre- and postmenopausal women before and after 12 weeks of aerobic high intensity exercise training. Twenty premenopausal and 16 early postmenopausal (3.1 ± 0.5 [mean ± SEM] years after final menstrual period) women only separated by 4 (50 ± 0 versus 54 ± 1) years of age were included. Before training, leg blood flow, O2 delivery, O2 uptake, and lactate release during knee-extensor exercise were similar in pre- and postmenopausal women. Exercise training reduced (P < 0.05) leg blood flow, O2 delivery, O2 uptake, lactate release, blood pressure and heart rate during the same absolute workloads in the postmenopausal women. These effects were not detected in the premenopausal women. Quadriceps muscle protein contents of mitochondrial complex II, III, and IV, endothelial nitric oxide synthase (eNOS), cyclooxygenase-1 (COX.1), COX-2, and oestrogen related receptor α (ERRα) were increased (P < 0.05) with training in the postmenopausal women whereas only the levels of mitochondrial complex V, eNOS, and COX-2 were increased (P < 0.05) in the premenopausal women. These findings demonstrate that vascular and skeletal muscle mitochondrial adaptations to aerobic high intensity exercise training are more pronounced in recent post- compared to premenopausal women, possibly as an effect of enhanced ERRα signalling. Also, the hyperaemic response to acute exercise appears to be preserved in the early postmenopausal phase. This article is protected by copyright. All rights reserved.

TidsskriftJournal of Physiology
Udgave nummer9
Sider (fra-til)2969-2983
Antal sider15
StatusUdgivet - 2017

Bibliografisk note

CURIS 2017 NEXS 104

ID: 173948019