Maternal exercise increases infant resting energy expenditure: preliminary results.

Maternal obesity is associated with lower infant resting energy expenditure (REE), predisposing them to more rapid weight and adiposity gain through early infancy. Maternal exercise (ME) decreases infant adiposity and risk for childhood obesity; however, it remains unknown if this is in part mediated by changes in infant energy expenditure. Thus, we measured REE in 1-month-old infants from pregnant individuals who performed moderate-intensity exercise during pregnancy and compared it to infants from non-exercising controls. We observed higher oxygen respiratory rates (p = 0.003 for VO2 and p = 0.007 for VCO2) and REE (p = 0.002) in infants exposed to exercise in utero, independent of any differences in infant body composition. Furthermore, maternal BMI was significantly and inversely associated with infant REE in the control (r = -0.86, R2 = 0.74, p = 0.029), but not the exercise group (r = 0.33, R2 = 0.11, p = 0.473). Together, these findings associate ME with increasing infant energy expenditure which could be protective of subsequent infant adiposity gain. Clinical Trial: ClinicalTrials.gov Identifier: NCT03838146 and NCT04805502.

Exercise FITT-V during pregnancy: Association with birth outcomes.

BACKGROUND: Prenatal exercise improves birth outcomes, but research into exercise dose-response effects is limited. METHODS: This study is a retrospective, secondary analysis of pooled data from three blinded, prospective, randomized controlled trials. Prenatal exercise frequency, intensity, type, time, and volume (FITT-V) were assessed in supervised sessions throughout pregnancy. Gestational age (GA), neonatal resting heart rate (rHR), morphometrics (body circumferences, weight-to-length and ponderal index) Apgar and reflex scores, and placental measures were obtained at birth. Stepwise regressions and Pearson correlations determined associations between FITT-V and birth outcomes. RESULTS: Prenatal exercise frequency reduces ponderal index (R2 = 0.15, F = 2.76, p = .05) and increased total number of reflexes present at birth (R2 = 0.24, F = 7.89, p < .001), while exercise intensity was related to greater gestational age and birth length (R2 = 0.08, F = 3.14; R2 = 0.12, F = 3.86, respectively; both p = .04); exercise weekly volume was associated with shorter hospital stay (R2 = 0.24, F = 4.73, p = .01). Furthermore, exercise type was associated with placenta size (R2 = 0.47, F = 3.51, p = .01). CONCLUSIONS: Prenatal exercise is positively related to birth and placental outcomes in a dose-dependent manner.

Effects of maternal exercise on infant mesenchymal stem cell mitochondrial function, insulin action, and body composition in infancy.

Maternal exercise (ME) has been established as a useful non-pharmacological intervention to improve infant metabolic health; however, mechanistic insight behind these adaptations remains mostly confined to animal models. Infant mesenchymal stem cells (MSCs) give rise to infant tissues (e.g., skeletal muscle), and remain involved in mature tissue maintenance. Importantly, these cells maintain metabolic characteristics of an offspring donor and provide a model for the investigation of mechanisms behind infant metabolic health improvements. We used undifferentiated MSC to investigate if ME affects infant MSC mitochondrial function and insulin action, and if these adaptations are associated with lower infant adiposity. We found that infants from exercising mothers have improvements in MSC insulin signaling related to higher MSC respiration and fat oxidation, and expression and activation of energy-sensing and redox-sensitive proteins. Further, we found that infants exposed to exercise in utero were leaner at 1 month of age, with a significant inverse correlation between infant MSC respiration and infant adiposity at 6 months of age. These data suggest that infants from exercising mothers are relatively leaner, and this is associated with higher infant MSC mitochondrial respiration, fat use, and insulin action.

NASA SPRINT exercise program efficacy for vastus lateralis and soleus skeletal muscle health during 70 days of simulated microgravity.

The efficacy of the NASA SPRINT exercise countermeasures program for quadriceps (vastus lateralis) and triceps surae (soleus) skeletal muscle health was investigated during 70 days of simulated microgravity. Individuals completed 6° head-down-tilt bedrest (BR, n = 9), bedrest with resistance and aerobic exercise (BRE, n = 9), or bedrest with resistance and aerobic exercise and low-dose testosterone (BRE + T, n = 8). All groups were periodically tested for muscle (n = 9 times) and aerobic (n = 4 times) power during bedrest. In BR, surprisingly, the typical bedrest-induced decrements in vastus lateralis myofiber size and power were either blunted (myosin heavy chain, MHC I) or eliminated (MHC IIa), along with no change (P > 0.05) in %MHC distribution and blunted quadriceps atrophy. In BRE, MHC I (vastus lateralis and soleus) and IIa (vastus lateralis) contractile performance was maintained (P > 0.05) or increased (P < 0.05). Vastus lateralis hybrid fiber percentage was reduced (P < 0.05) and energy metabolism enzymes and capillarization were generally maintained (P > 0.05), while not all of these positive responses were observed in the soleus. Exercise offsets 100% of quadriceps and approximately two-thirds of soleus whole muscle mass loss. Testosterone (BRE + T) did not provide any benefit over exercise alone for either muscle and for some myocellular parameters appeared detrimental. In summary, the periodic testing likely provided a partial exercise countermeasure for the quadriceps in the bedrest group, which is a novel finding given the extremely low exercise dose. The SPRINT exercise program appears to be viable for the quadriceps; however, refinement is needed to completely protect triceps surae myocellular and whole muscle health for astronauts on long-duration spaceflights.NEW & NOTEWORTHY This study provides unique exercise countermeasures development information for astronauts on long-duration spaceflights. The NASA SPRINT program was protective for quadriceps myocellular and whole muscle health, whereas the triceps surae (soleus) was only partially protected as has been shown with other programs. The bedrest control group data may provide beneficial information for overall exercise dose and targeting fast-twitch muscle fibers. Other unique approaches for the triceps surae are needed to supplement existing exercise programs.

A narrative review of exercise dose during pregnancy.

The current recommendations for prenatal exercise dose align with those from the American College of Sports Medicine; 150 min of moderate intensity every week of pregnancy. However, recent works suggest there may be a dose-dependent beneficial effect for mother and offspring; maternal and offspring health outcomes respond differently to low, medium, and high doses of prenatal exercise. It is, therefore, our aim to summarize the published evidence (years 1950-2023) for five metrics of prenatal exercise training commonly reported, that is, "FITT-V": Frequency (number of sessions), Intensity (metabolic equivalents "METs"), Time (duration of sessions), Type (exercise mode), Volume (exercise MET*mins). The target audience includes clinicians and health care professionals, as well as exercise professionals and physiologists. Data suggest that moderate exercise frequency (3-4 times weekly) appears safe and efficacious for mother and offspring, while there is contradictory evidence for the safety and further benefit of increased frequency beyond 5 sessions per week. Moderate (3-6 METs) and vigorous (>6 METs) intensity prenatal exercise have been shown to promote maternal and offspring health, while little research has been performed on low-intensity (<3 METs) exercise. Exercise sessions lasting less than 1 hr are safe for mother and fetus, while longer-duration exercise should be carefully considered and monitored. Taken together, aerobic, resistance, or a combination of exercise types is well tolerated at medium-to-high volumes and offers a variety of type-specific benefits. Still, research is needed to define (1) the "minimum" effective dose of exercise for mother and offspring health, as well as (2) the maximum tolerable dose from which more benefits may be seen. Additionally, there is a lack of randomized controlled trials addressing exercise doses during the three trimesters of pregnancy. Further, the protocols adopted in research studies should be more standardized and tested for efficacy in different populations of gravid women.

Myogenically differentiated mesenchymal stem cell insulin sensitivity is associated with infant adiposity at 1 and 6 months of age.

OBJECTIVE: In adults, skeletal muscle insulin sensitivity (SI ) and fatty acid oxidation (FAO) are linked with a predisposition to obesity. The current study aimed to determine the effects of maternal exercise on a model of infant skeletal muscle tissue (differentiated umbilical cord mesenchymal stem cells [MSCs]) SI and FAO and analyzed for associations with infant body composition. METHODS: Females <16 weeks' gestation were randomized to either 150 min/wk of moderate-intensity aerobic, resistance, or combination exercise or a nonexercising control. At delivery, MSCs were isolated from umbilical cords and myogenically differentiated, and SI and FAO were measured using radiolabeled substrates. Infant body fat percentage (BF%) and fat-free mass were calculated using standard equations at 1 and 6 months of age. RESULTS: MSCs from infants of all exercisers had significantly (p < 0.05) higher SI . MSC SI was inversely associated with infant BF% at 1 (r = -0.38, p < 0.05) and 6 (r = -0.65, p < 0.01) months of age. Infants with high SI had lower BF% at 1 (p = 0.06) and 6 (p < 0.01) months of age. MSCs in the high SI group had higher (p < 0.05) FAO. CONCLUSIONS: Exposure to any type of exercise in utero improves offspring SI and could reduce adiposity in early infancy.

Multitissue responses to exercise: a MoTrPAC feasibility study.

We assessed the feasibility of the Molecular Transducers of Physical Activity Consortium (MoTrPAC) human adult clinical exercise protocols, while also documenting select cardiovascular, metabolic, and molecular responses to these protocols. After phenotyping and familiarization sessions, 20 subjects (25 ± 2 yr, 12 M, 8 W) completed an endurance exercise bout (n = 8, 40 min cycling at 70% V̇o2max), a resistance exercise bout (n = 6, ∼45 min, 3 sets of ∼10 repetition maximum, 8 exercises), or a resting control period (n = 6, 40 min rest). Blood samples were taken before, during, and after (10 min, 2 h, and 3.5 h) exercise or rest for levels of catecholamines, cortisol, glucagon, insulin, glucose, free fatty acids, and lactate. Heart rate was recorded throughout exercise (or rest). Skeletal muscle (vastus lateralis) and adipose (periumbilical) biopsies were taken before and ∼4 h following exercise or rest for mRNA levels of genes related to energy metabolism, growth, angiogenesis, and circadian processes. Coordination of the timing of procedural components (e.g., local anesthetic delivery, biopsy incisions, tumescent delivery, intravenous line flushes, sample collection and processing, exercise transitions, and team dynamics) was reasonable to orchestrate while considering subject burden and scientific objectives. The cardiovascular and metabolic alterations reflected a dynamic and unique response to endurance and resistance exercise, whereas skeletal muscle was transcriptionally more responsive than adipose 4 h postexercise. In summary, the current report provides the first evidence of protocol execution and feasibility of key components of the MoTrPAC human adult clinical exercise protocols. Scientists should consider designing exercise studies in various populations to interface with the MoTrPAC protocols and DataHub.NEW & NOTEWORTHY This study highlights the feasibility of key aspects of the MoTrPAC adult human clinical protocols. This initial preview of what can be expected from acute exercise trial data from MoTrPAC provides an impetus for scientists to design exercise studies to interlace with the rich phenotypic and -omics data that will populate the MoTrPAC DataHub at the completion of the parent protocol.

Influence of Supervised Maternal Aerobic Exercise during Pregnancy on 1-Month-Old Neonatal Cardiac Function and Outflow: A Pilot Study.

PURPOSE: The objective of this study is to assess the effects of supervised, recommended levels of prenatal aerobic exercise on 1-month-old infant cardiac function. METHODS: Eligible pregnant women were randomly assigned to either an aerobic exercise group that participated in 150 min of supervised, moderate-intensity (40% to 59% V̇O 2peak , 12 to 14 on Borg rating of perceived exertion) aerobic exercise per week for 24 wk or more or a nonexercising group that consisted of 150 min·wk -1 of relaxation techniques. One-month-old infant echocardiogram was performed to assess infant cardiac function , including heart rate (HR), left-ventricular stroke volume, cardiac output, cardiac index, ejection fraction, fractional shortening, and velocity time integral at the aortic valve. Pearson correlation analyses and linear regression models were performed. RESULTS: Prenatal aerobic exercise was negatively correlated with infant resting HR ( r = -0.311, P = 0.02). Similarly, when controlling for infant sex and activity state, exercise level/volume ( ß = -0.316; 95% CI, -0.029 to -0.002; P = 0.02) predicted resting infant HR ( R2 = 0.18, P = 0.02). In infants of overweight/obese women, infants of aerobic exercisers had increased fractional shortening ( P = 0.03). In addition, infant ventricular ejection fraction was correlated with maternal exercise attendance ( r = 0.418, P = 0.03) as well as a trend for exercise level ( r = 0.351, P = 0.08). Similarly, the only significant regression model for infants of overweight/obese women controls infant activity state ( ß = -0.444; 95% CI, -0.05 to -0.01; P = 0.006) and maternal exercise level ( ß = 0.492; 95% CI, 5.46-28.74; P = 0.01) predicting infant resting HR ( F = 5.79, R2 = 0.40, P = 0.003). CONCLUSIONS: The findings of this study demonstrate that women participating in exercise in the second and third trimesters of their pregnancy may have infants with increased cardiac function at 1 month of age. Importantly, the cardiac function effects were further augmented for infants born to overweight/obese women.

Differences in substrate metabolism between African American and Caucasian infants: evidence from mesenchymal stem cells.

Type 2 diabetes is more prevalent in African American (AA) than Caucasian (C) adults. Furthermore, differential substrate utilization has been observed between AA and C adults, but data regarding metabolic differences between races at birth remains scarce. The purpose of the present study was to determine if there are racial differences in substrate metabolism evident at birth using a mesenchymal stem cells (MSCs) collected from offspring umbilical cords. Using radio-labeled tracers, MSCs from offspring of AA and C mothers were tested for glucose and fatty acid metabolism in the undifferentiated state and while undergoing myogenesis in vitro. Undifferentiated MSCs from AA exhibited greater partitioning of glucose toward nonoxidized glucose metabolites. In the myogenic state, AA displayed higher glucose oxidation, but similar fatty acid oxidation rates. In the presence of both glucose and palmitate, but not palmitate only, AA exhibit a higher rate of incomplete fatty acid oxidation evident by a greater production of acid-soluble metabolites. Myogenic differentiation of MSCs elicits an increase in glucose oxidation in AA, but not in C. Together, these data suggest that metabolic differences between AA and C races exist at birth.NEW & NOTEWORTHY African Americans, when compared with Caucasians, display greater insulin resistance in skeletal muscle. Differences in substrate utilization have been proposed as a factor for this health disparity; however, it remains unknown how early these differences manifest. Using infant umbilical cord-derived mesenchymal stem cells, we tested for in vitro glucose and fatty acid oxidation differences. Myogenically differentiated MSCs from African American offspring display higher rates of glucose oxidation and incomplete fatty acid oxidation.

Influence of aspirin on aging skeletal muscle: Insights from a cross-sectional cohort of septuagenarians.

Aspirin is one of the most commonly consumed cyclooxygenase (COX)-inhibitors and anti-inflammatory drugs and has been shown to block COX-produced regulators of inflammation and aging skeletal muscle size. We used propensity score matching to compare skeletal muscle characteristics of individuals from the Health ABC study that did not consume aspirin or any other COX-inhibiting drugs (non-consumers, n = 497, 74 ± 3 year, 168 ± 9 cm, 75.1 ± 13.8 kg, 33.1 ± 7.4% body fat, 37% women, 34% black) to those that consumed aspirin daily (and not any other COX-inhibiting drugs) and for at least 1 year (aspirin consumers, n = 515, 74 ± 3 year, 168 ± 9 cm, 76.2 ± 13.6 kg, 33.8 ± 7.1% body fat, 39% women, 30% black, average aspirin consumption: 6 year). Subjects were matched (p > 0.05) based on age, height, weight, % body fat, sex, and race (propensity scores: 0.33 ± 0.09 vs. 0.33 ± 0.09, p > 0.05). There was no difference between non-consumers and aspirin consumers for computed tomography-determined muscle size of the quadriceps (103.5 ± 0.9 vs. 104.9 ± 0.8 cm2 , p > 0.05) or hamstrings (54.6 ± 0.5 vs. 54.9 ± 0.5 cm2 , p > 0.05), or quadriceps muscle strength (111.1 ± 2.0 vs. 111.7 ± 2.0 Nm, p > 0.05). However, muscle attenuation (i.e., density) was higher in the aspirin consumers in the quadriceps (40.9 ± 0.3 vs. 44.4 ± 0.3 Hounsfield unit [HU], p < 0.05) and hamstrings (27.7 ± 0.4 vs. 33.2 ± 0.4 HU, p < 0.05). These cross sectional data suggest that chronic aspirin consumption does not influence age-related skeletal muscle atrophy, but does influence skeletal muscle composition in septuagenarians. Prospective longitudinal investigations remain necessary to better understand the influence of chronic COX regulation on aging skeletal muscle health.

Methods for analyzing infant heart rate variability: A preliminary study.

Heart rate (HR) and heart rate variability (HRV) reflect autonomic development in infants. To better understand the autonomic response in infants, reliable HRV recordings are vital, yet no protocol exists. The purpose of this paper is to present reliability of a common procedure for analysis from two different file types. In the procedure, continuous electrocardiograph recordings of 5-10 min are obtained at rest in infants at 1 month of age by using a Hexoskin Shirt-Junior's (Carre Technologies Inc., Montreal, QC, Canada). Electrocardiograph (ECG; .wav) and R-R interval (RRi; .csv) files are extracted. The RRi of the ECG signal is generated by VivoSense (Great Lakes NeuroTechnologies, Independence, OH). Two MATLAB (The MathWorks, Inc., Natick, MA) scripts converted files for analysis with Kubios HRV Premium (Kubios Oy, Kuopio, Finland). A comparison was made between RRi and ECG files for HR and HRV parameters, and then tested with t tests and correlations via SPSS. There are significant differences in root mean squared successive differences between recording types, with only HR and low-frequency measures significantly correlated together. Recording with Hexoskin and analysis with MATLAB and Kubios enable infant HRV analysis. Differences in outcomes exist between procedures, and standard methodology for infant HR analysis is needed.

Muscle group-specific skeletal muscle aging: a 5-yr longitudinal study in septuagenarians.

There is some evidence that the age-associated change in skeletal muscle mass is muscle specific, yet the number of specific muscles that have been studied to form our understanding in this area is limited. In addition, few aging investigations have examined multiple muscles in the same individuals. This longitudinal investigation compared changes in skeletal muscle size via computed tomography of the quadriceps (rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius), hamstrings (biceps femoris short and long heads, semitendinosus, and semimembranosus), psoas, rectus abdominis, lateral abdominals (obliques and transversus abdominis), and paraspinal muscles (erector spinae and multifidi) of older individuals from the Health, Aging, and Body Composition (Health ABC) study at baseline and 5.0 ± 0.1 years later (n = 469, 73 ± 3 yr and 78 ± 3 yr, 49% women, 33% black). Skeletal muscle size decreased (P < 0.05) in quadriceps (-3.3%), hamstrings (-5.9%), psoas (-0.4%), and rectus abdominis (-7.0%). The hamstrings and rectus abdominis atrophied approximately twice as much as the quadriceps (P < 0.05), whereas the quadriceps atrophied substantially more than the psoas (P < 0.05). The lateral abdominals (+5.9%) and paraspinals (+4.3%) hypertrophied (P < 0.05) to a similar degree (P > 0.05) over the 5 years. These data suggest that older individuals experience skeletal muscle atrophy and hypertrophy in a muscle group-specific fashion in the eighth decade, a critical time period in the aging process. A broader understanding of muscle group-specific skeletal muscle aging is needed to better guide exercise programs and other interventions that mitigate decrements in physical function with aging.NEW & NOTEWORTHY These longitudinal analyses of six muscle groups in septuagenarians provide novel information on the muscle group-specific aging process. Although the quadriceps, hamstrings, psoas, and rectus abdominis atrophied with different magnitudes, the lateral abdominals and paraspinals hypertrophied over the 5 years. These findings contribute to a better understanding of the skeletal muscle aging process and highlight the need to complete studies in this area with a muscle-specific focus.

Controlling Inflammation Improves Aging Skeletal Muscle Health.

Chronic inflammation is associated with a decline in aging skeletal muscle health. Inflammation also seems to interfere with the beneficial skeletal muscle adaptations conferred by exercise training in older individuals. We hypothesize that the cyclooxygenase pathway is partially responsible for this negative inflammatory influence on aging skeletal muscle health and plasticity.

Heart Rate Variability Reflects Similar Cardiac Autonomic Function in Explosive and Aerobically Trained Athletes.

Autonomic cardiac function can be indirectly detected non-invasively by measuring the variation in microtiming of heart beats by a method known as heart rate variability (HRV). Aerobic training for sport is associated with reduced risk for some factors associated with cardiovascular diseases (CVD), but effects on autonomic function in different athlete types are less known. To compare cardiac autonomic modulation using a standard protocol and established CVD risk factors in highly trained intercollegiate athletes competing in aerobic, explosive, and cross-trained sports. A total of 176 college athletes were categorized in distinct sports as explosive (EA), aerobic (AA), or cross-trained (mixed) athletes. Eight different HRV measures obtained at rest were compared across training type and five health factors: systolic (SBP), diastolic blood pressure (DBP), body weight (BW), sex, and race. All athletic types shared favorable HRV measures that correlated with low CVD risk factors and indicated normal sympathovagal balance. A significant correlation was reported between DBP and pNN50 (% RR intervals > 50 ms) (ß = -0.214, p = 0.011) and between BW and low-frequency (LF) power (ß = 0.205, p = 0.006). Caucasian and African American athletes differed significantly (p < 0.05) with respect to four HRV variables: pNN50, HF power, LF power, and LF/HF ratios. Explosive, aerobic and mixed athletes had similar cardiovascular and autonomic HRV results in all eight HRV parameters measured. All athletes reported LF and pNN50 values that were significantly correlated with two CVD risk factors: DBP and BW. Compared with Caucasian teammates, African American athletes demonstrated lower LF/HF and higher pNN50, indicating an even more favorable resting sympathovagal activity and healthy CV function.

Influence of low-dose aspirin, resistance exercise, and sex on human skeletal muscle PGE2 /COX pathway activity.

Prostaglandin (PG) E2  has been linked to increased inflammation and attenuated resistance exercise adaptations in skeletal muscle. Nonaspirin cyclooxygenase (COX) inhibitors have been shown to reduce these effects. This study examined the effect of low-dose aspirin on skeletal muscle COX production of PGE2 at rest and following resistance exercise. Skeletal muscle (vastus lateralis) biopsies were taken from six individuals (4 M/2 W) before and 3.5 hr after a single bout of resistance exercise for ex vivo PGE2 production under control and low (10 µM)- or standard (100 µM)-dose aspirin conditions. Sex-specific effects of aspirin were also examined by combining the current findings with our previous similar ex vivo skeletal muscle investigations (n = 20, 10 M/10 W). Low-dose aspirin inhibited skeletal muscle PGE2 production (p < 0.05). This inhibition was similar to standard-dose aspirin (p > 0.05) and was not influenced by resistance exercise (p > 0.05) (overall effect: -18 ± 5%). Men and women had similar uninhibited skeletal muscle PGE2 production at rest (men: 1.97 ± 0.33, women: 1.96 ± 0.29 pg/mg wet weight/min; p > 0.05). However, skeletal muscle of men was 60% more sensitive to aspirin inhibition than women (p < 0.05). In summary, the current findings 1) confirm low-dose aspirin inhibits the PGE2 /COX pathway in human skeletal muscle, 2) show that resistance exercise does not alter aspirin inhibitory efficacy, and 3) suggest the skeletal muscle of men and women could respond differently to long-term consumption of low-dose aspirin, one of the most common chronically consumed drugs in the world.

Low-dose aspirin and COX inhibition in human skeletal muscle.

Skeletal muscle health has been shown to benefit from regular consumption of cyclooxygenase (COX)-inhibiting drugs. Aspirin, especially at low doses, is one of the most commonly consumed COX inhibitors, yet investigations of low-dose aspirin effects on skeletal muscle are nonexistent. The goal of this study was to examine the efficacy of low-dose aspirin on skeletal muscle COX production of the inflammatory regulator prostaglandin (PG)E2 at rest and after exercise. Skeletal muscle biopsies (vastus lateralis) were taken from eight individuals [4 men, 4 women; 25 ± 1 yr; 81.4 ± 3.4 kg; maximal oxygen consumption (V̇o2max): 3.33 ± 0.21 L/min] before and 3.5 h after 40 min of cycling at 70% of V̇o2max for the measurement of ex vivo PGE2 production. Muscle strips were incubated in Krebs-Henseleit buffer (control) or supplemented with one of two aspirin concentrations that reflected blood levels after a low (10 µM; typical oral dose: 75-325 mg) or standard (100 µM; typical oral dose: 975-1,000 mg) dose. Low (-22 ± 5%)- and standard (-28 ± 5%)-dose aspirin concentrations both reduced skeletal muscle PGE2 production, independent of exercise (P < 0.05). There was no difference in PGE2 suppression between the two doses (P > 0.05). In summary, low-dose aspirin levels are sufficient to inhibit the COX enzyme in skeletal muscle and significantly reduce production of PGE2, a known regulator of skeletal muscle health. Aerobic exercise does not appear to alter the inhibitory efficacy of aspirin. These findings may have implications for the tens of millions of individuals who chronically consume low-dose aspirin.NEW & NOTEWORTHY This study demonstrated that even low-dose aspirin concentrations can significantly reduce the prostaglandin (PG)E2/cyclooxygenase (COX) pathway activity in human skeletal muscle and this effect is not altered during the recovery period following aerobic exercise. These findings are noteworthy since aspirin is one of the most commonly consumed drugs in the world and nonaspirin COX-inhibiting drugs have been shown to regulate skeletal muscle health in sedentary and exercise-training individuals.