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Impact of acute exercise on peripheral blood mononuclear cells nutrient sensing and mitochondrial oxidative capacity in healthy young adults.

ABSTRACT: Regular exercise is associated with changes in peripheral blood mononuclear cell (PBMC) proportions that have enhanced effector functions in young and old adults; however, the effects of acute exercise on PBMC nutrient sensors and metabolic function in active young adults is unknown. To fill this gap, activation status and nutrient-sensing mechanisms of PBMCs isolated from 21 healthy active adults (20-35 yr; 36.5 ± 6.3 V̇O_2peak ) were characterized before and after 30 min of moderate-to-vigorous cycling (65%-75% V̇O_2peak ). In addition, changes in PBMC mitochondrial respiratory function in response to exercise were assessed using high-resolution respirometry. There was an increase in the number of activated CD69+/CD4 (79% increase) and CD69+/CD8 (166% increase) T-cells in response to the acute bout of exercise, while the nutrient-sensing mechanisms remained unchanged. PBMC mitochondrial respiration did not increase on a cell-per-cell basis, however, mitochondrial oxidative capacity (OXPHOS) increased at the tissue level (18.6 pmol/(s*ml blood) versus 29.3 pmol/(s*ml blood); p < 0.05) in response to acute exercise. Thus, this study shows that acute exercise preferentially mobilizes activated T-cells while concomitantly increasing PBMC mitochondrial oxidative capacity at the tissue level, rather than acutely changing mitochondrial oxidative capacity at the cellular level in young adults.

SUBMITTER: Theall B

PROVIDER: S-EPMC8661513 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background Exercise is associated with a reduced risk of cardiovascular disease. Increased high-density lipoprotein cholesterol (HDL-C) levels are thought to contribute to these benefits, but much of the research in this area has been limited by lack of well-controlled subject selection and exercise interventions. We sought to study the effect of moderate and high-intensity exercise on HDL function, lipid/lipoprotein profile, and other cardiometabolic parameters in a homogeneous population where exercise, daily routine, sleep patterns, and living conditions were carefully controlled. Methods and Results Male Army recruits (n=115, age 22±0.3 years) completed a 12-week moderate-intensity exercise program. A subset of 51 subsequently completed a 15-week high-intensity exercise program. Fitness increased and body fat decreased after moderate- and high-intensity exercise (P<0.001). Moderate-intensity exercise increased HDL-C and apolipoprotein A-I levels (6.6%, 11.6% respectively), and decreased low-density lipoprotein cholesterol and apolipoprotein B levels (7.2%, 4.9% respectively) (all P<0.01). HDL-C and apolipoprotein A-I levels further increased by 8.2% (P<0.001) and 6.3% (P<0.05) after high-intensity exercise. Moderate-intensity exercise increased ABCA-1 (ATP-binding cassette transporter A1) mediated cholesterol efflux by 13.5% (P<0.001), which was sustained after high-intensity exercise. In a selected subset the ability of HDLs to inhibit ICAM-1 (intercellular adhesion molecule-1) expression decreased after the high (P<0.001) but not the moderate-intensity exercise program. Conclusions When controlling for exercise patterns, diet, and sleep, moderate-intensity exercise improved HDL function, lipid/lipoprotein profile, fitness, and body composition. A sequential moderate followed by high-intensity exercise program showed sustained or incremental benefits in these parameters. Improved HDL function may be part of the mechanism by which exercise reduces cardiovascular disease risk.

Project description:OBJECTIVES:Metabolic derangements in sepsis stem from mitochondrial injury and contribute significantly to organ failure and mortality; however, little is known about mitochondrial recovery in human sepsis. We sought to test markers of mitochondrial injury and recovery (mitochondrial biogenesis) noninvasively in peripheral blood mononuclear cells from patients with sepsis and correlate serial measurements with clinical outcomes. DESIGN:Prospective case-control study. SETTING:Academic Medical Center and Veterans Affairs Hospital. PATIENTS:Uninfected control patients (n = 20) and septic ICU patients (n = 37). INTERVENTIONS:Blood samples were collected once from control patients and serially with clinical data on days 1, 3, and 5 from septic patients. Gene products for HMOX1, NRF1, PPARGC1A, and TFAM, and mitochondrial DNA ND1 and D-loop were measured by quantitative reverse transcriptase-polymerase chain reaction. Proinflammatory cytokines were measured in plasma and neutrophil lysates. MEASUREMENTS AND MAIN RESULTS:Median (interquartile range) Acute Physiology and Chronic Health Evaluation II and Sequential Organ Failure Assessment scores were 21 (8) and 10 (4), respectively, and 90-day mortality was 19%. Transcript levels of all four genes in peripheral blood mononuclear cells were significantly reduced in septic patients on day 1 (p < 0.05), whereas mitochondrial DNA copy number fell and plasma D-loop increased (both p < 0.05), indicative of mitochondrial damage. D-loop content was directly proportional to tumor necrosis factor-α and high-mobility group protein B1 cytokine expression. By day 5, we observed transcriptional activation of mitochondrial biogenesis and restoration of mitochondrial DNA copy number (p < 0.05). Patients with early activation of mitochondrial biogenesis were ICU-free by 1 week. CONCLUSIONS:Our findings support data that sepsis-induced mitochondrial damage is reversed by activation of mitochondrial biogenesis and that gene transcripts measured noninvasively in peripheral blood mononuclear cells can serve as novel biomarkers of sepsis recovery.

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Impact of acute exercise on peripheral blood mononuclear cells nutrient sensing and mitochondrial oxidative capacity in healthy young adults.

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