Modeling the cumulative benefits of regular physical activity on type 2 diabetes progression.

BackgroundThe level of physical activity (PA) among patients with coronary heart disease (CHD) living in Chinese communities who do not participate in cardiac rehabilitation programs and the factors contributing to patient maintenance of PA are unclear.ObjectiveThis cross-sectional study, guided by the Transtheoretical Model, evaluated (1) the maintenance of PA in Chinese patients with CHD 12 months after hospital discharge and (2) the demographic, clinical, and psychological characteristics associated with maintenance of PA.MethodsA total of 1162 patients completed 6 questionnaires at 12 months posthospitalization to assess their maintenance of PA, stage of change, symptoms of depression and anxiety, and health-related quality of life and sleep.ResultsOnly 40% of patients with CHD maintained regular PA 12 months after hospital discharge. Walking was their primary PA. Thirty-seven percent of patients reported no intention of having regular PA. Male sex (odds ratio [OR], 1.69), awareness of PA's cardiac benefit (OR, 4.12), a history of regular PA before the cardiac event (OR, 6.08), history of chronic disease (OR, 1.43), mild depressive symptoms (OR, 1.40), moderate and severe depressive symptoms (OR, 0.41), smoking (OR, 0.54), and years of CHD (OR, 0.96) were related to maintenance of regular PA. Patients with CHD who maintained regular PA had better quality of life and sleep (P < .001) and fewer unplanned clinic visits (P = .001) and cardiac cause readmissions (P = .012) and reported fewer declines in PA capacity (P < .001).ConclusionsWalking is the most common form of PA 12 months posthospitalization among patients with CHD in China. Patient education and counseling about the cardiac benefits of PA, taking into account stage of change, are important considerations to improve maintenance of PA.

Benefits of exercise for community-dwelling older adults

Background and ObjectivesOwing to the lack of long-term observations or comprehensive adjustment for confounding factors, reliable conclusions regarding long-term effects of exercise and regular physical activity in Parkinson disease (PD) have yet to be drawn. Here, using data from the Parkinson's Progression Markers Initiative study that includes longitudinal and comprehensive evaluations of many clinical parameters, we examined the long-term effects of regular physical activity and exercise habits on the course of PD.MethodsIn this retrospective, observational cohort study, we primarily used the multivariate linear mixed-effects models to analyze the interaction effects of their regular physical activity and moderate to vigorous exercise levels, measured with the Physical Activity Scale for the Elderly questionnaire, on the progression of clinical parameters, after adjusting for age, sex, levodopa equivalent dose, and disease duration. We also calculated bootstrapping 95% confidence intervals (CIs) and conducted sensitivity analyses using the multiple imputation method and subgroup analyses using propensity score matching to match for all baseline background factors.ResultsTwo hundred thirty-seven patients with early PD (median [interquartile range] age, 63.0 [56.0–70.0] years, male 69.2%, follow-up duration 5.0 [4.0–6.0] years) were included. Regular physical activity and moderate to vigorous exercise levels at baseline did not significantly affect the subsequent clinical progression of PD. However, average regular overall physical activity levels over time were significantly associated with slower deterioration of postural and gait stability (standardized fixed-effects coefficients of the interaction term [βinteraction] = −0.10 [95% CI −0.14 to −0.06]), activities of daily living (βinteraction = 0.08 [95% CI 0.04–0.12]), and processing speed (βinteraction = 0.05 [95% CI 0.03–0.08]) in patients with PD. Moderate to vigorous exercise levels were preferentially associated with slower decline of postural and gait stability (βinteraction = −0.09 [95% CI −0.13 to −0.05]), and work-related activity levels were primarily associated with slower deterioration of processing speed (βinteraction = 0.07 [95% CI 0.04–0.09]). Multiple imputation and propensity score matching confirmed the robustness of our results.DiscussionIn the long term, the maintenance of high regular physical activity levels and exercise habits was robustly associated with better clinical course of PD, with each type of physical activity having different effects.Trial Registration InformationClinicalTrials.gov Identifier: NCT01176565.Classification of EvidenceThis study provides Class II evidence that sustained increase in overall regular physical activity levels in patients with early PD was associated with slower decline of several clinical parameters.

In “Long-term effect of regular physical activity and exercise habits in patients with early Parkinson disease,” Tsukita et al. reported that average regular physical activity levels over time were associated with slower deterioration of gait stability, activities of daily living, and processing speed in patients with Parkinson disease (PD). Darweesh et al. contextualized these findings by noting they are consistent with the results of other studies, suggesting that regular exercise may slow progression of PD. They further proposed that vigorous exercise may reduce the risk of PD, implying that the findings of Tsukita et al. may also be attributed to reverse causality. Tsukita et al. agreed that reverse causality is feasible, although other data suggest that exercise may change the brain, modifying the course of PD. However, Gupta questioned the pathophysiologic mechanism by which exercise changes the brain and affects disease progression in PD, commenting that perhaps motivation to exercise may be relevant to disease progression in PD. In light of these comments, Tsukita et al. reinforced the need for the following types of future research: (1) international, multicenter randomized controlled trials on the effect of exercise on disease progression (for patients with PD) and development of clinical symptoms of PD (for patients with prodromal PD) which include neuroimaging; (2) evaluation of the motivation for patients with PD to exercise; and (3) animal studies on the effect of exercise on the brain, which include neuropathology assessment of α-synuclein. In “Long-term effect of regular physical activity and exercise habits in patients with early Parkinson disease,” Tsukita et al. reported that average regular physical activity levels over time were associated with slower deterioration of gait stability, activities of daily living, and processing speed in patients with Parkinson disease (PD). Darweesh et al. contextualized these findings by noting they are consistent with the results of other studies, suggesting that regular exercise may slow progression of PD. They further proposed that vigorous exercise may reduce the risk of PD, implying that the findings of Tsukita et al. may also be attributed to reverse causality. Tsukita et al. agreed that reverse causality is feasible, although other data suggest that exercise may change the brain, modifying the course of PD. However, Gupta questioned the pathophysiologic mechanism by which exercise changes the brain and affects disease progression in PD, commenting that perhaps motivation to exercise may be relevant to disease progression in PD. In light of these comments, Tsukita et al. reinforced the need for the following types of future research: (1) international, multicenter randomized controlled trials on the effect of exercise on disease progression (for patients with PD) and development of clinical symptoms of PD (for patients with prodromal PD) which include neuroimaging; (2) evaluation of the motivation for patients with PD to exercise; and (3) animal studies on the effect of exercise on the brain, which include neuropathology assessment of α-synuclein.

Rx Exercise: Physical Activity Is Good Medicine

Advances in exercise, physical activity, and diabetes mellitus.

Type 2 diabetes (T2D) has become a significant global health threat, yet its precise causes and mechanisms remain unclear. This study aims to identify gene expression patterns specific to T2D pancreatic islet cells and to explore the potential role of pancreatic stellate cells (PSCs) in T2D progression through regulatory networks involving lncRNA-mRNA interactions. In this study, we screened for upregulated genes in T2D pancreatic islet samples using bulk sequencing (bulkseq) datasets and mapped these gene expression profiles onto three T2D single-cell RNA sequencing (scRNAseq) datasets. The identified T2D-specific gene features were further validated in an additional T2D scRNAseq dataset, a T1D scRNAseq dataset, and a T2D bulkseq dataset. To investigate regulatory networks, we analyzed the potential lncRNA-mRNA interactions within T2D peripheral blood mononuclear cell (PBMC) bulkseq data. Our analysis identified a specific gene panel-COL1A2, VCAN, and SULF1-that was consistently upregulated in T2D pancreatic islet samples. Expression of this gene panel was strongly associated with the activation of pancreatic stellate cells (PSCs), suggesting a unique T2D-specific signature characterized by COL1A2hi/VCANhi/SULF1hi PSCs. This signature was exclusive to T2D and was not observed in Type 1 diabetes (T1D) samples, indicating a distinct role for activated PSCs in T2D progression. Furthermore, we identified six long non-coding RNAs (lncRNAs) that potentially interact with the COL1A2hi/VCANhi/SULF1hi PSCs. These lncRNAs were mapped to a lncRNA-mRNA network, suggesting they may modulate immune responses and potentially reshape the immune microenvironment in T2D. Our findings highlight the potential immune-regulatory role of PSCs in T2D and suggest that PSC-related lncRNA-mRNA networks could serve as novel therapeutic targets for T2D treatment. This research provides insights into PSCs as a modulator in T2D progression, paving the way for innovative treatment strategies.

Rheumatoid arthritis (RA) is an autoimmune disease, which not only affects the joints but can also impact on general well-being and risk for cardiovascular disease. Regular physical activity and exercise in patients with RA have numerous health benefits. Nevertheless, the majority of patients with RA are physically inactive. This indicates that people with RA might experience additional or more severe barriers to physical activity or exercise than the general population. This narrative review provides an overview of perceived barriers, benefits and facilitators of physical activity and exercise in RA. Databases were searched for articles published until September 2014 using the terms ‘rheumatoid arthritis’, ‘physical activity’, ‘exercise’, ‘barriers’, ‘facilitators’, ‘benefits’, ‘motivation’, ‘motivators’ and ‘enablers’. Similarities were found between disease-specific barriers and benefits of physical activity and exercise, e.g. pain and fatigue are frequently mentioned as barriers, but reductions in pain and fatigue are perceived benefits of physical activity and exercise. Even though exercise does not influence the existence of barriers, physically active patients appear to be more capable of overcoming them. Therefore, exercise programmes should enhance self-efficacy for exercise in order to achieve long-term physical activity and exercise behaviour. Encouragement from health professionals and friends/family are facilitators for physical activity and exercise. There is a need for interventions that support RA patients in overcoming barriers to physical activity and exercise and help sustain this important health behaviour.

High fitness levels attenuate the increased risk of heart failure due to low socioeconomic status: A cohort study

Exercise and type 1 diabetes: overcoming the barriers

Although the MTNR1B single nucleotide polymorphism rs10830963 has been strongly associated with the onset of type 2 diabetes (T2D), its association with the progression and prognosis of T2D has been understudied. We conducted this prospective analysis based on the UK Biobank cohort study. Microvascular complications (MIC) of T2D in this study included diabetic retinopathy, diabetic neuropathy, and diabetic kidney disease. Macrovascular complications (MAC) of T2D included diabetic coronary artery disease, diabetic cerebrovascular disease, and diabetic peripheral vascular disease. The multi-state model was used to analyze the association between the polymorphism of rs10830963 and the trajectory of T2D. The accelerated failure time (AFT) model was used to assess the association between rs10830963 and the onset of T2D and T2D comorbidities. A total of 283,531 middle- and old-age participants were included. During a median follow-up of 13.7 years, 11,947 participants developed T2D, 1556 participants developed MIC, 1797 participants developed MAC, and 618 participants died. In the additive model, the G risk allele of rs10830963 was significantly associated with an increased risk of the transition from T2D-free to T2D (HR = 1.050, 95% CI: 1.020, 1.079) and a decreased risk of the transition from T2D to MIC (HR = 0.918, 95% CI: 0.850, 0.992), particularly from T2D to diabetic retinopathy (HR = 0.882, 95% CI: 0.782, 0.995). Besides, the G risk allele of rs10830963 accelerated the transition from T2D-free to T2D (Time Ratio [TR] = 0.966, 95% CI: 0.947, 0.986) and slowed down the transition from T2D to MIC (TR = 1.067, 95% CI: 1.030, 1.105). The MTNR1B single nucleotide polymorphism rs10830963 was associated with an increased risk of T2D and a decreased risk of MIC, particularly diabetic retinopathy among T2D individuals. Our results highlight that rs10830963 might play differential roles in the onset and progression of T2D.

Finding The Clinical Exercise Physiologist's Collective Voice During the COVID-19 Pandemic

Disclosure: K. Girdhar: None. E. Elko: None. A. Pina: None. M. Atkinson: None. J. Ludvigsson: None. J. Ladner: None. E. Altindis: None. Type 1 diabetes (T1D) is an autoimmune disorder characterized by the immune-mediated destruction of insulin-producing beta cells. The etiological factors triggering the immunogenicity of endogenous β-cell antigens remain a focal point of investigation. Viral infections, particularly enteroviruses, coxsackieviruses, and rotaviruses, have been proposed as potential contributors to T1D onset and progression. However, the causal relationship between viral infections and T1D pathogenesis remains elusive. To address this, we conducted an in-depth analysis of viral infection histories of T1D patients and pediatric T1D progressors compared to the controls. To this end, we employed highly multiplexed serology using PepSeq sequencing, an in vitro platform designed for conducting proteomic assays against customizable targets via DNA-barcoded peptides. Utilizing samples from the All Babies in Sweden (ABIS) study (n=58) and the TrialNet study (n=116 new-onset T1D, n=25 established T1D, n=128 controls), we assessed seropositivity against 79 different human viruses. Contrary to previous reports, no significant differences were identified in viral infection histories between T1D individuals and controls. Subsequent analyses of enriched Peptide Count and Viral Homology Search (VHS) species provided further confirmation of the absence of distinctions in T1D progression. Next, we determined whether there are any differences in the markers of systematic inflammation in spite of their similar viral history profile. Therefore, we employed Luminex assays to investigate cytokine profiles in established T1D individuals (n=25). While we could not identify any differences when we compared T1D patients to controls, we identified notable sex-specific differences. Anti-inflammatory cytokines (IL-4, IL-13, IL-22) were lower in female T1D patients compared to female controls. Likewise, female T1D patients had higher pro-inflammatory cytokines (IL-17E, TNF-β). On the other hand, male T1D patients exhibited increased levels of epidermal growth factor and platelet-derived growth factor compared to male controls, with IL-22 uniquely elevated. Our findings challenge the direct association between viral infections and T1D, highlighting the importance of investigating alternative factors. Moreover, the observed sex-specific cytokine alterations underscore the complex interplay between immune responses and T1D, emphasizing the need for sex-specific therapeutic strategies. This research contributes valuable insights into the intricate dynamics of viral infections, systemic inflammation, and their potential roles in T1D pathogenesis. Presentation: 6/2/2024

Physical Activity Intensity Measurement and Association With Adolescent Health: Chartering New Frontiers

<h3>Objective:</h3> Owing to the lack of long-term observations and/or comprehensive adjustment for confounding factors, reliable conclusions regarding long-term effects of exercise and regular physical activity in Parkinson’s disease (PD) have...