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The use of continuous glucose monitors (CGMs) in individuals living without diabetes is increasing. The purpose of this study was to profile various CGM metrics around nutritional intake, sleep and exercise in a large cohort of physically active men and women living without any known metabolic disease diagnosis to better understand the normative glycemic response to these common stimuli. A total of 12,504 physically active adults (age 40 ± 11 years, BMI 23.8 ± 3.6 kg/m2; 23% self-identified as women) wore a real-time CGM (Abbott Libre Sense Sport Glucose Biosensor, Abbott, USA) and used a smartphone application (Supersapiens Inc., Atlanta, GA, USA) to log meals, sleep and exercise activities. A total of >1 M exercise events and 274,344 meal events were analyzed. A majority of participants (85%) presented an overall (24 h) average glucose profile between 90 and 110 mg/dL, with the highest glucose levels associated with meals and exercise and the lowest glucose levels associated with sleep. Men had higher mean 24 h glucose levels than women (24 h—men: 100 ± 11 mg/dL, women: 96 ± 10 mg/dL). During exercise, the % time above >140 mg/dL was 10.3 ± 16.7%, while the % time <70 mg/dL was 11.9 ± 11.6%, with the remaining % within the so-called glycemic tight target range (70–140 mg/dL). Average glycemia was also lower for females during exercise and sleep events (p < 0.001). Overall, we see small differences in glucose trends during activity and sleep in females as compared to males and higher levels of both TAR and TBR when these active individuals are undertaking or competing in endurance exercise training and/or competitive events.

Atherosclerotic cardiovascular disease is the leading cause of mortality worldwide, with arterial stiffness being an important predictor of cardiovascular mortality. This study aimed to examine in the Swedish longitudinal cohort of males and females (SPAF-1958) whether aerobic capacity measured at early- (34 years) and mid-adulthood (52 years) can predict arterial stiffness assessed by pulse wave velocity later in life (63 years). Further, we determined whether this association is modified by traditional cardiovascular risk factors such as obesity, smoking, blood pressure, advanced lipoprotein profiles and high-density lipoprotein (HDL) function determined as cholesterol efflux capacity. Multiple regression analysis revealed that a higher aerobic capacity at ages 34 (B = − 0.04, P = 0.002) and 52 (B = − 0.04, P = 0.005) significantly predicted lower arterial stiffness at age 63, independent of obesity, smoking, blood pressure, HDL, and HDL-cholesterol efflux capacity. In contrast, lipoprotein profiles and HDL-mediated cholesterol efflux at age 52 were not associated with arterial stiffness at age 63 (P > 0.05). These findings suggest that maintaining aerobic capacity from early adulthood can reduce arterial stiffness and cardiovascular risk in later life, independently of traditional and contemporary cardiovascular factors. This study emphasizes the need for further research on lifestyle modifications to enhance cardiovascular health.

Women have a lower age-matched cardiovascular risk than men, largely due to estrogen’s protective role in endothelial function. While exercise improves vascular health, acute vascular responses are influenced by factors such as age, fitness level, metabolic status, and exercise modality. In premenopausal women, fluctuations in estrogen levels during the menstrual cycle may further affect vascular reactivity. Here, we review current evidence on acute exercise-induced vascular responses in women, emphasizing menstrual phase influences and key biomarkers such as flow-mediated dilation (FMD), along with others including vascular conductance and pulse wave velocity (PWV). Despite limited and heterogeneous evidence, shear-induced vascular responses, (including FMD) following acute exercise, appear to be relatively stable across menstrual cycle phase, suggesting that strict phasic control may not always be necessary. However, future high-quality studies are needed to further clarify this response. In contrast, other vascular assessments that rely more heavily on neural components—such as vascular conductance and PWV—show greater estrogen sensitivity. Nonetheless, the inconsistencies between studies again underscore the need for future research with hormonal verification. Morever, adequate sample sizes, and standardized exercise protocols will improve both consistency and help develop and promote the inclusion of women in vascular research.

Angiogenesis, the formation of new blood vessels from pre-existing vasculature, is a complex and tightly regulated biological process that plays a fundamental role in both physiological and pathological tissue remodeling by facilitating the delivery of oxygen and nutrients. Over recent decades, extensive research has identified a wide array of factors that regulate the balance between endothelial cell quiescence and activation. This review discusses the cellular events and molecular mechanisms that regulate angiogenesis within skeletal muscle, considering dynamic interactions with the extracellular matrix and highlighting the critical involvement of multiple resident and infiltrating cell types—including myofibres, satellite cells, fibro-adipogenic progenitors, immune cells and pericytes. The current understanding of these regulatory networks is examined in both healthy muscle tissue as part of the phenotype changes that occur during exercise and in pathological conditions that affect skeletal muscle angiogenesis. Particular attention is given to introduce data of emerging high-resolution techniques, especially omics-based approaches such as single-cell RNA sequencing (scRNA-seq) of skeletal muscle tissue. These methodologies hold significant promise for elucidating cell-type-specific roles and intercellular interactions that drive angiogenic processes in both physiological and disease contexts. Despite substantial progress, the precise mechanisms governing angiogenesis in skeletal muscle remain only partially understood.

Eccentric exercise has been extensively used as a model to study the contraction-induced muscle damage and its consequent processes. This study aimed at examining molecular responses associated with tissue remodelling, inflammation and angiogenesis in skeletal muscle during the recovery period after eccentric exercise in humans. Ten healthy men performed 50 maximal eccentric muscle actions with the knee extensors and muscle biopsies were collected from the vastus lateralis before and 6 h, 48 h and 120 h post eccentric exercise. Real Time-PCR was utilized to investigate alterations in gene expression of various tissue remodelling-, inflammation- and angiogenesis-related factors: uPA, uPA-R, TGF-β1, MMP-9, TNF-α, IL-6, IL-8, VEGF, VEGFR-2, HIF-1a, Ang-1, Ang-2 and Tie-2. The uPA/uPA-R system exhibited a similar time-expression pattern increasing 6 h post exercise (p < 0.05), while the other tissue remodelling factors TGF-β1 and MMP-9 did not change significantly over time. Transcriptional responses of inflammatory factors TNF-α and IL-8 increased significantly and peaked 6 h post eccentric exercise (p < 0.05), while IL-6 exhibited a similar, though not statistically significant, expression profile (p > 0.05). Similarly, the expression of angiopoietin receptor Tie-2 showed an early increase only at 6 h after the completion of exercise (p < 0.05), while the other angiogenic factors failed to reach statistical significance due a high interindividual variability in the gene expression responses. The early transcriptional upregulation of tissue remodelling, inflammation- and angiogenesis-related factors post eccentric exercise may indicate the acute intramuscular activation of these processes functionally related to muscle damage-induced adaptation.

Purpose Animal studies have shown that endothelial denudation abolishes vasodilation in response to increased shear stress. Interestingly, shear-mediated dilation has been reported to be reduced, but not abolished, in coronary artery disease (CAD) patients following catheterization. However, it is not known whether this resulted from a priori endothelial dysfunction in this diseased population. In this study, we evaluated shear-mediated dilation following catheterization in healthy young men. Methods Twenty-six (age: 24.4 ± 3.8 years, BMI: 24.3 ± 2.8 kg m −2 , V O 2peak : 50.5 ± 8.8 ml/kg/min) healthy males underwent unilateral transradial catheterization. Shear-mediated dilation of both radial arteries was measured using flow-mediated dilation (FMD) pre-, and 7 days post-catheterization. Results FMD was reduced in the catheterized arm [9.3 ± 4.1% to 4.3 ± 4.1% ( P  < 0.001)] post-catheterization, whereas no change was observed in the control arm [8.4 ± 3.8% to 7.3 ± 3.8% ( P  = 0.168)]. FMD was completely abolished in the catheterized arm in five participants. Baseline diameter ( P  = 0.001) and peak diameter during FMD ( P  = 0.035) were increased in the catheterized arm 7 days post-catheterization (baseline: 2.3 ± 0.3 to 2.6 ± 0.2 mm, P  < 0.001, peak: 2.5 ± 0.3 to 2.7 ± 0.3 mm, P  = 0.001), with no change in the control arm (baseline: 2.3 ± 0.3 to 2.3 ± 0.3 mm, P  = 0.288, peak: 2.5 ± 0.3 to 2.5 ± 0.3 mm, P  = 0.608). Conclusion This is the first study in young healthy individuals with intact a priori endothelial function to provide evidence of impaired shear-mediated dilation following catheterization. When combined with earlier studies in CAD patients, our data suggest the catheterization impairs artery function in humans.

Background: Peripheral myopathy consists a hallmark of heart failure (HF) and has been associated with poor prognosis. Inflammation has been suggested to dominate this pathology, while exercise training is typically associated with the induction of anti-inflammatory mechanisms. However, the current knowledge regarding the involvement of inflammation-related genes in the exercise training-induced muscle adaptations in HF patients is very limited. Given that high-intensity interval training (HIIT) alone or combined with strength training (COM) has gained ground in HF cardiac rehabilitation, this study aimed to investigate the local muscle expression of inflammatory and tissue remodeling factors in HF patients, who underwent 3 months of these training schemes. In addition, we examined whether these exercise training-induced gene expression responses are associated with changes in exercise capacity in those patients. Methods: Thirteen male patients with chronic HF (age: 51 ± 13 y; body mass index (BMI): 27 ± 4 kg/m2) were randomly assigned to a 3-month exercise program consisted of either HIIT (N = 6) or COM training (N = 7). Muscle tissue biopsies were obtained from vastus lateralis pre- and post-training and transcriptional changes in interleukin 6 (IL-6), interleukin 8 (IL-8), tumor necrosis factor-1 alpha (TNF-1α), urokinase-type plasminogen activator (uPA), urokinase-type plasminogen activator receptor (uPAR), and transforming growth factor-beta 1 (TGF-β1) were quantified by RT-PCR. Results: An overall increase in the expression levels of selected inflammatory (IL-8, TNF-1α) and remodeling factors (uPAR) was found post-training (p < 0.05), while IL-6, uPA and TGF-β1 gene expression remained unchanged (p > 0.05). The observed alterations did not differ between training groups. Additionally, IL-8 changes were found to be correlated with the improvement in exercise capacity post-training (p < 0.05). Conclusions: This is the first study demonstrating an increase in intramuscular inflammatory and remodeling key factors induced by HIIT or COM training in HF patients. Combining these observations with our previous findings of improved muscle hypertrophy and capillarization post-training in these patients, the findings of the present study may suggest that inflammatory responses are part of an ongoing remodeling process in the exercising skeletal muscle. Clinical Trial Registration: NCT02387411.

Peripheral myopathy consists of a hallmark of heart failure (HF). Exercise enhanced skeletal muscle angiogenesis, and thus, it can be further beneficial towards the HF-induced myopathy. However, there is limited evidence regarding the exercise type that elicits optimum angiogenic responses of skeletal muscle in HF patients. This study aimed to (a) compare the effects of a high-intensity-interval-training (HIIT) or combined HIIT with strength training (COM) exercise protocol on the expression of angiogenesis-related factors in skeletal muscle of HF patients, and (b) examine the potential associations between the expression of those genes and capillarization in the trained muscles. Thirteen male patients with chronic HF (age: 51 ± 13 y; BMI: 27 ± 4 kg/m2) were randomly assigned to a 3-month exercise program that consisted of either HIIT (N = 6) or COM training (N = 7). Vastus lateralis muscle biopsies were performed pre- and post-training. RT-PCR was used to quantify the fold changes in mRNA expression of vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 2 (VEGFR-2), hypoxia-inducible factor 1 alpha (HIF-1α), angiopoietin 1 (Ang-1), angiopoietin 2 (Ang-2), angiopoietin receptor (Tie2), and matrix metallopeptidase 9 (MMP-9), and immunohistochemistry to assess capillarization in skeletal muscle post-training. There was an overall increase in the expression levels of VEGF, VEGFR-2, HIF-1α, Ang2, and MMP9 post-training, while these changes were not different among groups. Changes in capillary-to-fibre ratio were found to be strongly associated with Tie2 and HIF-1α expression. This was the first study demonstrating that both HIIT and combined HIIT with strength training enhanced similarly the expression profile of angiogenic factors in skeletal muscle of HF patients, possibly driving the angiogenic program in the trained muscles, although those gene expression increases were found to be only partially related with muscle capillarization.

Background Post‐COVID condition (PCC) affects ~10% of SARS‐CoV‐2–infected individuals and manifests as persistent symptoms such as fatigue, exercise intolerance and muscle weakness. This study aimed to assess the skeletal muscle of these patients and compare them with healthy controls. Methods Biopsies were obtained from the vastus lateralis muscle of 28 nonhospitalised PCC patients without concomitant diseases (75% women, mean age 46.4 ± 10.4 years) and 28 age‐ and sex‐matched healthy controls (79% women, mean age 46.6 ± 8.7 years). The analysis included morphological and pathological alterations, fibre type composition, fibre cross‐sectional area, capillarisation, number of myonuclei, presence of developmental myosin, CD68+ cells, macroautophagy markers, mitochondrial respiration, lipidomics and RNA sequencing. Results PCC patients, compared to controls, had a higher percentage of angulated fibres (median [IQR] 0.43 [0.00–3.20] vs. 0.00 [0.00–0.00]; p < 0.001), small, rounded fibres (0.21 [0.00–1.20] vs. 0.00 [0.00–0.00]; p < 0.001) and fibres expressing fetal myosin (0.26 [0.00–1.15] vs. 0.00 [0.00–0.17]; p = 0.015). Semiquantitative analysis showed nuclear clumps (18/27, 66.6%), hypertrophic fibres (9/27, 33.3%) and fibrosis (22/27, 81.4%) in PCC patients. Fibre cross‐sectional area was significantly lower in PCC patients (4031 ± 1365 vs. 4982 ± 1463 μm2; p = 0.018), largely driven by differences in type 2 fibre size (3533 ± 1249 vs. 4275 ± 1646 μm2; p = 0.068) than type 1 fibre size (4553 ± 1422 vs. 4932 ± 1380 μm2; p = 0.325). There was a significantly lower number of myonuclei per fibre in PCC (3.4 ± 1.1 vs. 4.1 ± 1.0; p = 0.012), but no difference in the presence of CD68+ per fibre (0.28 ± 0.15 vs. 0.22 ± 1.0; p = 0.115). No group differences were observed in macroautophagy markers LC3B (0.0032 ± 0.0007 vs. 0.0030 ± 0.0006; p = 0.232) or p62 (0.0072 ± 0.0023 vs. 0.0079 ± 0.0016; p = 0.814). Capillary‐to‐fibre ratio in PCC patients was lower for both type 1 (2.2 ± 0.7 vs. 2.6 ± 0.9; p = 0.044) and type 2 fibres (1.8 ± 0.6, vs. 2.2 ± 0.8; p = 0.022). Mitochondrial respiration was 11–28% lower in PCC patients, although not statistically significant. Lipidomics showed a lower number of phospholipids, and RNA sequencing revealed downregulation of eight metabolic pathways, primarily related to oxidative phosphorylation in PCC patients compared to controls (FDR < 0.05). Conclusions Nonhospitalised patients with PCC show signs of morphological and pathological muscle changes suggestive of degeneration and regeneration. The smaller overall fibre size, lower number of phospholipids, reduced mitochondrial oxidative capacity and lower capillarisation in these patients may be a consequence of reduced physical activity levels. The presence of clusters of atrophied angular and round‐shaped fibres, signs of inflammation and fibrosis and increased expression of fetal myosin may reflect myopathic and neurogenic post‐viral effects. Trial Registration ClinicalTrials.gov Identifier: NCT05445830.

Hypertension and arterial stiffness are significant factors contributing to cardiovascular disease. L-citrulline, a nitric oxide precursor, has been proposed as a nutritional, non-pharmacological blood pressure-lowering intervention. This study aimed to investigate the impact of L-citrulline on central and peripheral blood pressure, pulse wave reflection, and central arterial stiffness at rest and during an isometric knee extension exercise protocol. Twelve older males received 6 g of L-citrulline or a placebo for six days using a double-blind crossover design. Blood hemodynamics parameters (i.e., aortic and brachial systolic and diastolic blood pressure, mean arterial pressure, pulse pressure, heart rate), pulse wave reflection (i.e., augmented pressure, augmentation index, forward/backward wave pressure), and arterial stiffness (i.e., carotid–femoral pulse wave velocity) were measured at baseline, post-supplementation, and during isometric exercise. No significant effects of L-citrulline supplementation were observed at rest or during exercise on blood pressure, pulse wave reflection, or arterial stiffness. Both central and peripheral blood pressure were increased during the exercise, which is consistent with isometric contractions. The results of the present study do not support any blood pressure-lowering effect of short-term L-citrulline at rest or during low-intensity isometric exercise compared to the pre-exercise values in older males.