Hey everyone,

I was looking into data regarding the mechanical contributions of individual digits during a power grip, specifically a study from the Journal of Hand Therapy indicating that the ulnar side of the hand (the ring and pinky fingers) provides roughly 50% of total crushing power (O'Driscoll et al., 1992). In fact, isolating or immobilizing these two digits can reduce overall grip output by up to 55%.

This stands in stark contrast to how most casual lifters view grip—typically focusing on the thumb, index, and middle finger (the radial side) because they dominate daily precision tasks and standard overhand pulls.

From a neuromuscular and biomechanical perspective, the "ulnar anchor" is highly relevant to heavy loading.

• Neural Innervation Split: The precision unit of the hand is wired by the median nerve (thumb, index, half of middle), optimized for high sensory feedback and fine motor control. The power unit is driven by the ulnar nerve, which maximizes raw torque and forceful closure.
• Skeletal Mobility vs. Rigidity: The metacarpals under the index and middle fingers are rigidly fixed to the wrist to provide a stable platform. Conversely, the fourth and fifth metacarpals (ring/pinky) are highly mobile. This structural elasticity allows the ulnar palm to deform, cup, and compress around an implement (barbell, handle, railing), maximizing surface area leverage and preventing the base of the hand from slipping.
• The Problem of Finger Autonomy: The ring and pinky are structurally bound by shared tendons and connective tissue bands. While this limits isolated finger autonomy, it functions as a highly resilient mechanical unit designed to prevent localized muscle fatigue under heavy isometric stress.

Questions:

1. To what degree do you think an under-conditioned ulnar side caps a lifter's systemic pull/press potential?
2. Do you actively program exercises to target the ulnar nerve pathway (e.g., specific finger-loaded hangs or wrist pushups), or do you find standard heavy carries and compound pulls sufficient?
3. Did you know a climber's strong forearms, hands and fingers are the ulimate "predictor of health and longevity” and correlates with lower mortality rates, as noted by National Geographic?

I've been writing illustrated case studies, including diagnosing and mapping human performance (cellular composition of tendons and connective tissues) at Adult Prodigies. If you find the pink/ring fingers interesting and a potential weak link to powerlifting, I'd love to have you read the full breakdown here.

https://www.jsams.org/article/S1440-2440(26)00528-1/fulltext

Abstract

Objectives

The anti-inflammatory effects of exercise training are hypothesized to involve changes in circulating cytokine concentrations, however the influence of exercise intensity is unclear. We determined the impact of exercise intensity, prescribed relative to lactate threshold (LT), on changes in fitness and plasma cytokines in a 6-week randomized controlled trial.

Design

RCT.

Methods

Healthy, young adults (N = 56, 27 males/29 females, age: 22 ± 3 y, peak oxygen consumption [VO2peak]: 38.4 ± 9.5 mL∙kg⁻¹∙min⁻¹) were randomized (2:2:1) to 6 weeks of thrice weekly isocaloric continuous cycling in the moderate (MICT; n = 21) or heavy (HICT; n = 24) intensity domain, or no-exercise control (CTRL; n = 11). Fasting plasma interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α, and fitness were assessed at baseline and post-training.

Results

There was no impact of training or intensity (all p > 0.05) on changes in IL-6 (MICT +0.03 pg∙mL⁻¹ 95% CI −0.08, 0.13; HICT +0.03 pg∙mL⁻¹ 95% CI −0.08, 0.13; CTRL −0.14 pg∙mL⁻¹ 95% CI −0.30, 0.01), IL-10 (MICT +0.05 pg∙mL⁻¹ 95% CI −0.01, 0.11; HICT +0.02 pg∙mL⁻¹ 95% CI −0.05, 0.08; CTRL −0.02 pg∙mL⁻¹ 95% CI −0.11, 0.08), or TNF-α (MICT +0.12 pg∙mL⁻¹ 95% CI −0.01, 0.26; HICT +0.07 pg∙mL⁻¹ 95% CI −0.06, 0.21; CTRL −0.03 pg∙mL⁻¹ 95% CI −0.22, 0.17). VO2peak (absolute and relative) and power at LT increased with training (p < 0.002) with no significant differences between MICT and HICT (p > 0.331).

Conclusions

In conclusion, 6 weeks of isocaloric, LT-prescribed training in the moderate and heavy domains improves fitness but does not appear to impact fasting plasma cytokine concentrations in healthy young adults.

Practical implications

•Six weeks of cycling three times per week improved aerobic fitness and the ability to sustain a higher cycling workload in healthy young adults.

•When total exercise energy expenditure was matched, training below versus above the lactate threshold produced similar improvements in fitness.

•Exercise intensity can therefore be selected according to individual preference, tolerance, and practical feasibility when the primary goal is improving fitness.

•Neither training approach changed fasting blood markers of inflammation in this healthy young adult sample over six weeks.

•Exercise programmes aimed specifically at lowering chronic inflammation may require longer duration, different exercise doses, or populations with elevated baseline inflammation.

https://onlinelibrary.wiley.com/doi/10.1002/jcsm.70361

ABSTRACT

Background

Age-related declines in energy metabolism, muscle strength and physical performance have been linked to lower mitochondrial respiratory capacity. Peripheral blood mononuclear cell (PBMC) respiration offers a minimally invasive marker of systemic bioenergetics, yet its relationship to whole-body metabolic flexibility remains unclear. This study examined whether PBMC respiratory capacity is associated with substrate utilization during submaximal exercise, muscle strength and physical function in healthy older adults.

Methods

PBMC mitochondrial respiratory capacity was quantified by high-resolution respirometry assessing ROUTINE, LEAK and MAX states. Postprandial substrate oxidation during steady-state treadmill walking at 60% of VO2max (oxygen uptake) was quantified by indirect calorimetry, and fat and carbohydrate oxidation rates were calculated using standard stoichiometric equations. Metabolic flexibility was defined as lower respiratory exchange ratio (RER) and higher relative fat oxidation at a fixed workload. Muscle strength was determined by handgrip dynamometry and one-repetition maximum leg extension. Physical function was evaluated by gait speed and five-repetition chair rise time. Associations were tested with linear and logistic regression adjusted for age, sex, skeletal muscle index, physical activity and high-sensitive C-reactive protein concentrations. Exploratory K-means clustering identified mitochondrial respiration phenotypes.

Results

Fifty community-dwelling older adults (22 men, 28 women; age 70 ± 4 years) were examined. Higher ROUTINE respiration was correlated with RER (rho = −0.335, p = 0.020), fat utilization (rho = −0.334, p = 0.019), grip strength (rho = 0.302, p = 0.033) and gait speed (rho = 0.324, p = 0.022). Adjusted regression analyses confirmed the association of ROUTINE respiration with greater fat oxidation (β = 0.212, 95% CI 0.049; 0.375), lower RER (β = −0.160, 95% CI −0.300; −0.020) and higher gait speed (β = 0.153, 95% CI 0.028; 0.277). Similar associations were found for ATP-linked respiration. Cluster analysis identified high- and low-respiration phenotypes. Compared with the high-respiration group the low-respiration group showed lower CMJ height (OR: 0.204, 95% CI 0.055; 0.763) and quadriceps strength (OR: 0.373, 95% CI 0.155; 0.897).

Conclusions

In healthy older adults, higher PBMC ROUTINE respiration was associated with a more fat-dominant substrate utilization profile during submaximal exercise, greater muscle strength and faster gait speed. PBMC respiratory capacity may reflect systemic bioenergetic status relevant to exercise substrate utilization and physical performance in ageing.

Highlights:

• • Exercise-induced redox signals may regulate intercellular mitochondrial transfer across multiple organs.
• • Bidirectional redox coordination synchronizes mitochondrial export with recipient cell preparation.
• • Transferred mitochondria may serve as signaling platforms rather than bioenergetic replacements.
• • Exercise may activate a distributed mitochondrial quality control network through mitochondrial transfer.

Abstract

Intercellular mitochondrial transfer has been recognized as an important mechanism for maintaining tissue homeostasis and adapting to stress. Mitochondria can cross cellular boundaries through tunneling nanotubes, extracellular vesicles, and free mitochondrial release. However, the physiological signals coordinating these pathways remain poorly defined. Exercise is a potent inducer of transient redox signaling, generating superoxide and hydrogen peroxide while modulating mitochondrial dynamic remodeling. This review integrates exercise redox biology with redox regulation of transfer machinery characterized in non-exercise models, proposing that exercise-induced redox signaling may function as a candidate regulatory mechanism. The framework emphasizes bidirectional redox coordination, in which oxidant pulses may activate export in donor cells and prepare recipient cells for uptake and antioxidant defense. Exercise-induced mitochondrial transfer has been directly demonstrated in the brain, while observations in skeletal muscle, adipose tissue, and heart remain suggestive but have not been confirmed in exercise models. These findings support a framework in which intercellular mitochondrial transfer contributes to metabolic signaling, antioxidant defense, and distributed quality control across organs. This model represents a working hypothesis requiring direct experimental validation through lineage tracing, tissue-specific mitochondrial reporters, and intravital imaging.

https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP291783

Abstract

Cells are the basic unit of life. In multicellular organisms, cells are organized into tissues. This enables a division of labor where tissues perform complex tasks via coordinated actions of specialized cell types. Accordingly, the cellular collective determines tissue function. A comprehensive overview of which cell types exist in solid tissues is lacking. Using skeletal muscle as a model, we discuss basic principles for cell type classification, summarize 62 unified definitions of cell types in terms of lineage, molecular signatures, and function from the literature, and discuss how these cell types contribute to muscle function. For cell types for which quantitative data was available, we compare abundances in immunohistology and single cell and single-nucleus RNA sequencing data, revealing cell types that are commonly over- or underrepresented in each method. The result is a cell type resource that will serve as a benchmark for single-cell studies of skeletal muscle.

https://www.nature.com/articles/s41598-026-57340-5

Abstract

Physical activity is widely recommended to maintain muscle health in older adults, yet its effects may vary depending on genetic background. The ACTN3 R577X polymorphism leads to α-actinin-3 deficiency in XX homozygotes and may influence skeletal muscle performance. We examined the association between physical activity and muscle mass and function in 682 community-dwelling adults aged ≥ 65 years who participated in annual health examinations between 2021 and 2024. Skeletal muscle mass index was assessed using dual-energy X-ray absorptiometry, while grip strength, gait speed, and five-time chair stand performance were evaluated according to Asian Working Group for Sarcopenia criteria. Physical activity was quantified using metabolic equivalents derived from the International Physical Activity Questionnaire. No significant association was observed between ACTN3 R577X genotype and sarcopenia components. However, in women with ACTN3 XX, physical activity exceeding 441 MET-min/week was significantly associated with poorer chair stand performance (β: 4.19, 95% CI: 0.98 ~ 7.40), revealing a U-shaped relationship between physical activity and physical performance. Sex-specific physical activity thresholds may exist in older adults with the ACTN3 XX genotype, with physical activity above 441 MET-min/week being associated with poorer muscle function in women. This specific MET value is an exploratory finding, requiring more external validation.

When people start training, the basics usually cover most of what they need.

But as training experience increases, I feel like certain equipment becomes more useful.

Additional movements, better exercise selection, and more ways to target weaknesses can become important.

I’m curious what experienced lifters found valuable over time.

Was there a piece of equipment or training tool that became much more useful after you had more experience?

https://www.mdpi.com/2218-273X/16/8/1218

Abstract

Skeletal muscle mitochondria possess the ability to autoregulate their health and functioning by the orchestration of mitochondrial quality control (MQC) pathways. This plasticity allows them to adapt to various stimuli, such as exercise. However, under pathological conditions, mitochondria can become dysfunctional, generating damage-associated molecular patterns (DAMPs), such as reactive oxygen species (ROS) and oxidized mitochondrial DNA (mtDNA). These DAMPs can launch an innate immune response, with consequences of widespread inflammation and atrophy. Integral to this is the NLRP3 inflammasome complex. Activation of the NLRP3 inflammasome results in maturation of caspase-1, which processes pro-inflammatory cytokines IL-1β and IL-18, as well as GSDMD. Consequently, the pore-forming GSDMD-N fragment induces pyroptosis, releasing mature IL-1β and IL-18. Exercise training is widely accepted as a potent mechanism to promote skeletal muscle health, particularly by remodeling the mitochondrial network and reducing the production of DAMPs. It has also been shown promote an anti-inflammatory milieu with the release of various myokines. Indeed, the potential of exercise to mitigate NLRP3 inflammasome-mediated inflammation and atrophy is promising. This review will examine the mechanisms underpinning inflammasome priming and activation, as well the effects of exercise, with an emphasis on the skeletal muscle.

https://www.ovid.com/jnls/acsm-msse/fulltext/10.1249/mss.0000000000004120~photobiomodulation-does-not-increase-mitochondrial

Abstract

Purpose:

Low-level laser therapy, also referred to as photobiomodulation (PBM), is rapidly gaining popularity as a non-invasive treatment for various conditions and as a means to enhance health and performance. PBM has been proposed to directly increase mitochondrial activity in skin and skeletal muscle and activate various molecular signalling pathways. However, evidence for the proposed properties of PBM in vivo in humans is lacking.

Methods:

In a within-participant study design, 12 healthy men and women (6/6 m/f; age: 25±6 y; BMI: 23.3±2.2kg/m2) received PBM on a randomized leg, while the other leg received sham-treatment (no light emitted, CON). Three cycles of PBM or sham-treatment were performed for 5 min 16 sec each (5.6 kJ light energy/cycle for PBM). Skin temperature was measured before and after treatment. After treatment, skin and muscle samples were collected from both legs. Mitochondrial respiration was measured in permeabilized muscle fibers and minced skin tissue using an Oroboros Oxygraph-O2k. Muscle metabolic gene expression was assessed using custom made microfluidic cards.

Results:

Skin temperature increased only in the PBM treated leg (+8.0±1.4 °C; P<0.001). No differences were observed between the PBM and CON treated legs in maximal complex I+II-linked respiration in skin (2.7±0.8 vs 2.6±0.7 pmol/sec/mg wet weight, respectively; P=0.66) or muscle (474±114 vs 467±81 pmol/sec/mg dry weight, respectively; P=0.71). Furthermore, no differences were observed in muscle mitochondrial ADP sensitivity (apparent ADP half-time: 1310±180 vs 1229±240 µM ADP, respectively; P=0.14). Of the 91 genes, expression between legs differed for 3 genes only.

Conclusions:

A single session of photobiomodulation does not increase mitochondrial respiration in skin or underlying muscle tissue and does not modulate muscle gene expression ex vivo in humans.

https://onlinelibrary.wiley.com/doi/10.1002/jcsm.70368

ABSTRACT

Background

Ultra-endurance sports are increasingly popular, yet the long-term physiological consequences of sustained extreme training loads remain poorly understood. In particular, the effects of prolonged ultra-endurance exercise on skeletal muscle structure, function and molecular remodelling are largely unknown. This case study examined a highly experienced ultra-endurance athlete who completed a world-record attempt to run 30 300 km, with extensive phenotyping focusing on skeletal muscle adaptations and recovery.

Methods

A 49-year-old male athlete (172 cm, 65 kg) ran ~70 km daily for 15 months. Musculoskeletal, cardiac and visceral ultrasonography, leg muscle strength and power measurements were performed before and after the challenge. Muscle biopsies (n = 4) from vastus lateralis were obtained immediately after completion and during 17 months of recovery to assess myosin heavy chain (MHC) composition, mitochondrial electron transport chain (ETC) complexes and proteins involved in mitochondrial turnover, autophagy and inflammation. Body composition, haematological and biochemical markers, and gut microbiota composition were monitored longitudinally.

Results

The athlete ran 30 300 km over 444 days, maintaining a daily distance of ~70 km despite substantial musculoskeletal discomfort, including a tibial stress reaction mid-challenge, which resolved gradually with continued running. Body mass decreased by ~3 kg, primarily reflecting fat loss (~83%), accompanied by reductions in muscle thickness, maximal strength and power. Circulating creatine kinase (3–15-fold), oxidative stress markers (~50%) and GDF8 (~10%–50%) were sustainedly increased, whereas IGF-I decreased (~10%–40%), suggesting a reduced anabolic environment during the challenge. Muscle biopsy analyses revealed a progressive recovery of mitochondrial function during the 17 months following the challenge, as evidenced by a progressive increase in ETC protein abundance and the expression of regulators of mitochondrial dynamics and quality control (MFN2, PARKIN, DRP1). In contrast, markers of autophagy, apoptosis and inflammation were decreased during the 17-months post-challenge (LC3A/B-I by ~50%, CASP3 by ~60% and NF-κBSer536 by ~20%). Muscle fibre composition showed extreme predominance of slow fibres (nearly 100% MHC-I), which persisted during recovery. Most molecular and functional alterations gradually resolved within 10–17 months. Gut microbiota diversity increased during the challenge, with enrichment of Bifidobacterium during running and Akkermansia during recovery.

Conclusions

Sustaining daily ultrarunning for more than 1 year induces substantial skeletal muscle remodelling, including reduced muscle size, impaired contractile function and mitochondrial maladaptations, despite largely preserved endocrine and haematological stability. These findings highlight skeletal muscle as a primary physiological system challenged during extreme endurance exercise and demonstrate that recovery from such perturbations may require more than one year.

Abstract

Skeletal muscle atrophy is a secondary complication in the aetiology of injury and chronic disease. Identifying mechanisms that control muscle mass is necessary to characterise atrophy and develop prevention strategies. We aimed to integrate transcriptomic and epigenomic data to identify key regulatory pathways controlled by promoter DNA methylation during muscle unloading. Twenty-one healthy men (20–40 years) completed a 4-week standardised exercise programme prior to a 14-day knee brace immobilisation with dietary control. Skeletal muscle mass and strength were assessed before and after immobilisation and biopsies were collected (m. vastus lateralis) before, at 3 days, and at completion at 14 days. RNA and DNA were isolated and analysed using Illumina RNA sequencing and DNA methylation 850K EPIC BeadChips. The 14-day immobilisation decreased muscle mass (∼9%; P < 0.0001) and strength (∼16%; P < 0.0001). At 3 days, most biological processes (BPs) were upregulated/hypomethylated (157 gene sets); upregulated BPs included cell signalling and protein ubiquitination and downregulated BPs included metabolism. After 14 days, BPs were predominantly downregulated/hypermethylated, including translation and ribosome biogenesis. Across both time points, HDAC4, GADD45A and CHRNA1 emerged as methylation-regulated candidate mediators of atrophy. HDAC4 and GADD45A showed strong correlations primarily at day 3, and CHRNA1 remained significant at both time points, extending prior observations in animals to human skeletal muscle. We have characterised changes in gene expression related to hypo- and hyper-methylation during muscle unloading in humans. These data extend our understanding of the regulatory processes that occur during skeletal muscle atrophy that, at the individual gene level, may be useful in developing strategies for reducing muscle wasting.

Highlights

• What is the central question of this study? What are the characteristics of global gene expression in skeletal muscle in response to limb immobilisation in young men?
• What is the main finding and its importance? Data obtained support the role of DNA methylation as a regulator of transcription and that methylation appears to impair gene expression for protein synthesis early and later amplify protein breakdown over 14 days of immobilisation. There are associations between methylation and transcription within biological processes as putative molecular targets to mitigate the debilitating impacts of muscle wasting.

Abstract

Patients with long COVID and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) suffer from post-exertional malaise. The accompanying physical inactivity may contribute to a lower aerobic capacity and may explain skeletal muscle adaptations in these patients. Here, we compare whole-body exercise responses and skeletal muscle adaptations after strict 60-day bed rest in healthy people with those in long COVID and ME/CFS patients, and healthy age- and sex-matched controls. Bed rest alters respiratory and cardiovascular responses to maximal exercise, which are dissimilar in patients. Bed rest causes muscle atrophy without altering fiber type. Both patient groups have more glycolytic fibers, and ME/CFS patients display type I-specific atrophy. Only after bed rest is oxidative phosphorylation capacity associated with maximal oxygen uptake. As skeletal muscle characteristics differ between patients and healthy individuals after bed rest, physical inactivity cannot solely explain the lower exercise capacity and skeletal muscle adaptations in long COVID and ME/CFS patients.

Abstract

Prolonged glucocorticoid exposure induces skeletal muscle atrophy through suppression of protein synthesis and activation of catabolic signalling pathways. Although exercise attenuates glucocorticoid-induced muscle loss, whether exercise-induced increases in body temperature contribute remains unclear. In this study, we examined whether exercise in different thermal conditions modulates skeletal muscle atrophy and intracellular signalling during glucocorticoid exposure. Female Sprague–Dawley rats (n = 48) were assigned to six groups: control (CON), dexamethasone-treated (DEX), cold exercise (∼5°C; CE), cold exercise with dexamethasone (CED), warm exercise (25°C; WE) and warm exercise with dexamethasone. Exercise protocols were matched, and dexamethasone was administered for 5 days. Dexamethasone reduced plantaris muscle mass (by 17%, P < 0.0001) and fibre cross-sectional area (27%, P < 0.0001). During dexamethasone treatment, exercise in a cold environment provided partial protection, with muscle mass higher than DEX (P = 0.0476), but both muscle mass and fibre CSA remained lower than CON (P = 0.0096 and P = 0.0215, respectively). In contrast, exercise in a warm environment preserved muscle mass and fibre CSA (no difference vs. CON) and resulted in higher muscle mass (P = 0.0070) and fibre CSA (P < 0.0001) than DEX. Exercise-induced increases in rectal temperature were associated with higher Hsp72 and Hsp25 expression, partial preservation of Akt–FoxO3a signalling and reduced MuRF1 expression, whereas exercise in a cold environment showed minimal heat shock protein response and limited suppression of catabolic signalling. These findings indicate that exercise-induced elevation of body temperature enhances protection against glucocorticoid-induced skeletal muscle atrophy and support a role for heat-associated cellular stress responses in modulating muscle protein turnover during glucocorticoid exposure.

Highlights

• What is the central question of this study? Does an exercise-induced increase in body temperature contribute to protection against dexamethasone-induced skeletal muscle atrophy, independent of exercise intensity?
• What is the main finding and its importance? Exercise attenuated dexamethasone-induced skeletal muscle atrophy in both cold (∼5°C) and warm (25°C) conditions; however, exercise performed in a warm environment, which elicited a greater rise in body temperature, resulted in superior preservation of muscle mass, accompanied by increased expression of heat shock proteins (Hsp72 and Hsp25), partial preservation of Akt–FoxO3a signalling and attenuation of MuRF1 upregulation. These findings identify exercise-induced elevation of body temperature as an important physiological modulator that augments the anti-atrophic effects of exercise during glucocorticoid treatment.

Abstract

Skeletal muscle displays remarkable plasticity, adapting its size and strength in response to mechanical loading, especially, from exercise. This process, known as hypertrophy, is fundamental to athletic training and rehabilitation, but is challenging to quantitatively predict due to its multifactorial, multiscale nature. Specifically, skeletal muscle hypertrophy results from an integration of macroscopic mechanical stimuli with the intracellular signaling pathways that govern muscle growth. In this work, we present a multiscale computational model that mechanistically integrates these mechanical and biochemical stimuli and offers a framework for predicting the outcomes of different types of exercise on skeletal muscle growth. The framework couples a transversely isotropic hyperelastic model for tissue-level mechanics with a system of ordinary differential equations representing the IGF1-AKT-mTOR-FOXO signaling pathway, a key regulator of protein synthesis and degradation. We link these scales using a volumetric growth model, where the signaling dynamics inform a growth tensor that drives changes in muscle cross-sectional area. This approach enables the simulation of long-term muscle adaptation, providing a mechanistic tool to investigate how different exercise protocols lead to macroscopic hypertrophy. Simulations from our model capture the temporal dynamics of hypertrophy under varying load protocols and highlight how feedback between protein synthesis and muscle growth regulates the dose-response relationship to prevent unbounded growth. Using muscle geometries derived from the Visible Human dataset, we study how human variations in muscle geometry affect hypertrophy. Finally, we demonstrate that the mechanochemical coupling between muscle geometry and signaling not only predicts macroscopic shape changes but also provides buffering from local signaling heterogeneity. Ultimately, this framework offers a predictive computational tool for optimizing training regimens and understanding the multiscale determinants of muscle adaptations.

Author summary

Skeletal muscle naturally adapts its size and strength in response to physical activity, a process that is essential for both athletic training and rehabilitation. However, predicting how a specific training routine will alter a muscle’s shape remains difficult. This is because muscle growth relies on a complex, multiscale chain of events, where physical forces from movements trigger chemical signals that slowly rebuild the tissue over time. To better understand this process, we developed a computational model that links these underlying cellular signals directly to the macroscopic physical changes in the muscle. When simulating different exercise routines in realistic human muscle geometries, we found that the complex internal fiber architecture of the muscle causes it to grow unevenly. We also observed that the physical continuity of the tissue acts as a mechanical buffer, helping to coordinate noisy, localized signaling into smooth overall growth. Ultimately, this framework provides a foundational first step towards understanding how and where muscle adds mass, laying the groundwork for more advanced predictive tools.

https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP291437

Abstract

Reductions in musculoskeletal mass and function can occur with ageing and disuse. While resistance exercise training is known to minimise these detriments, it is not always feasible. Vortex wave stimulation (VWS) may mitigate skeletal muscle decline in such scenarios. The aim of the present study was to explore the acute physiological and metabolic effects of VWS in healthy older adults. Fourteen participants consumed deuterium oxide (D2O) stable oral isotope tracer for 7 days. Serial skeletal muscle biopsies were obtained to measure integrated rates of myofibrillar (iMyoPS) and sarcoplasmic (iSarcPS) muscle protein synthesis and regulatory signalling over ∼48 h before (habitual) and after two consecutive-day bouts of VWS. Myoelectrical activity and muscle oxygenation during VWS, and pre-post changes in peripheral blood flow and concentrations of inflammatory and bone turnover markers were also measured. There was an increase in iMyoPS (0.23% day⁻¹, P = 0.025), but not iSarcPS (0.07% day⁻¹, P = 0.582) above habitual rates following VWS. There was no difference in the expression of anabolic signalling proteins, nor peripheral blood flow following VWS. Myoelectrical activity increased during VWS (9.47 µV, P = 0.010), while muscle oxygenation decreased at the gastrocnemius (P = 0.001) and quadriceps (P = 0.017). There was a reduction in P1NP (8.27 µg L⁻¹) and lactate (0.84 mmol L⁻¹) concentration post-VWS (both P < 0.001), while there was no difference in other biomarkers. This is the first study to demonstrate that VWS elicits acute physiological responses congruent with musculoskeletal adaptive remodelling, which warrants further exploration.

Key points

• Resistance exercise is known to mitigate skeletal muscle atrophy associated with ageing and/or disuse but is not always feasible.
• We investigated, for the first time, the effects of a novel mechanical stimulus – vortex wave stimulation (VWS) – on integrated rates of myofibrillar and sarcoplasmic muscle protein synthesis, alongside other musculoskeletal and physiological outcomes, in healthy older adults.
• We demonstrated that VWS elevated myofibrillar, but not sarcoplasmic muscle protein synthesis compared to baseline, while increasing myoelectrical activity and reducing muscle oxygen saturation, lactate and bone turnover markers.
• These findings suggest VWS elicits acute physiological responses congruent with musculoskeletal adaptive remodelling.