Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.10.06.757082

Does increasing the dose of relaxation strain augment the sarcomerogenic response to isometric resistance exercise?

Abstract

Increases in serial sarcomere number (SSN) have been suggested to reduce muscle strain injury risk and improve muscle mechanical performance, however the environmental loading conditions optimizing sarcomerogenesis are not well known. It has been suggested that the magnitude of lengthening which fibres are subject to upon deactivation (i.e., the relaxation strain) may provide a stimulus for sarcomerogenesis. However, no study has attempted to amplify this relaxation strain stimulus to directly test this possible mechanism. Sprague-Dawley rats underwent six weeks (twice weekly) of isometric plantar flexion training, either sustained near-maximal contractions, or intermittent burst type contractions (i.e., contract-relax) in which each repetition consisted of eight brief high-frequency trains to magnify the overall incidence of relaxation strain occurrences across the training period. Groups were otherwise matched for peak torque and torque-time integral. Following training, the torque-angle relationship adapted similarly between groups (training x group interaction P=0.249), with active torque increasing ~30-40% across the angles tested (P<0.001). No changes in maximal shortening velocity were observed with training in either group (P=0.577), however peak power output increased by ~19% in Isometric and ~49% in Burst (training effect P=0.002; interaction P=0.152). For SSN, the gastrocnemius showed a divergent training response (Lateral gastrocnemius: Burst +~11%; Isometric +~2%; interaction P=0.001; Medial gastrocnemius: Burst +~9%; Isometric +~3%; interaction P=0.052), while soleus SSN increased similarly between groups (~2-3%) (training effect P=0.029, interaction P=0.543). Overall, amplifying the relaxation strain stimulus may have a positive effect on stimulating sarcomerogenesis, however further research is needed to clarify the extent of this effect, as well as any underpinning mechanisms.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

MacDougall, K. B., MacIntosh, B. R., Power, G. A.. 2026-10-14. Does increasing the dose of relaxation strain augment the sarcomerogenic response to isometric resistance exercise?. https://doi.org/10.64898/2026.10.06.757082

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Speed judgments during smooth pursuit reflect low gain efference copy

During smooth pursuit eye movements, the visual system must compensate for self-generated retinal motion to achieve stable perception of motion in the environment. This compensation primarily depends on an efferent copy of motor commands. Systematically under- or overweighting the strength of efference copy should lead to correlations between eye movement velocity and perceived object velocity. However, previous examinations of these trial-by-trial perceptual correlations have produced mixed results. It remains unclear how effectively the brain compensates for eye movement induced retinal motion during pursuit, and what this reveals about the way efference copy influences perception. To address this, we developed a speed perturbation paradigm in which 29 participants tracked a moving target that underwent brief speed changes. On each trial, we recorded eye velocity along with perceptual judgments of the sign of the speed change (faster or slower) and confidence ratings for those judgments. Across participants, perceptual and oculomotor sensitivity were correlated (r =0.53), but trial-by-trial perceptual and oculomotor responses appeared independent. A logistic regression model incorporating efference copy gain to predict perceptual reports from stimulus speed and eye speed revealed systematic under-compensation for eye movements; faster eye movements were associated with lower changes in perceived speed. Confidence ratings were well-calibrated to perceptual accuracy and showed a consistent negative relationship with eye movement speed. Collectively, these results are consistent with systematic under compensation for eye movements through the use of efference copy during motion perception.

physiology↗

AN INTEGRATED HEART-ON-A-CHIP NAM RESOLVES DISTINCT CLINICAL PHENOTYPES OF MYOCARDIAL ISCHEMIA-REPERFUSION INJURY

Background: Reperfusion is required for myocardial salvage yet itself injures the heart, and cardioprotective interventions that reduce infarct size experimentally have repeatedly failed to improve outcomes in patients. These interventions are evaluated against viability or infarct size alone, whereas ischemia-reperfusion (I/R) injury produces structural, biochemical, and contractile dysfunction in the same tissue. No in vitro new approach methodology (NAM), however, resolves all three within one system. Methods: A NAM was created within a heart-on-a-chip platform, which was constructed by culturing neonatal rat ventricular myocytes (NRVMs) on muscular thin films. Cardiomyocytes were subjected to normoxia, 2 hours of ischemia, and ischemia followed by 2 hours of reperfusion. Sarcomeric architecture was quantified by immunofluorescence, cardiomyocyte injury by LIVE/DEAD staining and cardiac troponin I release into conditioned media, while contractile stress and spontaneous beat frequency were recorded on the same films before and after each condition. Results: Under ischemia, z-line density decreased while architectural metrics were preserved, indicating cell loss rather than sarcomere disorganization. Furthermore, viability decreased, troponin elevated, and every contractile stress component declined, while spontaneous beat frequency was unchanged. Reperfusion fractured this uniform depression. Cell death and troponin release increased further, yet structure was unchanged from ischemia, so every functional change occurred on a depleted but architecturally intact cardiomyocyte population. Systolic stress recovered partially, whereas diastolic stress exceeded baseline, leaving active stress suppressed despite oxygen recovery. Beat frequency increased with pronounced variability. Conclusions: This heart-on-a-chip NAM resolved structural, biochemical, and contractile injury that global indices conflate, distinguishing ischemic from reperfusion pathophysiology. Interestingly, individual readouts corresponded to distinct clinical syndromes of ischemic injury, positioning this platform for future testing of cardioprotective candidates against the full injury phenotype.

physiology↗

Proteomic profiling of experimental acute alcohol intoxication reveals FGF21 as a specific ethanol-induced hormone

Background: The effects of acute alcohol intoxication on the human plasma proteome are still largely unexplored. Gaining insights into this relationship could identify factors that are influenced by and influence alcohol consumption. Fibroblast Growth Factor 21 (FGF21), a hormone produced by the liver and associated with alcohol preferences, is currently undergoing Phase 2 clinical trials for metabolic dysfunction and alcohol-related liver disease. We hypothesized that FGF21 is a key endocrine responsive hormone to alcohol in humans. Methods: In a post hoc analysis, we evaluated the effects of five standard units of alcoholic beverages on the plasma proteome in 12 healthy Caucasian men. Participants, fasting for 10 hours, received 0.7 g of alcohol per kg of body weight via gastric infusion, with blood samples collected before and after consumption. Results: The proteomic response to this level of alcohol intoxication was highly specific. Of 1,462 proteins measured, only 11 changed significantly and FGF21 exhibited by far the largest increase (10.5-fold). Conclusion: This study highlights a unique proteomic response to acute alcohol ingestion and supports further exploration of FGF21 mimetics as potential treatments for alcohol-related disorders.

physiology↗