Scientific Programme
Biomechanics & Motor control
IS-BM02 - The power of eccentric contractions on muscle adaptation, remodeling, and function in old age: The positives of negatives
Date: 02.07.2025, Time: 09:30 - 10:45, Session Room: Arengo
Description
Content: In our symposium on eccentric contractions and aging, we will explore the latest insights on how eccentric resistance exercise impacts molecular signalling pathways, adaptation, and muscle form and function in older adults. Eccentric contractions - those involving muscle lengthening under tension - hold unique potential in preserving muscle function and structure as we age. This symposium brings together leading experts who will share cutting-edge research on this important topic. Dr. Colleen Deane will open with her work on the transcriptional responses triggered by eccentric exercise, shedding light on the cellular mechanisms that drive adaptation in aging muscle. Following her, Dr. Martino Franchi will discuss how eccentric contractions influence muscle morphology, with a focus on structural changes and adaptations that can preserve muscle function in old age. Lastly, Dr. Geoff Power will address how eccentric training can stimulate sarcomerogenesis, providing insight into how eccentric stimuli promote sarcomere addition and potentially counteract age-related muscle decline and impairments in muscle mechanical performance. Relevance: This will surely be a thought-provoking session as we examine how eccentric training may serve as a powerful tool to promote and maintain healthy adult aging. Target Audience: Given the basic and applied nature of research being presented, this symposium is geared towards both practitioners and basic scientists.
Chair(s)
Geoffrey A. Power
College of Biological Sciences, University of Guleph, Human Health and Nutritional Sciences
Canada
Speaker A
Colleen Deane
University of Southampton, Clinical, Metabolic and Molecular Physiology
United Kingdom
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Molecular responses to eccentric exercise across age
Traditional resistance exercise involves both shortening (concentric) and lengthening (eccentric) contractions. Compared to concentric contractions, isolated lengthening eccentric contractions represent a potential therapeutic intervention for combating muscle decline in ageing as they are the least metabolically demanding for a given load and produce the most force. However, the safety and efficacy of eccentric exercise as a training mode is often questioned, especially for ageing populations, due to the associated muscle “damage”. This talk will describe the physiological and molecular responses to eccentric exercise across age drawing upon both animal and human evidence. This first part of this talk will describe, with high temporal resolution, the physiological and targeted molecular responses to a bout of eccentric exercise in young and older exercise naïve males. Unpublished observations from our lab demonstrate that functional decline and recovery trajectories are similar across age, yet there was a general pattern of blunted anabolic signaling in older versus younger adults, which might provide the molecular basis for impaired functional adaptations over repeated eccentric exercise bouts. The second part of this talk will explore the application and utility of omics for gaining deeper insight into the age-related molecular responses to eccentric exercise. Using a transcriptional approach, we identified contraction ‘responsive’ modules (related to ‘cell adhesion’ and ‘transcription factor’ processes) that correlated with the magnitude of post-eccentric exercise muscle strength decline, and thus may be novel molecular candidates of functional relevance to ageing muscle adaptation. The third and final part of this talk will explore the impaired adaptability of ageing muscle to eccentric exercise training. Using a mouse model, we found 5 weeks of eccentric training increased strength in younger but not older mice, which was associated with downregulated cellular respiration/oxidative phosphorylation, and upregulated extracellular matrix organization, gene responses in older mice. These molecular signatures may reveal, in part, why older muscles do not appear to be as adaptive to eccentric exercise training as young muscles. Combined, our data detail physiological and molecular responses to acute and chronic eccentric exercise, highlighting several potential molecular candidates worthy of further research as potential therapeutics for optimising adaptation to eccentric exercise.
Speaker B
Martino Franchi
University of Padova, Institute of Physiology, Department of Biomedical Sciences
Italy
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Human muscle adaptations to eccentric exercise through an integrative physiology approach: matching morphology to contractile performance
Eccentric exercise is regarded as one of the most potent stimuli for muscle remodelling owing to the marked tension produced during eccentric contractions. Nevertheless, within the last decades, a limited number of studies have focused on eccentric contraction-induced remodelling with an integrative physiological approach (from the macro-to-the-micro), trying to unravel either with models or in humans the possible connections between changes in structure and function. The first part of this talk will provide an up-to-date description of evidence for the mechanisms responsible for regulating muscle structural and molecular adaptations to different modalities of eccentric training, where I discuss the role of mechanotransduction in muscle remodelling in young and older age. The second part of the talk will present unpublished data on muscle morphological, functional and molecular response to concentric vs. eccentric loading in young vs. older age. This part will be linked to the first talk by Dr Colleen Deane, as data in older males on downregulation of cellular respiration/oxidative phosphorylation to eccentric training will be presented in support of Dr Deane’s data in animal models. In fact, skeletal muscle aging is not only characterized by loss of muscle mass and power but also by mitochondrial impairments and reduced oxidative function. Despite the positive effect on muscle mass and strength, our data point towards dampened mitochondrial biogenesis, reduced mitochondrial content, and promoted fission in older males in response to moderate-load eccentric training. This is of particular interest, as eccentric training often shows positive neuromuscular adaptations in elderly populations but may not be entirely suitable for counteracting reductions in oxidative function. I will conclude with unpublished data related to muscle structural and functional adaptations to 6 weeks of conventional resistance training (concentric + eccentric phase) performed with or without the use of eccentric overload. Using ad hoc ultrasound protocols during ramped isometric contractions and synchronized High-Density EMG, I will discuss changes in architectural behaviour of fascicles at rest and during contraction, and their relation to motor unit properties and muscle function. From our pilot data, it appears that distinct structural adaptations provided by eccentric overload match differences in muscle fascicle behaviour and mechanical function. This topic Is of broad interest for sport scientists, kinesiologists, biomechanics professionals and researchers, physiologists, and will complement Dr Deane’s talk, while laying the ground for Dr Geoff Power’s work on how sarcomerogenesis can influence muscle mechanical function in older age. Our intention is to provide the most updated view on eccentric loading in skeletal muscle.
Speaker C
Geoffrey A. Power
College of Biological Sciences, University of Guleph, Human Health and Nutritional Sciences
Canada
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Implications of eccentric exercise-induced serial sarcomerogenesis in old age on muscle mechanical function
My Lab is interested in the effects of chronic changes to muscle fascicle length on mechanical function in old age. Here we use a F344BN aged rodent model (~32 month) to explore how eccentric exercise may stimulate sarcomerogenesis - the addition of sarcomeres in series – for improvement of muscle mechanical function. Understanding muscle design helps predict functional changes and counteract effects of aging. Muscle fascicle length gets shorter with age due to the loss of sarcomeres aligned in series. This loss of serial sarcomere number (SSN) contributes to declining muscle mechanical function including reduced active force, power, and increased passive stiffness. Due to the relationship between SSN and biomechanical properties of muscle, interventions promoting the addition of sarcomeres in series have been suggested to mitigate age-related impairments in muscle mechanical function. A common intervention for serial sarcomerogenesis is resistance training biased to active lengthening (i.e., eccentric) contractions. In young healthy rats and rabbits, eccentric training has increased SSN by up to 8%, and in humans SSN adaptations have been mostly assumed by increases in FL as measured by ultrasound. Through a series of studies, we investigated the ability for aged muscle to add sarcomeres in series and improve muscle mechanical function during re-ambulation after casting and following eccentric training. In 3 studies age-related differences in sarcomerogenesis and mechanical function were investigated following: (1) 2 weeks of plantar flexor immobilization then 4 weeks of ambulatory recovery; (2) 4 weeks of maximal eccentric plantar flexion training; and (3) 4 weeks of submaximal eccentric training. The soleus was assessed for SSN via laser diffraction. In-vivo measures of strength, passive stiffness, and power assessed changes in mechanical function. (1) Immobilization induced similar losses of SSN (-20%) and isometric strength (-40%) in young and old. Both young and old recovered SSN following immobilization, however, old took twice as long as young, and only young recovered strength. (2) Following maximal eccentric training, young exhibited increased SSN and strength, however, old exhibited no changes in SSN and became 35% weaker, 63% less powerful, and 51% stiffer. (3) Following submaximal eccentric training SSN increased 11%. Training also shifted optimal torque production towards longer muscle lengths, reduced passive torque 42%, and increased peak isotonic power 23%. Our results indicate that old retain the ability to re-add SSN following disuse, but did not increase SSN following maximal eccentric training. Impressively, submaximal eccentric training brought SSN in old back to the level of young rats and improved muscle function. Our results show, for the first time, that aged muscle retains the ability for serial sarcomerogenesis, making SSN an appealing target to improve mechanical function in older adults. Supported by: NSERC