Abstract Background The age-related progressive decline in skeletal muscle function is characterised by declining mitochondrial quality control and perturbed fatty acid metabolism, contributing to frailty and increased mortality. The actin cytoskeleton, a key structural component of skeletal muscle, has recently been implicated in mitochondrial anchoring and dynamics. However, the role of actin-regulating proteins, including the Rho GTPase Rac1, in mitochondrial function and age-associated metabolic and functional muscle deterioration remains undefined. Methods Skeletal muscle from mice with inducible muscle-specific deletion of Rac1 (Rac1 imKO) underwent unbiased mass spectrometry-based proteomic profiling. Mitochondrial morphology was assessed by transmission electron microscopy, and physiological parameters, including muscle mass and contraction-stimulated palmitate oxidation in isolated soleus muscle, were evaluated. Mitochondrial respiratory function was determined by high-resolution respirometry in permeabilised gastrocnemius skeletal muscle fibre bundles. Biochemically, muscular triacylglycerol (TG) content, mRNA (qPCR) and protein (immunoblotting) content were determined. In vastus lateralis muscle biopsies from healthy, untrained young (20-30 years) and old, sarcopenic (83-94 years) men, Rac1 and mitochondrial respiratory protein abundances were measured. A complementary human genetic association analysis was performed using the FinnGen dataset. Results Rac1 deficiency triggered muscle wasting in middle-aged mice (Gastrocnemius: -10%; Quadriceps: -7%). Preceding muscle wasting, gene set enrichment analysis identified enrichment in fatty acid metabolism and oxidative phosphorylation pathways, consistent with increased mitochondrial volume density in Rac1 imKO muscle (subsarcolemmal: +467%; intermyofibrillar: +166%). Despite mitochondrial expansion at this stage, Rac1 deficiency attenuated the increase in palmitate oxidation in response to muscle contraction (-62%). At the muscle-wasting stage, Rac1 imKO muscle exhibited reduced mitochondrial respiratory capacity (-25-32%). Additionally, the mitochondrial dysfunction was associated with an accumulation of muscle TG (+78%, p = 0.096) and upregulation of fatty acid transporter, CD36 protein content (+25%), indicative of altered fatty acid handling. In humans, Rac1 muscle protein content was increased in old, sarcopenic subjects compared to young (+41%), and negatively correlated with quadriceps cross-sectional area (CSA) (r = -0.475) and type II fibre CSA (r = -0.466). In old, sarcopenic muscle, Rac1 protein content correlated negatively with protein content of multiple mitochondrial respiratory complexes (CI: r = -0.690, CIV: r = -0.938, CV: r = -0.704). GWAS further identified associations between Rac1 SNP variants and lipid metabolic and muscle-wasting diseases. Conclusions Muscle Rac1 deficiency reduces mitochondrial respiratory capacity and metabolic flexibility through impaired fatty acid metabolism, leading to muscle wasting and highlighting a potential therapeutic target in age-related functional decline.

Aging is associated with declines in skeletal muscle function, mitochondrial capacity, and changes in redox balance, which collectively contribute to frailty and chronic disease risk. This study investigated the effects of a 12-week resistance training (RT) program combined with a small dose of high-intensity interval training (HIIT), with or without polyphenol supplementation, on mitochondrial respiratory capacity (MRC) and oxidative stress in middle-aged and older adults (55–70 years). Forty-one participants were randomized to receive either a polyphenol supplement or a placebo for 30 days before the training intervention. Following the training intervention, aerobic capacity, lean mass, and strength improved significantly in both groups. Training also increased MRC in the placebo group but not in the polyphenol group, which displayed higher MRC following the supplementation phase, possibly reflecting either a supplement effect or baseline variation. The training resulted in a 20% decrease in skeletal muscle H2O2 emission across both groups, suggesting enhanced mitochondrial efficiency or antioxidant defenses. However, gene expression of selected antioxidants was unchanged, and plasma oxidative stress markers malondialdehyde (MDA) increased, and 3-nitrotyrosine (3-NT) remained unchanged. Circulating antioxidants showed distinct changes with training, as ascorbic acid increased with training in both groups, while α-tocopherol increased only in the placebo group and β-cryptoxanthin and retinol declined in the polyphenol group, suggesting potential supplement–nutrient interactions. Uric acid increased in both groups, likely reflecting exercise-induced purine turnover. In conclusion, combined RT and HIIT improved mitochondrial bioenergetics and muscle redox balance in middle-aged and older adults, whereas polyphenol supplementation did not augment these adaptations and may have blunted some vitamin-related responses. These findings underscore resistance-based exercise as a potent intervention for maintaining physical and mitochondrial health with age.

Aging is associated with declines in muscle mass, strength, aerobic capacity, and metabolic health, accompanied by increased low-grade inflammation. The purpose of this study was to assess the effects of 12 weeks of resistance training (RT) combined with minimal high-intensity interval training (HIIT), with or without polyphenol supplementation, on muscular, cardiovascular, metabolic, and inflammatory adaptations in healthy older adults. Forty-one men and women aged 55–70 years ingested either polyphenol supplementation or placebo for 30 days, then underwent 12 weeks of supervised RT combined with once-weekly HIIT, continuing polyphenol supplementation or placebo throughout. The training intervention increased whole-body and thigh lean mass, vastus lateralis cross-sectional area, type II fiber size, and muscle and functional strength (all p < 0.001). Maximal oxygen uptake significantly increased (p = 0.0001), accompanied by reductions in heart rate and plasma lactate during submaximal exercise, as well as increases in total blood volume and hemoglobin mass (p < 0.05). Training led to reductions in respiratory exchange ratio and plasma cortisol during exercise, which, together with decreased cholesterol levels and trends toward increased peak fat oxidation, may suggest enhanced substrate utilization. Polyphenols alone lowered cholesterol levels but had no other effects. Although no changes were observed in basal systemic or muscle inflammation, the exercise intervention attenuated the acute exercise-induced inflammatory responses of IL-10, IFN-γ, and TNF-α (p < 0.05). These results indicate that a combined RT and minimal HIIT program improves muscular, aerobic, and metabolic health, and may improve inflammatory regulation in aging adults.

Training can improve insulin sensitivity in individuals with type 2 diabetes, but a clear understanding of the mechanisms remains elusive. To further our knowledge in this area, we aimed to examine the effect of type 2 diabetes and of high-intensity interval training (HIIT) on the nuclear transcriptional response in skeletal muscle. We performed single-nucleus RNA-sequencing (snRNA-seq) and immunofluorescence analysis on muscle biopsies from the trained and the untrained legs of participants with and without type 2 diabetes, after 2 weeks of one-legged HIIT on a cycle ergometer. Surprisingly, the type 2 diabetes condition only seemed to have a minor effect on transcriptional activity in myonuclei related to major metabolic pathways when comparing the untrained legs. However, while in particular the type IIA myonuclei in the control group displayed a considerable metabolic response to HIIT, with increases in genes related to glycogen breakdown and glycolysis primarily in the type IIA myonuclei of the trained leg, this response was blunted in the diabetes group, despite a marked increase in glucose clearance in both groups. Additionally, we observed that fibre type distribution assessed by immunofluorescence significantly correlated with the proportion of myonuclei in the snRNA-seq analysis. In conclusion, the type 2 diabetes condition blunts the metabolic transcriptional response to HIIT in the type IIA myonuclei without affecting the improvement in insulin sensitivity. Additionally, our results indicate that snRNA-seq can be used as a surrogate marker for fibre type distribution in sedentary middle-aged adults. KEY POINTS: The study utilized single-nucleus RNA sequencing (snRNA-seq) to analyse 38 skeletal muscle biopsies, revealing distinct transcriptional profiles in myonuclei from individuals with and without type 2 diabetes (T2D) after 2 weeks of HIIT. snRNA-seq identified significant differences in gene expression, with 14 differentially expressed genes (DEGs) in type IIA myonuclei of the control group, specifically related to glycogen breakdown and glycolysis, which were blunted in the T2D group. In the control group, HIIT induced a substantial transcriptional response in type IIA myonuclei, enhancing metabolic pathways associated with insulin sensitivity, while the T2D group showed minimal transcriptional changes despite improved insulin sensitivity. The T2D group exhibited a blunted response in metabolic gene expression, indicating that the training effect on muscle adaptation was significantly impaired compared to healthy controls. Overall, the findings highlight the differential impact of HIIT on muscle metabolism, emphasizing the need for tailored exercise interventions for individuals with T2D.

Abstract Prematurity has physical consequences, such as lower birth weight, decreased muscle mass and increased risk of adult‐onset metabolic disease. Insulin‐like growth factor 1 (IGF‐1) has therapeutic potential to improve the growth and quality of muscle and tendon in premature births, and thus attenuate some of these sequalae. We investigated the effect of IGF‐1 on extensor carpi radialis muscle and biceps brachii tendon of preterm piglets. The preterm group consisted of 19‐day‐old preterm (10 days early) piglets, treated with either IGF‐1 or vehicle. Term controls consisted of groups of 9‐day‐old piglets (D9) and 19‐day‐old piglets (D19). Muscle samples were analysed by immunofluorescence to determine the cross‐sectional area (CSA) of muscle fibres, fibre type composition, satellite cell content and central nuclei‐containing fibres in the muscle. Tendon samples were analysed for CSA, collagen content and maturation, and vascularization. Gene expression of the tendon was measured by RT‐qPCR. Across all endpoints, we found no significant effect of IGF‐1 treatment on preterm piglets. Preterm piglets had smaller muscle fibre CSA compared to D9 and D19 control group. Satellite cell content was similar across all groups. For tendon, we found an effect of age on tendon CSA, and mRNA levels of COL1A1, tenomodulin and scleraxis. Immunoreactivity for elastin and CD31, and several markers of tendon maturation, were increased in D9 compared to the preterm piglets. Collagen content was similar across groups. IGF‐1 treatment of preterm‐born piglets does not influence the growth and maturation of skeletal muscle and tendon.

INTRODUCTION:While the use of camping stoves in poorly ventilated areas is discouraged, the need to address dehydration challenges in harsh arctic conditions has led to their unconventional use inside snow caves for snow melting, subjecting occupants to unknown carbon monoxide (CO) levels. This study, located at sea level in northeastern Greenland, aimed to assess CO levels and dynamics during short cooking sessions in newly constructed emergency snow caves.METHODS:In 5 snow caves, constructed according to the same design principles by 4 different individuals, a single MSR Whisperlite multifuel burner, primed with ethanol and burning white gas, was used to melt snow. CO concentrations were monitored every minute until all the snow in a 5-L pot was converted to water and CO levels returned to below 10 ppm.RESULTS:A total of 16 experiments conducted showed that the priming phase generated the highest CO peaks, with a maximum of 120 ppm. Time-weighted averages ranged from 14 ppm to 67 ppm, with trial durations of 15 to 21 min. A single trial with a dirty burner resulted in up to a 10-fold increase in CO levels.CONCLUSIONS:While single, short cooking sessions of less than 10 min burn time in newly constructed snow caves may be tolerated under specific conditions, the study highlighted substantial variation between caves and the importance of using clean burners, emphasizing the need for further research to gain a comprehensive understanding of CO exposure dynamics in snow caves.

BACKGROUND:Age-related loss of strength is disproportionally greater than the loss of mass, suggesting maladaptations in the neuro-myo-tendinous system. Myofibers are often misshaped in aged and diseased muscle, but systematic analyses of large sample sets are lacking. Our aim was to investigate myofiber shape in relation to age, exercise, myofiber type, species and sex. METHODS:Vastus lateralis muscle biopsies (n = 265) from 197 males and females, covering an age span of 20-97 years, were examined. The gastrocnemius and soleus muscles of 11 + 22-month-old male C57BL/6 mice were also examined. Immunofluorescence and ATPase stainings of muscle cross-sections were used to measure myofiber cross-sectional area (CSA) and perimeter. From these, a shape factor index (SFI) was calculated in a fibre-type-specific manner (type I/II in humans; type I/IIa/IIx/IIb in mice), with higher values indicating increased deformity. Heavy resistance training (RT) was performed three times per week for 3-4 months by a subgroup (n = 59). Correlation analyses were performed comparing SFI and CSA with age, muscle mass, maximal voluntary contraction (MVC), rate of force development and specific force (MVC/muscle mass). RESULTS:In human muscle, SFI was positively correlated with age for both type I (R2 = 0.20) and II (R2 = 0.38) myofibers. When subjects were separated into age cohorts, SFI was lower for type I (4%, P < 0.001) and II (6%, P < 0.001) myofibers in young (20-36) compared with old (60-80) and higher for type I (5%, P < 0.05) and II (14%, P < 0.001) myofibers in the oldest old (>80) compared with old. The increased SFI in old muscle was observed in myofibers of all sizes. Within all three age cohorts, type II myofiber SFI was higher than that for type I myofiber (4-13%, P < 0.001), which was also the case in mice muscles (8-9%, P < 0.001). Across age cohorts, there was no difference between males and females in SFI for either type I (P = 0.496/0.734) or II (P = 0.176/0.585) myofibers. Multiple linear regression revealed that SFI, after adjusting for age and myofiber CSA, has independent explanatory power for 8/10 indices of muscle mass and function. RT reduced SFI of type II myofibers in both young and old (3-4%, P < 0.001). CONCLUSIONS:Here, we identify type I and II myofiber shape in humans as a hallmark of muscle ageing that independently predicts volumetric and functional assessments of muscle health. RT reverts the shape of type II myofibers, suggesting that a lack of myofiber recruitment might lead to myofiber deformity.

The myotendinous junction (MTJ) is a specialized domain of the multinucleated myofibre that is faced with the challenge of maintaining robust cell-matrix contact with the tendon under high mechanical stress and strain. Here, we profiled 24,124 nuclei in semitendinosus muscle-tendon samples from three healthy males by using single-nucleus RNA sequencing (snRNA-seq), alongside spatial transcriptomics, to gain insight into the genes characterizing this specialization in humans. We identified a cluster of MTJ myonuclei represented by 47 enriched transcripts, of which the presence of ABI3BP, ABLIM1, ADAMTSL1, BICD1, CPM, FHOD3, FRAS1 and FREM2 was confirmed at the MTJ at the protein level in immunofluorescence assays. Four distinct subclusters of MTJ myonuclei were apparent, comprising two COL22A1-expressing subclusters and two subclusters lacking COL22A1 expression but with differing fibre type profiles characterized by expression of either MYH7orMYH1 and/orMYH2. Our findings reveal distinct myonuclei profiles of the human MTJ, which represents a weak link in the musculoskeletal system that is selectively affected in pathological conditions ranging from muscle strains to muscular dystrophies.

Skeletal muscle injury in aged rodents is characterized by an asynchronous infiltration of pro-and anti-inflammatory macrophage waves, leading to improper and incomplete regeneration. It is unclear whether this aberration also occurs in aged human muscle. In this study, we quantified the macrophage responses in a human model of muscle damage and regeneration induced by electrical stimulation in 7 young and 21 older adults. At baseline, total resident macrophage (CD68+/DAPI+) content was not different between young and old subjects, but pro-inflammatory (CD206-/CD68+/DAPI+) macrophage content was lower in the old. Following damage, muscle Infiltration of CD206-/CD68+/DAPI+ macrophages was lower in old relative to young subjects. Further, only the increase in CD206-/CD68+ macrophages correlated with the change in muscle satellite cell content. Our data show that older individuals have a compromised macrophage response during muscle regeneration, pointing to an altered inflammatory response as a potential mechanism for reduced muscle regenerative efficacy in aged humans.

Proteomics analysis of skeletal muscle has recently progressed from whole muscle tissue to single myofibers. Here, we further focus on a specific myofiber domain crucial for force transmission from muscle to tendon, the myotendinous junction (MTJ). To overcome the anatomical constraints preventing the isolation of pure MTJs, we performed in-depth analysis of the MTJ by progressive removal of the muscle component in semitendinosus muscle-tendon samples. Using detergents with increasing stringency we quantified >3000 proteins across all samples, and identified 112 significantly enriched MTJ-proteins, including 24 known MTJ-enriched proteins. Of the 88 novel MTJ markers, immunofluorescence analysis confirmed the presence of tetraspanin-24 (CD151), kindlin-2 (FERMT2), cartilage intermediate layer protein 1 (CILP), and integrin-alpha10 (ITGA10), at the human MTJ. Together, these human data constitute the first detailed MTJ proteomics resource that will contribute to advance understanding of the biology of the MTJ and its failure in pathological conditions.

Objective: NAD+ is a co-factor and substrate for enzymes maintaining energy homeostasis. Nicotinamide phosphoribosyltransferase (NAMPT) controls NAD+ synthesis, and in skeletal muscle, NAD+ is essential for muscle integrity. However, the underlying molecular mechanisms by which NAD+ synthesis affects muscle health remain poorly understood. Thus, the objective of the current study was to delineate the role of NAMPT-mediated NAD+ biosynthesis in skeletal muscle development and function. Methods: To determine the role of Nampt in muscle development and function, we generated skeletal muscle-specific Nampt KO (SMNKO) mice. We performed a comprehensive phenotypic characterization of the SMNKO mice, including metabolic measurements, histological examinations, and RNA sequencing analyses of skeletal muscle from SMNKO mice and WT littermates. Results: SMNKO mice were smaller, with phenotypic changes in skeletal muscle, including reduced fiber area and increased number of centralized nuclei. The majority of SMNKO mice died prematurely. Transcriptomic analysis identified that the gene encoding the mitochondrial permeability transition pore (mPTP) regulator Cyclophilin D (Ppif) was upregulated in skeletal muscle of SMNKO mice from 2 weeks of age, with associated increased sensitivity of mitochondria to the Ca2+-stimulated mPTP opening. Treatment of SMNKO mice with the Cyclophilin D inhibitor, Cyclosporine A, increased membrane integrity, decreased the number of centralized nuclei, and increased survival. Conclusions: Our study demonstrates that NAMPT is crucial for maintaining cellular Ca2+ homeostasis and skeletal muscle development, which is vital for juvenile survival.

The decline in muscle mass and function with age is partly caused by a loss of muscle fibres through denervation. The purpose of this study was to investigate the potential of exercise to influence molecular targets involved in neuromuscular junction (NMJ) stability in healthy elderly individuals. Participants from two studies (one group of 12 young and 12 elderly females and another group of 25 elderly males) performed a unilateral bout of resistance exercise. Muscle biopsies were collected at 4.5 h and up to 7 days post exercise for tissue analysis and cell culture. Molecular targets related to denervation and NMJ stability were analysed by immunohistochemistry and real-time reverse transcription polymerase chain reaction. In addition to a greater presence of denervated fibres, the muscle samples and cultured myotubes from the elderly individuals displayed altered gene expression levels of acetylcholine receptor (AChR) subunits. A single bout of exercise induced general changes in AChR subunit gene expression within the biopsy sampling timeframe, suggesting a sustained plasticity of the NMJ in elderly individuals. These data support the role of exercise in maintaining NMJ stability, even in elderly inactive individuals. Furthermore, the cell culture findings suggest that the transcriptional capacity of satellite cells for AChR subunit genes is negatively affected by ageing.

ABSTRACT Aim This study aimed to examine changes in lean mass during hospitalization in geriatric patients and the effect of muscle activation by neuromuscular electrical stimulation. Methods Thirteen patients (69–94 yr) at a geriatric ward completed tests at hospital admission (days 2–3) and discharge (days 8–10). One leg received daily stimulation of the knee extensors, whereas the other leg served as a control leg. Lean mass was evaluated by dual-energy x-ray absorptiometry scans and muscle thickness by ultrasound scans. Muscle biopsies were collected from both legs at admission and discharge in nine patients and analyzed for fiber size, satellite cell number, and activation and expression of genes associated with muscle protein synthesis and breakdown, connective tissue, and cellular stress. Results The relative decline in leg lean mass and midthigh region lean mass was larger in the control (−2.8% ± 1.5%) versus the stimulated leg (−0.5% ± 1.4%, P < 0.05). Although there were no changes in fiber size or satellite cell number, the mRNA data revealed that, compared with control, the stimulation resulted in a downregulation of myostatin ( P < 0.05) and a similar trend for MAFbx ( P = 0.099), together with an upregulation of Collagen I ( P < 0.001), TenascinC ( P < 0.001), CD68 ( P < 0.01), and Ki67 ( P < 0.05) mRNA. Conclusion These findings demonstrate a moderate decline in leg lean mass during a hospital stay in geriatric patients, whereas leg lean mass was preserved with daily neuromuscular electrical muscle activation. At the cellular level, the stimulation had a clear influence on suppression of atrophy signaling pathways in parallel with a stimulation of connective tissue and cellular remodeling processes.

There is growing evidence for a link between loss of skeletal muscle, impaired muscle performance, and systemic markers of acute inflammation in hospitalized geriatric patients. The present literature suggests a negative effect of acute inflammation at the time of hospital admission upon muscle performance and the change of this during the hospital stay, particularly in patients with persistent rather than resolved inflammation. Further, a few studies have reported a positive effect of anti-inflammatory medication upon recovery of muscle function in geriatric patients, but how this is mediated (e.g. inhibition of inflammatory cytokines) is not clear. In conclusion, a negative association between the presence of acute and persistent systemic markers of inflammation and various aspects of muscle function and its recovery after bedrest is observed in geriatric patients.

Blunted muscle hypertrophy and impaired regeneration with aging have been partly attributed to satellite cell (SC) dysfunction. However, true muscle regeneration has not yet been studied in elderly individuals. To investigate this, muscle injury was induced by 200 electrically stimulated (ES) eccentric contractions of the vastus lateralis (VL) of one leg in seven young (20-31 years) and 19 elderly men (60-73 years). This was followed by 13 weeks of resistance training (RT) for both legs to investigate the capacity for hypertrophy. Muscle biopsies were collected Pre- and Post-RT, and 9 days after ES, for immunohistochemistry and RT-PCR. Hypertrophy was assessed by MRI, DEXA, and immunohistochemistry. Overall, surprisingly comparable responses were observed between the young and elderly. Nine days after ES, Pax7+ SC number had doubled (P < .05), alongside necrosis and substantial changes in expression of genes related to matrix, myogenesis, and innervation (P < .05). Post-RT, VL cross-sectional area had increased in both legs (15%, P < .05) and SCs/type II fiber had increased 2-4 times more with ES+RT vs RT alone (P < .001). Together these novel findings demonstrate "youthful" regeneration and hypertrophy responses in human elderly muscle. Furthermore, boosting SC availability in healthy elderly men does not enhance the subsequent muscle hypertrophy response to RT.

AIMS:To examine satellite cell and myonuclear content in very old (≥83 years) individuals, and the response to heavy resistance training.METHODS:A group of very old men and women (Old, 83-94 years, n = 29) was randomized to 12 weeks of heavy resistance training or untrained controls. A group of young men who did not resistance train (Young, 19-27 years, n = 9) were included for comparison.RESULTS:Compared to young men, prior to training the old men had smaller type II fibres (-38%, P < 0.001), lower satellite cell content (-52%, P < 0.001), smaller myonuclear domain (-30%, P < 0.001), and a trend for lower myonuclear content (-13%, P = 0.09). Old women were significantly different from old men for these parameters, except for satellite cell content. Resistance training had no effect on these parameters in these old men and women. Fibre-size specific analysis showed strong correlations between fibre size and myonuclei per fibre and between fibre size and myonuclear domain for both fibre types (r = 0.94-0.99, P < 0.0001). In contrast, muscle fibre perimeter per myonucleus seemed to be constant across the range in fibre size, particularly in type I fibres (r = -0.31, P = 0.17).CONCLUSIONS:The present data demonstrate that type II fibre size, satellite cell content and myonuclear domain is significantly smaller in very old men compared to young men, while myonuclear content is less affected. These parameters were not improved with heavy resistance training at the most advanced stage of ageing.

Muscle fiber denervation is a major contributor to the decline in physical function observed with aging. Denervation can occur through breakdown of the neuromuscular junctions (NMJ) itself, affecting only that particular fiber, or through the death of a motor neuron, which can lead to a loss of all the muscle fibers in that motor unit. In this review, we discuss the muscle-nerve relationship, where signaling from both the motor neuron and the muscle fiber is required for maximal preservation of neuromuscular function in old age. Physical activity is likely to be the most important single factor that can contribute to this preservation. Furthermore, we propose that inactivity is not an innocent bystander, but plays an active role in denervation through the production of signals hostile to neuron survival. Investigating denervation in human muscle tissue samples is challenging due to the shared protein profile of regenerating and denervated muscle fibers. In this review, we provide a detailed overview of the key traits observed in immunohistochemical preparations of muscle biopsies from healthy, young, and elderly individuals. Overall, a combination of assessing tissue samples, circulating biomarkers, and electrophysiological assessments in humans will prove fruitful in the quest to gain more understanding of denervation of skeletal muscle. In addition, cell culture models represent a valuable tool in the search for key signaling factors exchanged between muscle and nerve, and which exercise has the capacity to alter.

Background and purposeHospital admission for older patients has been linked to loss of muscle mass and function, and the former can be measured with ultrasonography during hospitalization. MethodsTwo studies were carried out. In Study 1, 69 patients' (85 8 years) activity level was measured with ActivPal and quadriceps thickness measured twice with ultrasonography during hospitalization. In Study 2, 10 older patients (85 8 years) and 10 healthy young subjects (23 +/- 2 years) had their quadriceps thickness measured on two consecutive days with ultrasonography that included a pressure calibrator. ResultsIn Study 1, the results revealed that the older patients had a reduction in thigh muscle thickness together with very low levels of activity level during hospitalization. Patients with a <95% inactivity level show a 1.8% reduction in muscle thickness, and those with a >95% inactivity level had a 7.0% reduction. In Study 2, ultrasonographic measurements were performed using a pressure calibrator, and these results yielded very good reproducibility. Typical error was 1.7% for the young and 7.2% for the old persons. This high reproducibility and low error improve the ability to detect significant changes over time. ConclusionImproving the ultrasonography method including use of a pressure calibrator can result in greater reproducibility.

Background: Hospitalization of older medical patients may lead to functional decline. This study investigated whether simultaneously applied neuromuscular electrical stimulation (NMES) can enhance the effects of a functional training program in hospitalized geriatric patients. Method: This was a quasi-randomized controlled trial in geriatric hospitalized patients (N = 16, age = 83.1 +/- 8.1 years, mean +/- SD). The patients performed a simple and time efficient chair-stand based functional exercise program daily, either with (FT+NMES, N = 8) or without (FT, N = 8) simultaneous NMES to the knee extensor muscles. Physical function was assessed at day 2 and 6-10 of the hospitalization with the De Morton Mobility Index (DEMMI), a 30-second chair stand test (30 s-CST) and a 4-meter gait speed test (4 mGST). Additionally, the pooled results of training from the two training groups (TRAINING, N = 16) was compared to a similar historical control-group (CON, N = 48) receiving only standard-care. Results: Eight patients were assigned to FT, 12 to FT+NMES with 4 dropouts during intervention. During the 6-10 days of hospitalization, both groups improved in all functional measures (p < 0.05), but with no difference between groups (p > 0.05). The training sessions within the FT+NMES-group were more time consuming (similar to 11 vs similar to 7 min) and entailed higher levels of discomfort than FT-training sessions. Compared to standard-care, training resulted in significantly larger improvements in the 30 s-CST (TRAINING: +3.8 repetitions; CON: +1.4 repetitions, p < 0.01), but not in the DEMMI-test and the 4 m-GST. Conclusion: A short-duration daily functional training program improves chair stand performance in hospitalized geriatric patients, with no additional effect of simultaneous electrical muscle stimulation.