Sofie K Hansen, Pernille Hansen, Tania W Berry, Hans D Grønbæk, Camilla M Olsen, Youssif Merhi, Shweta Agarwala, Per Aagaard, Lars G Hvid, Jakob Agergaard, Flemming Dela, Charlotte Suetta
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引用次数: 0
Abstract
Disuse induces a disproportionate loss of muscle force compared with muscle mass, with unclear effects on voluntary muscle activation (VA) and peripheral contractility. Furthermore, the effect of neuromuscular electrical stimulation (NMES) as a disuse countermeasure remains uncertain. We investigated the effects of NMES during bed rest on neuromechanical function to improve our understanding of the mechanisms underlying disuse-induced reductions in muscular force. Young (n = 16, 25 years old) and old (n = 16, 71 years old) adults underwent 5 days of bed rest. One leg received NMES (3 × 30 min/day), while the other served as the control (CON). Maximal isometric knee-extensor strength (MVIC), VA and peripheral muscle contractility were assessed before and after bed rest using the interpolated twitch technique, along with biomarkers of neuromuscular junction instability (C-terminal agrin fragment (CAF)) and muscle damage (creatine kinase (CK)). MVIC decreased in both age groups, regardless of NMES (young: CON, -21.7 Nm and NMES, -23.8 Nm; old: CON, -18.5 Nm and NMES, -16.4 Nm). VA was preserved with NMES, while decreasing in CON legs (young, -8.1%; old, -5.6%) following bed rest. Peripheral contractility (resting doublet twitch force) was reduced in CON and NMES legs in both age groups (young: CON, -4.0 Nm and NMES, -11.5 Nm; old: CON, -5.9 Nm and NMES, -10.8 Nm), with a greater decrease in NMES legs. CAF remained unchanged, whereas CK levels increased in young participants, albeit remaining within the normal range. In conclusion, a decline in neuromechanical function was observed after 5 days of bed rest in young and old adults. Although NMES appeared to preserve VA, peripheral muscle contractility was altered, resulting in reduced MVIC.
期刊介绍:
Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged.
Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.