The purpose of this study was to examine the effects of lifelong aerobic exercise (LLE) on VOmax and skeletal muscle metabolic fitness in trained females (n=7, 72±2y) and males (n=21, 74±1y), and compare them to old healthy non-exercisers (OH; females: n=10, 75±1y; males: n=10, 75±1y), and young exercisers (YE; females: n=10, 25±1y; males: n=10, 25±1y). LLE males were further subdivided based on intensity of lifelong exercise and competitive status into performance (LLE-P, n=14) and fitness (LLE-F, n=7). On average, LLE exercised 5d/wk for 7h/wk over the past 52±1y. Each subject performed a maximal cycle test to assess VOmax and had a vastus lateralis muscle biopsy to examine capillarization and metabolic enzymes (citrate synthase, β-HAD, and glycogen phosphorylase). VOmax had a hierarchical pattern (YE>LLE>OH, P<0.05) for females (44±2>26±2>18±1 ml•kg•min) and males (53±3>34±1>22±1 ml•kg•min), and was greater (P<0.05) in LLE-P (38±1 ml•kg•min) than LLE-F (27±2 ml•kg•min). LLE males, regardless of intensity, and females had similar capillarization and aerobic enzyme activity (citrate synthase and β-HAD) as YE, which were 20-90% greater (P<0.05) than OH. In summary, these data show a substantial VOmax benefit with LLE that tracked similarly between the sexes, with further enhancement in performance trained males. For skeletal muscle, 50+ years of aerobic exercise fully preserved capillarization and aerobic enzymes, regardless of intensity. These data suggest that skeletal muscle metabolic fitness may easier to maintain with lifelong aerobic exercise than more central aspects of the cardiovascular system.

Age-associated chronic basal inflammation compromises muscle mass and adaptability, but exercise training may exert an anti-inflammatory effect. This investigation assessed basal and exercise-induced inflammation in three cohorts of men: young exercisers [YE; n = 10 men; 25 ± 1 yr; maximal oxygen consumption (V̇o2max), 53 ± 3 mL·kg−1·min−1; quadriceps area, 78 ± 3 cm2; means ± SE], old healthy nonexercisers (OH; n = 10; 75 ± 1 yr; V̇o2max, 22 ± 1 mL·kg−1·min−1; quadriceps area, 56 ± 3 cm2), and lifelong exercisers with an aerobic training history of 53 ± 1 yr (LLE; n = 21; 74 ± 1 yr; V̇o2max, 34 ± 1 mL·kg−1·min−1; quadriceps area, 67 ± 2 cm2). Resting serum IL-6, TNF-α, C-reactive protein, and IGF-1 levels were measured. Vastus lateralis muscle biopsies were obtained at rest (basal) and 4 h after an acute exercise challenge (3 × 10 repetitions, 70% 1-repetition maximum) to assess gene expression of cytokines [IL-6, TNF-α, IL-1β, IL-10, IL-4, interleukin-1 receptor antagonist (IL-1Ra), and transforming growth factor-β (TGF-β)], chemokines [IL-8 and monocyte chemoattractant protein-1 (MCP-1)], cyclooxygenase enzymes [cyclooxygenase-1 and -2 (COX-1 and COX-2, respectively), prostaglandin E2 synthases [microsomal prostaglandin E synthase 1 (mPGES-1) and cytosolic prostaglandin E2 synthase (cPGES)] and receptors [prostaglandin E2 receptor EP3 and EP4 subtypes (EP3 and EP4, respectively), and macrophage markers [cluster of differentiation 16b (CD16b) and CD163], as well as basal macrophage abundance (CD68+ cells). Aging led to higher ( P ≤ 0.05) circulating IL-6 and skeletal muscle COX-1, mPGES-1, and CD163 expression. However, LLE had significantly lower serum IL-6 levels ( P ≤ 0.05 vs. OH) and a predominantly anti-inflammatory muscle profile [higher IL-10 ( P ≤ 0.05 vs. YE), TNF-α, TGF-β, and EP4 levels ( P ≤ 0.05 vs. OH)]. In OH only, acute exercise increased expression of proinflammatory factors TNF-α, TGF-β, and IL-8 ( P ≤ 0.05). LLE had postexercise gene expression similar to YE, except lower IL-10 ( P ≤ 0.10), mPGES-1, and EP3 expression ( P ≤ 0.05). Thus, although aging led to a proinflammatory profile within blood and muscle, lifelong exercise partially prevented this and generally preserved the acute inflammatory response to exercise seen in young exercising men. Lifelong exercise may positively impact muscle health throughout aging by promoting anti-inflammation in skeletal muscle. NEW & NOTEWORTHY This study assessed a unique population of lifelong aerobic exercising men and demonstrated that their activity status exerts an anti-inflammatory effect in skeletal muscle and circulation. Furthermore, we provide evidence that the inflammatory response to acute exercise is dysregulated by aging but preserved with lifelong exercise, which might improve skeletal muscle resilience to unaccustomed loading and adaptability into late life.

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Background Cystic Fibrosis (CF) is a chronic multi-system disease best cared for at Care centers with routine monitoring by interdisciplinary teams. Previously, remote home monitoring technology has been explored to augment in-person care. During the COVID-19 pandemic, traditional in-person care was limited and CF centers rapidly adapted to a telehealth delivery model. The purpose of this study was to understand how people with CF (PwCF) and families of PwCF experienced the shift to telehealthcare delivery. Methods This was a cross-sectional survey-based study conducted in 11 CF Centers. Two surveys were designed (one for adult PwCF and one for parents/guardians of PwCF) by participating CF center members with patient and family partner input. Surveys were disseminated electronically via email/text to all patients who completed a telehealth visit, and data were collected on secure Google Forms. Results Respondents rated their telehealth experiences as positive. Most were highly satisfied with their telehealth visit (77% adult, 72% pediatric) and found the visits to be highly convenient (85% for all surveyed). A majority of patients reported they had adequate time during the visit and had all questions and concerns addressed. Importantly, we also identified concerns regarding lack of in-person assessments including pulmonary function testing (PFT) and throat/sputum culture. Conclusion Telehealth was a feasible and well-accepted mechanism for delivering care in a chronic CF care model during the COVID-19 pandemic and may be useful in the post-pandemic era. Further work is needed to understand the impact of telehealth on patient outcomes, healthcare utilization and associated cost.

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Although aspirin is one of the most common anti-inflammatory drugs in the world, the effect of aspirin on human skeletal muscle inflammation is almost completely unknown. This study examined the potential effects and related time course of an orally consumed aspirin dose on the inflammatory prostaglandin E (PGE)/cyclooxygenase (COX) pathway in human skeletal muscle. Skeletal muscle biopsies were taken from the vastus lateralis of 10 healthy adults (5 male and 5 female, 25 ± 2 yr old) before (Pre) and 2, 4, and 24 h after (Post) a standard dose (975mg) of aspirin and partitioned for analysis of 1) in vivo PGE levels in resting skeletal muscle and 2) ex vivo skeletal muscle PGE production when stimulated with the COX substrate arachidonic acid (5 μM). PGE levels in vivo and PGE production ex vivo were generally unchanged at each time point after aspirin consumption. However, most individuals clearly showed suppression of PGE, but at varying time points after aspirin consumption. When the maximum suppression after aspirin consumption was examined for each individual, independent of time, PGE levels in vivo (184 ± 17 and 104 ± 23pg/g wet wt at Pre and Post, respectively) and PGE production ex vivo (2.74 ± 0.17 and 2.09 ± 0.11pg·mg wet wt·min at Pre and Post, respectively) were reduced ( P < 0.05) by 44% and 24%, respectively. These results provide evidence that orally consumed aspirin can inhibit the COX pathway and reduce the inflammatory mediator PGE in human skeletal muscle. Findings from this study highlight the need to expand our knowledge regarding the potential role for aspirin regulation of the deleterious influence of inflammation on skeletal muscle health in aging and exercising individuals. NEW & NOTEWORTHY This study demonstrated that orally consumed aspirin can target the prostaglandin/cyclooxygenase pathway in human skeletal muscle. This pathway has been shown to regulate skeletal muscle metabolism and inflammation in aging and exercising individuals. Given the prevalence of aspirin consumption, these findings may have implications for skeletal muscle health in a large segment of the population.

The integrated resistance and aerobic training protocol on a device maintains several key myocellular characteristics during prolonged unloading, but further refinement of the exercise approach to fully protect the SOL is warranted.

Low muscle mass and frailty are especially prevalent in older women and may be accelerated by age-related inflammation. Habitual physical activity throughout the lifespan (lifelong exercise) may prevent muscle inflammation and associated pathologies, but this is unexplored in women. This investigation assessed basal and acute exercise-induced inflammation in three cohorts of women: young exercisers (YE, n=10, 25±1y, VO2max:44±2mL/kg/min, quadriceps size:59±2cm2), old healthy non-exercisers (OH, n=10, 75±1y, VO2max:18±1mL/kg/min, quadriceps size:40±1cm2), and lifelong aerobic exercisers with a 48±2y aerobic training history (LLE, n=7, 72±2y, VO2max:26±2mL/kg/min, quadriceps size:42±2cm2). Resting serum IL-6, TNF-α, CRP, and IGF-1 were measured. Vastus lateralis muscle biopsies were obtained at rest (basal) and 4h after an acute exercise challenge (3x10reps, 70%1RM) to assess gene expression of cytokines (IL-6, TNF-α, IL-1β, IL-10, IL-4, IL-1Ra, TGF-β), chemokines (IL-8, MCP-1), cyclooxygenase enzymes (COX-1, COX-2), prostaglandin E2 synthases (mPGES-1, cPGES) and receptors (EP3-4), and macrophage markers (CD16b, CD163), as well as basal macrophage abundance (CD68+ cells). The older cohorts (LLE+OH combined) demonstrated higher muscle IL-6 and COX-1 (P≤0.05) than YE, while LLE expressed lower muscle IL-1β (P≤0.05 vs. OH). Acute exercise increased muscle IL-6 expression in YE only, whereas the older cohorts combined had higher postexercise expression of IL-8 and TNF-α (P≤0.05 vs. YE). Only LLE had increased postexercise expression of muscle IL-1β and MCP-1 (P≤0.05 vs. preexercise). Thus, aging in women led to mild basal and exercise-induced inflammation that was unaffected by lifelong aerobic exercise, which may have implications for long-term function and adaptability.