The aging process is associated with many functional decrements. It is important to consider the additive acute functional decreases that may occur following eccentric exercise-induced muscle damage (EIMD). This study aimed to examine the effect of age on muscle damage metrics following EIMD. Ten younger (age=20±2 years, BMI=22.49±3.97 kg/m2) and six older (age=68±2 years, BMI=24.45±2.82 kg/m2) females participated in this study. Participants performed a maximal knee extensor EIMD protocol. Additionally, participants completed various assessments before, immediately after, 24-, 48-, and 72-hours after the EIMD protocol to evaluate the presence of and recovery from muscle damage. Assessments included B-mode ultrasound imaging of the rectus femoris (RF) and vastus lateralis (VL) to assess cross sectional area (CSA) and echo intensity (EI), soreness measures, and neuromuscular assessments (i.e., peak torque [PT] and rapid torque [RT]). A 2×5 ANOVA was used to compare age groups by time for all variables. Significant age × time interactions were found for RT at 200ms and 250ms (p<0.001) indicating a slower rate of recovery for the older group. Significant main effects for age were found for PT (p<0.001), maximal eccentric torque (p<0.001), VL CSA (p<0.001), RF CSA (p=0.03), RF EI (p=0.03), and all soreness measures (p<0.05). Overall, there were significant differences in performance, muscle morphology, and soreness between the younger and older females as well as significant differences in the late-phase RT recovery timeline. Practitioners should remain aware of the decreased functional abilities of female clients as they age and prescribe exercises appropriately.

IntroductionGlycemic dysregulation is a hallmark of type 2 diabetes (T2D) and contributes to skeletal muscle (SKM) loss and frailty risk, especially in older adults. Glycemic control and physical function are supported by SKM capillarization and mitochondrial function, and their impairment contributes to T2D development. While high-intensity interval training (HIIT) is a promising intervention, adherence and effectiveness remain concerns for prescribing HIIT among older adults at risk for T2D. Local heat therapy (LHT) may be a more practical initial strategy to improve SKM architectural factors and precondition SKM, enhancing physiological adaptations to exercise in this population.Methods and analysisHeat and Exercise in Aging as Therapy (HEAT) is a two-phase, randomized, sham-controlled clinical trial investigating the efficacy of LHT to improve glycemic control and decrease frailty risk via improved SKM architecture among older adults with prediabetes. LHT is tested as a standalone intervention and as a means to precondition SKM for subsequent HIIT, improving exercise adaptations. In Phase 1, LHT and sham (CON) groups apply heat pads for 90 minutes/day, 6 days/week, for 12 weeks. A separate HIIT group completes 4x4-minute cycling intervals at 90-95% VO₂peak, 3 days/week. In Phase 2, LHT and CON groups begin HIIT. Participants (≥50 years) have impaired fasting glucose (100-125 mg/dL) and/or HbA1c (5.7-6.4%). Biospecimen collection and clinical assessments occur at baseline (T1), after Phase 1 (T2), and Phase 2 (T3). To our knowledge, this is the first study to determine the use of local heat pad on pre-diabetic older population. If successful, LHT may be a practical, scalable, non-invasive intervention to improve glycemic control and reduce frailty risk in older adults with prediabetes, preventing progression to T2D.

Exercising under dehydrated conditions is common among physically active individuals, yet its impact on immune cell mitochondrial quality control, oxidative stress and inflammatory signaling, and systemic inflammatory mediators remains poorly defined. This study investigated mitochondrial quality control and systemic inflammatory responses to high-volume resistance exercise (HVRE) under hydrated (HYD) and dehydrated (DEH) conditions in 10 young men (21 ± 1 yr, 175 ± 6 cm, 76.9 ± 10.5 kg, 18.5 ± 6.3% fat). Participants completed two identical HVRE sessions following either normal hydration or 24-h fluid restriction. Peripheral blood mononuclear cells (PBMCs) collected before (PRE) and at 1 h and 3 h post-HVRE were analyzed for proteins related to mitochondrial quality control (PINK1, Parkin, DRP1, p-DRP1S616, and MFN2), oxidative stress and inflammatory signaling (p-NF-κBS536, NF-κB, SOD2, and H2O2), autophagy machinery and degradation (LC3-I, LC3-II, p62, and cathepsin-L), and blood samples for systemic inflammatory mediators (IL-6, TNF-α, CRP, and H2O2). Significant time × condition interaction effects revealed that LC3-II/I was greater in DEH than HYD at PRE and 3 h. In DEH, LC3-II/I returned to PRE levels at 3 h, whereas in HYD, it was greatest at 3 h. PINK1 was greater at 1 h and 3 h, and pDRP1S616 was greater at 3 h in DEH than HYD. Also, PINK1 and pDRP1S616 were greatest at 3 h post-HVRE in DEH. Lastly, significant condition main effects revealed greater MFN2, p62, LC3-II, and H2O2 in PBMCs and greater IL-6 and CRP in serum in DEH than in HYD. These results provide novel evidence that 24 h of fluid restriction before metabolically demanding resistance exercise activates mitochondrial quality control in PBMCs and elevates systemic inflammatory mediators.NEW & NOTEWORTHY This study examined how 24-h fluid restriction affects mitochondrial stress and inflammatory responses in peripheral blood mononuclear cells (PBMCs) after high-volume resistance exercise in young men. Dehydration increased markers of mitophagy (PINK1 and p-DRP1S616), autophagosome formation (LC3-II and p62), and oxidative stress (H2O2), while systemic IL-6 and CRP were elevated compared with euhydration. Findings suggest dehydration amplifies mitochondrial stress and proinflammatory signaling, highlighting the importance of proper hydration during exercise and its implications on cellular homeostasis.

AIMS:Alcohol misuse may adversely impact health-promoting behaviors. Our objective was to evaluate health-related behaviors in people with HIV with alcohol misuse during the early phase of the COVID-19 pandemic, aiming to understand how alcohol misuse influences these behaviors during health-related emergencies. METHODS:Eighty people with HIV (64% male, 51 ± 11 years of age), enrolled in the ALIVE-Ex Study (NCT03299205), consented to a cross-sectional phone survey during the Louisiana stay-at-home order. Alcohol use, dietary intake, physical activity (PA), and emotional well-being over the previous week were assessed. Based on their pre-pandemic Alcohol Use Disorders Identification Test-Consumption (AUDIT-C) score, participants were categorized into having alcohol misuse (AUDIT-C ≥ 3 female (F)/4 male (M)) or having no/low use (AUDIT-C < 3F/4M). Descriptive statistics, Spearman correlations, and crude and adjusted logistic regression models were estimated. RESULTS:Participants with alcohol misuse reported more alcohol use, more frequent meat and salty snack intake, and higher frequency of feeling tense and panicked over the previous week than people with HIV having no/low use (P < .05). Higher alcohol use was associated with more meat and salty snack intake, more frequent vigorous PA, higher PA level, and more emotional distress (P < .05). CONCLUSIONS:Overall, participants having alcohol misuse and those reporting higher alcohol use during the stay-at-home order reported less healthy dietary patterns and more emotional distress, while engaging in more PA, compared to participants with lower alcohol use. These data suggest that during health-related emergencies, consideration of patients' prior and current alcohol use is necessary when encouraging healthy behavioral patterns.

Dehydration is prevalent and adversely affects exercise performance; however, its influence on cellular responses to exercise remains unclear. Thus, this study examined the intramuscular responses to resistance-exercise (RE) in RE-trained men under dehydrated and euhydrated states. Eleven men (21 ± 1 years, 175.9 ± 6.2 cm, 79.2 ± 12.3 kg, 18.4% ± 6.7% fat) completed two identical lower-body RE sessions, either with (DEHY) or without (EUHY) fluid-restriction from 24 h before to 3 h after RE. At pre-RE (PRE), 1 h, and 3 h post-RE, muscle samples were collected and analysed for protein content of AKT/mTOR/p70S6K/rpS6 and their corresponding phosphorylation sites, REDD1 and selected autophagy markers, cathepsin L, H2O2 concentration, fibre cross-sectional area (CSA), and muscle water content. Significant time × condition interaction effects revealed that p-rpS6S240/244 was greater in DEHY than EUHY at PRE and increased from PRE to 1 h and 3 h in both conditions. In DEHY, REDD1 increased from PRE to 1 h and 3 h, active-cathepsin L decreased from 1 h to 3 h and was greater than EUHY at 1 h, and muscle water content increased from 1 h to 3 h. Significant condition main effects revealed that p-S6KT389 and H2O2 were greater, and CSA was smaller, in DEHY versus EUHY. Significant time main effects revealed that p-AKTS473 and p-mTORS2448 increased from PRE to 1 h and 3 h, LC3-I decreased from PRE and 1 h to 3 h, LC3-II decreased from PRE to 1 h and 3 h, and LC3-II/LC3-I decreased from PRE to 1 h and increased from 1 h to 3 h. These results suggest that performing RE in a dehydrated state imposes additional stress on the muscle, leading to greater cellular stress and growth signalling. KEY POINTS: Dehydration can negatively impact exercise performance, overall health, and cognitive function in humans. Water makes up about 70% of muscle mass, and dehydration has been shown to decrease muscle size in humans. However, the mechanisms by which dehydration affects muscle response on anabolic and catabolic signalling have only been observed in in vitro studies, leaving the processes in humans still not fully understood. Following 24 h of dehydration, there was an increase in the activation of rpS6 at rest. Additionally, young men exhibited greater activation of S6K during resistance exercise (RE) while dehydrated compared to when they were adequately hydrated. Concurrently, stress (H2O2 and REDD1) and proteolytic (active-cathepsin L) responses were elevated after RE in a dehydrated state compared to an adequately hydrated state. Our research offers new insights into the importance of hydration in muscle responses to exercise, particularly for individuals who are frequently dehydrated.

In recent decades, global temperature and humidity levels have surged. These increases in temperature and humidity are associated with higher risk of heat-related illnesses and impaired exercise performance, thereby prompting investigation into physiological responses to heat stress. Preconditioning strategies, including heat acclimation/acclimatization (HA), elicit physiological adaptations to enhance response to future heat exposures. Within HA research, an area of growing interest is examination of subcellular adaptations that contribute to whole-body acclimation, such as changes to/within mitochondria. External heat stress alters molecular pathways involved in mitochondrial biogenesis and bioenergetic function, but the relationship between these alterations and whole-body HA adaptations remains relatively unknown. Therefore, this review provides a detailed examination of the impact of HA on mitochondria across cell models, rodent models, and humans, linking these changes to exercise performance. Based on the current evidence, we propose a HA protocol aimed at promoting mitochondrial adaptations while maximizing traditional HA benefits. Lastly, we identify key areas for future research to further explore and enhance our understanding of mitochondrial responses to HA.

BACKGROUND:Alcohol misuse is prevalent among firefighters, and associated adverse cardiometabolic health consequences could negatively impact readiness for duty. Mental health conditions may confer additional risk. Therefore, we aimed to determine whether alcohol misuse increases cardiometabolic risk among firefighters and whether mental health conditions modify these relationships. METHODS:Deidentified data from firefighters (N = 2405; 95.8% males, 38 ± 9 years, 29.6 ± 4.6 kg/m2) included demographics, Alcohol Use Disorders Identification Test (AUDIT) and AUDIT-C scores, mental health screening scores, anthropometrics, metabolic panel, and cardiorespiratory testing results. Differences in cardiometabolic parameters between firefighters with low AUDIT-C (<3 [females] or <4 [males]; no or low-risk alcohol use) or high AUDIT-C (≥3 [females] or ≥4 [males]; hazardous alcohol use) were determined and odds ratios for clinical risk factors were calculated. Posttraumatic stress disorder (PTSD), insomnia, depression, and anxiety were assessed as moderators. RESULTS:Firefighters with high AUDIT-C had significantly (p < 0.05) higher total cholesterol (TC), high-density lipoprotein (HDL-C), and systolic blood pressure (SBP) and diastolic blood pressure (DBP) and lower hemoglobin A1C (HbA1c) than those with low AUDIT-C. In unadjusted and/or adjusted analyses, those with high AUDIT-C had increased risk for overweight/obesity, hypercholesterolemia, and prehypertension/hypertension, and decreased risk for low HDL and elevated HbA1c. There were inverse moderation effects by posttraumatic stress disorder (PTSD), depression, and anxiety on relationships between AUDIT-C score and BP. Insomnia (directly) and anxiety (inversely) moderated relationships between AUDIT-C score and circulating lipids. CONCLUSIONS:Firefighters with high AUDIT-C have differential cardiometabolic risk, with specific relationships altered by mental health status. Whether higher HDL and lower HbA1c with high AUDIT-C in firefighters is protective long-term remains to be explored. Overall, these results underscore the need for alcohol screening and intervention to maintain cardiometabolic health and long-term occupational readiness among firefighters.

Muscle recovery after damage is mediated by circulating factors and intracellular signaling pathways. Our previous studies have demonstrated that resistance exercise (RE)‐induced circulating factors elicited sex‐differential responses in damaged muscle. However, the global effects of these circulating factors on damaged muscle are largely understudied. We examined the differential effects of RE‐induced circulating factors and sex on the damaged muscle proteome. Damaged vastus lateralis muscle from 3 men and 3 women from a parent study were analyzed. Participants completed 2 identical bouts of unilateral eccentric knee extensions immediately followed by either upper body RE to induce circulating factors (EXE) or 20‐min seated rest (CON). Muscle biopsies collected from the damaged leg at 24 h were used. 900 proteins were identified by LC–MS/MS analysis. Ingenuity Pathway Analysis was used to detect activation prediction using z‐scores for functional and pathway analyses. In men, 79 proteins were downregulated and 15 were upregulated in EXE versus CON. These differentially expressed proteins were associated with immunological and inflammatory signaling pathways. Biological functions of the differentially expressed proteins in EXE vs. CON in men include inactivating acute inflammatory signaling, neutrophil extracellular trap signaling, ROS production, and activating IL‐12 signaling. These results underline that RE‐induced circulating factors have a sex‐specific effect on the damaged muscle proteome, where immune signaling is altered in men but not women. Given that the immune response is critical for recovery from muscle damage, these results highlight the potential role of RE‐induced circulating factors that could be essential in mediating muscle recovery.

Alcohol misuse and HIV independently induce myopathy. We previously showed that chronic binge alcohol (CBA) administration, with or without simian immunodeficiency virus (SIV), decreases differentiation capacity of male rhesus macaque myoblasts. We hypothesized that short-term alcohol and CBA/SIV would synergistically decrease differentiation capacity and impair bioenergetic parameters in female macaque myoblasts. Myoblasts from naïve (CBA−/SIV−), vehicle [VEH]/SIV, and CBA/SIV (N = 4–6/group) groups were proliferated (3 days) and differentiated (5 days) with 0 or 50 mM ethanol (short-term). CBA/SIV decreased differentiation and increased non-mitochondrial oxygen consumption rate (OCR) versus naïve and/or VEH/SIV. Short-term alcohol decreased differentiation; increased maximal and non-mitochondrial OCR, mitochondrial reactive oxygen species (ROS) production, and aldolase activity; and decreased glycolytic measures, ATP production, mitochondrial membrane potential (ΔΨm), and pyruvate kinase activity. Mitochondrial ROS production was closely associated with mitochondrial network volume, and differentiation indices were closely associated with key bioenergetic health and function parameters. Results indicate that short-term alcohol and CBA non-synergistically decrease myoblast differentiation capacity. Short-term alcohol impaired myoblast glycolytic function, driving the bioenergetic deficit. Results suggest potentially differing mechanisms underlying decreased differentiation capacity with short-term alcohol and CBA, highlighting the need to elucidate the impact of different alcohol use patterns on myopathy.

Alcohol-mediated myopathy frequently accompanies chronic alcohol misuse. This decreased skeletal muscle mass and function increases risk for frailty and falls, decreases quality of life, and worsens prognosis for other comorbid conditions. After muscle injury or atrophy, satellite cells are activated as myoblasts, which proliferate, differentiate, and fuse with myofibers to aid in repairing and rebuilding skeletal muscle. While decreased myoblast differentiation with ethanol (EtOH) is well-documented, we have also observed fewer myoblasts with in vitro EtOH after the proliferative phase of myogenesis. The extent of this decrease and whether this is due primarily to increased cell death, decreased cell division, or a combination thereof remains unanswered. Therefore, the objective of this study is to quantify effects of EtOH on myoblast cell division and death during the proliferative phase. C2C12 myoblasts were proliferated in the presence or absence of 50 mM EtOH for 24, 48, and 72 hrs. Nuclei were stained with DAPI to quantify differences in cell count at each time point. Lactate dehydrogenase (LDH) activity was measured in cell culture supernatant at 48 and 72 hrs and normalized to cell count to assess overall cytotoxicity. T-tests were used to determine differences between conditions at each time point. There were no significant differences in cell counts between cells grown with 0 and 50 mM EtOH at 24 or 48 hrs. At 72 hrs, EtOH significantly decreased cell count (p=0.03). There were no significant differences for LDH activity at 48 hrs. At 72 hrs, LDH activity was significantly lower in the 50 mM group (p=0.05). These preliminary results suggest that EtOH decreases cell count in a time-dependent manner. Cytotoxicity appeared lower with EtOH, although this is likely due to lower intracellular LDH activity given our previously observed adverse impacts of EtOH on myoblast glycolytic function. Regardless, the present data do not support increased cytotoxicity with 50 mM EtOH. Next steps will be to assess alterations in myoblast apoptosis and cell division with EtOH. Future work based on the results of these experiments will examine possible nutraceutical supplements and exercise-like stimulation as interventions to rescue alcohol-mediated effects on myoblast proliferation, which may improve subsequent differentiation and therefore regenerative capacity. This work was supported by Texas Tech University (TTU) startup funds and a TTU College of Arts & Sciences Undergraduate Research Experiences grant (DL). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Infants born preterm face an increased risk of deleterious effects on lung and brain health that can significantly alter long-term function and quality of life and even lead to death. Moreover, preterm birth is also associated with a heightened risk of diabetes and obesity later in life, leading to an increased risk of all-cause mortality in young adults born prematurely. While these preterm-birth-related conditions have been well characterized, less is known about the long-term effects of preterm birth on skeletal muscle health and, specifically, an individual’s skeletal muscle hypertrophic potential later in life. In this review, we discuss how a confluence of potentially interrelated and self-perpetuating elements associated with preterm birth might converge on anabolic and catabolic pathways to ultimately blunt skeletal muscle hypertrophy, identifying critical areas for future research.

Infants born preterm face an increased risk of deleterious effects on lung and brain health that can significantly alter long-term function and quality of life and even lead to death. Moreover, preterm birth is also associated with a heightened risk of diabetes and obesity later in life, leading to an increased risk of all-cause mortality in young adults born prematurely. While these preterm-birth-related conditions have been well characterized, less is known about the long-term effects of preterm birth on skeletal muscle health and, specifically, an individual's skeletal muscle hypertrophic potential later in life. In this review, we discuss how a confluence of potentially interrelated and self-perpetuating elements associated with preterm birth might converge on anabolic and catabolic pathways to ultimately blunt skeletal muscle hypertrophy, identifying critical areas for future research.

Recovery from muscle damage is tightly orchestrated by multiple physiological processes that can be altered by circulating factors (e.g., cytokines, growth factors) and intracellular signaling pathways (e.g., autophagy). Our previous studies have demonstrated that resistance exercise (RE)-induced circulating factors alter the expression of intramuscular cytokine mRNA and autophagic and myogenic markers in exercise-induced skeletal muscle damage (EIMD). However, the global effects of these circulating factors on damaged muscle are largely understudied. Purpose: To identify global changes in the proteome and functional pathways in skeletal muscle when EIMD is followed by an upper body RE-induced circulating milieu. Hypothesis: RE-induced circulating factors alter protein expression profile in damaged muscle. Methods: Vastus lateralis samples from 3 men included in the parent study were utilized for this report. Untrained men (age: 23 ± 5yr; height: 181.6 ± 5.9cm; weight: 86.0 ± 15.8kg) completed 2 identical bouts of maximal unilateral eccentric knee extensions for 8 sets of 10 repetitions, which were immediately followed by either heavy upper body RE to induce changes in circulating factors (EX) or 20 min seated rest (CON). Muscle samples from the damaged leg at 24h were used to compare between conditions. The total number of proteins was measured using LC-MS/MS. Bioinformatic analyses were performed via Qiagen Ingenuity Pathway Analysis software. For identifying enriched biological processes and functions, proteins had to have at least 1.0-fold differential expression with an FDR-adjusted significance level < 0.05. Z scores were calculated to predict changes in biological functions. Results: A total of 900 proteins were identified. For EX, 79 proteins were downregulated, and 15 were upregulated compared to CON at 24h. Pathway analyses demonstrated that for EX, there was decreased activation in acute phase response signaling, liver X receptor/retinoid X receptor activation, nitric oxide production and reactive oxygen species in macrophages, and neutrophil extracellular trap signaling pathways compared to CON. In addition, for EX, there was an increase in macrophage IL-12 signaling and production than CON. Conclusion: RE-induced changes in circulating factors modulated pathways associated with the immune response and cytokine signaling in untrained men. Given that immune response is critical for recovery from muscle damage, these results highlight the potential role of RE-induced circulating factors (e.g., hormones, growth factors, etc.) which could play a role in mediating muscle recovery. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Alcohol misuse in people with HIV (PWH) and chronic binge alcohol (CBA) administration in simian immunodeficiency virus (SIV)-infected macaques are associated with increased physical frailty and impaired functional skeletal muscle mass, respectively. Previous studies by our group demonstrate that muscle-enriched microRNAs (myomiRs) are differentially expressed in skeletal muscle (SKM) from CBA-administered SIV-infected male macaques and their altered expression contributes to impaired differentiation of SKM stem cells, or myoblasts. MicroRNAs can be transported in extracellular vesicles (EVs) to mediate numerous cellular responses through intercellular communication. The current study tested the hypothesis that EV-mediated delivery of miR-206 can ameliorate CBA-mediated decreased myoblast differentiation. Myoblasts were isolated from SKM of female SIV-infected, antiretroviral therapy-treated macaques that received either CBA (2.5g/kg/day, CBA/SIV) or water (VEH/SIV) for 14.5 months. Myotube and myotube derived EV myomiR expression, including miR-206, was lower in the CBA/SIV group. Overexpression of miR-206 decreased histone deacetylase 4 ( HDAC4) and paired box 7 ( PAX7) expression in myotubes and increased fusion index, a differentiation index, in CBA/SIV-derived myotubes. Similarly, EV-mediated delivery of miR-206 increased both fusion index and myotube density of CBA/SIV-derived myoblasts. These results support the potential therapeutic utility of EVs in delivering myomiRs to improve SKM stem cell differentiation.

Bioenergetic pathways uniquely support sarcomere function which, in turn, helps to maintain functional skeletal muscle (SKM) mass. Emerging evidence supports alcohol (EtOH)-induced bioenergetic impairments in SKM and muscle precursor cells. We performed a scoping review to synthesize existing evidence regarding the effects of EtOH on SKM bioenergetics. Eligible articles from six databases were identified, and titles, abstracts, and full texts for potentially relevant articles were screened against inclusion criteria. Through the search, we identified 555 unique articles, and 21 met inclusion criteria. Three studies investigated EtOH effects on the adenosine triphosphate (ATP)-phosphocreatine (PCr) system, twelve investigated EtOH effects on glycolytic metabolism, and seventeen investigated EtOH effects on mitochondrial metabolism. Despite increased ATP-PCr system reliance, EtOH led to an overall decrease in bioenergetic function through decreased expression and activity of glycolytic and mitochondrial pathway components. However, effects varied depending on the EtOH dose and duration, model system, and sample type. The results detail the EtOH-induced shifts in energy metabolism, which may adversely affect sarcomere function and contribute to myopathy. These findings should be used to develop targeted interventions that improve SKM bioenergetic function, and thus sarcomere function, in people with Alcohol Use Disorder (AUD). Key areas in need of further investigation are also identified.

IntroductionPeople with pre-existing conditions, including metabolic comorbidities, are at greater risk for complications of SARS-CoV-2 infection and expression of machinery required for viral entry into host cells may be a contributing factor. This study tested the hypothesis that high fat, high sucrose diet (HFSD) and alcohol use increase expression of angiotensin converting enzyme 2 (ACE2) receptor and transmembrane serine protease 2 (TMPRSS2) in tissues isolated from simian immunodeficiency virus (SIV) infected macaques, the most clinically relevant model for the study of HIV.MethodsBiospecimens obtained from a longitudinal study of SIV-infected, antiretroviral therapy (ART)-treated female rhesus macaques (Macaca mulatta) were used to determine whether HFSD and chronic binge alcohol (CBA) increased ACE2 and TMPRSS2 protein and gene expression. Macaques (n = 10) were assigned to HFSD or standard diet (SD) for 3 months before CBA or vehicle administration. Three months later, macaques were infected with SIV; ART was initiated 2.5 months thereafter. Tissue samples including lung, pancreas, and kidney were collected at study endpoint (12 months post-SIV infection).ResultsProtein expression of ACE2 in the lung, whole pancreas, and pancreatic islets was significantly greater in HFSD- than SD-fed macaques with no significant differences in protein expression of TMPRSS2 or mRNA expression of ACE2 or TMPRSS2. CBA did not significantly alter any measures.DiscussionThe increased ACE2 receptor expression observed in lung and pancreas of SIV-infected HFSD-fed female rhesus macaques aligns with reports that diet may increase susceptibility to COVID-19. These data provide direct evidence for a link between dietary quality and cellular adaptations that may increase the risk for SARS-CoV-2 infection.

IntroductionPsychological aspects of sport are key in maintaining athlete motivation and make a difference in competitive outcomes. Adjustments to training may be necessary according to athletes’ emotional state. Therefore, it is important to assess and quantify mood states throughout the season in team sports, including among soccer players. The Profile of Mood States (POMS) is a widely used questionnaire that assesses emotional states characterized by positive or negative feelings and can be administered repeatedly to assess changes in mood state. This review aims to assess and summarize the current literature on mood state variation in soccer players with a specific focus on training loads, training modalities, and competitive performance.MethodsA literature search was systematically conducted and resulted in 156 records. After removing duplicates, items with irrelevant titles and abstracts were screened out, and full texts were then screened for relevance and compared with inclusion and exclusion criteria. The remaining 37 articles were included in the final qualitative synthesis.ResultsPOMS scores were related to variability in training load, intensity of the training period, modality of training exercises, competitive performance and time of day in soccer players. Common recommendations include monitoring the mood state of soccer players during training sessions, matches, and throughout training periods to detect early signs of psychological disturbance and aid in optimizing high-level training performance.ConclusionThe POMS allows for monitoring of players’ psychological state, providing coaches with data to aid in adjusting acute program variables according to players’ psychological states and improve performance. Results offer practical support for the use of a simple POMS measurement as part of an overall program to monitor the players’ psychological states. Results also highlight how training choices (i.e., load and exercise modality) and competitive performance are related to mood states (i.e., tension, anger, confusion, depression, fatigue, and vigor).

Background Effective antiretroviral therapy (ART) in people living with HIV (PLWH) has improved life expectancy and increased risk of age-associated cardiometabolic comorbidities. At-risk alcohol use is more frequent among PLWH and increases the risk of health challenges. PLWH with at-risk alcohol use are more likely to meet criteria for prediabetes/diabetes and this is associated with impaired whole-body glucose-insulin dynamics. Methods The Alcohol & Metabolic Comorbidities in PLWH: Evidence Driven Interventions Study (ALIVE-Ex Study, NCT03299205) is a longitudinal, prospective, interventional study to determine the effects of an aerobic exercise protocol on improving dysglycemia among PLWH with at-risk alcohol use. The intervention is a moderate intensity aerobic exercise protocol implemented 3 days per week for 10 weeks at the Louisiana State University Health Sciences Center-New Orleans. Participants who have a fasting blood glucose level between 94 and 125 mg/dl will be enrolled in the study. Oral glucose tolerance tests, fitness assessments, and skeletal muscle biopsies will be performed pre- and post-exercise intervention. The primary outcome is to determine whether the exercise protocol improves measures of whole-body glucose-insulin dynamics, cardiorespiratory fitness, and skeletal muscle metabolic and bioenergetic function. Secondary outcomes are to determine whether the exercise intervention improves cognitive function and overall quality of life. Results generated will demonstrate the effect of exercise on glycemic measures in PLWH with subclinical dysglycemia and at-risk alcohol use. Conclusions The proposed intervention will also have the potential to be scalable to promote lifestyle changes among PLWH, particularly in underserved communities.