Acute Exercise Stress Research Articles

Ulk1 phosphorylation at S555 is not required for endurance training-induced improvements in exercise and metabolic capacity in mice.

Endurance exercise training improves exercise capacity as well as skeletal muscle and whole body metabolism, which are hallmarks of high quality-of-life and healthy aging. However, its mechanisms are not yet fully understood. Exercise-induced mitophagy has emerged as an important step in mitochondrial remodeling. Unc-51-like autophagy-activating kinase 1, ULK1, specifically its activation by phosphorylation at serine 555, was discovered as an autophagy driver and to be important for energetic stress-induced mitophagy in skeletal muscle, making it a potential mediator of the beneficial effects of exercise on mitochondrial remodeling. Here, we used CRISPR/Cas9-mediated gene editing and generated knock-in mice with a serine-to-alanine mutation of Ulk1 on serine 555. We now report that these mice displayed normal endurance capacity and cardiac function at baseline with a mild impairment in energy metabolism as indicated by an accelerated increase of respiratory exchange ratio (RER) during acute exercise stress; however, this was completely corrected by 8 wk of voluntary running. Ulk1-S555A mice also retained the exercise-mediated improvements in exercise capacity and metabolic flux. We conclude that Ulk1 phosphorylation at S555 is not required for exercise-mediated improvements of exercise and metabolic capacity in healthy mice.NEW & NOTEWORTHY We have used CRISPR/Cas9-mediated gene editing to generate Ulk1-S555A knock-in mice to show that loss of phosphorylation of Ulk1 at S555 blunted exercise-induced mitophagy and mildly impairs energy metabolism during exercise in healthy mice. However, the knock-in mice retained exercise training-mediated improvements of endurance capacity and energy metabolism during exercise. These findings suggest that exercise-induced mitophagy through Ulk1 activation is not required for the metabolic adaptation and improved exercise capacity in young, healthy mice.

Exercise Preconditioning Preserves Cardiac Function and Enhances Cardiac Recovery Following Dobutamine Stimulation in Doxorubicin-Treated Rat Hearts.

Exercise preconditioning has been shown to protect against doxorubicin (DOX)-induced cardiac dysfunction when hearts are maintained under resting conditions. However, it is unclear whether this exercise-induced protective effect is maintained when the heart is challenged with the β 1 -adrenergic receptor agonist dobutamine (DOB), which mimics acute exercise stress. Fischer 344 rats were randomly assigned to sedentary (SED) or voluntary wheel running (WR) groups for 10 weeks. At week 11, rats were treated with either 15 mg/kg DOX or saline. Five days later, ex vivo cardiac function was assessed using an isolated working heart model at baseline, during the infusion of 7.5 μg·kg -1 ·min -1 DOB, and during recovery. DOB infusion significantly increased left ventricular developed pressure (LVDP), maximal (dP/dt max ) and minimal (dP/dt min ) rate of left ventricular pressure development, and heart rate in all groups ( P < 0.05). SED + DOX also showed a lower baseline and recovery LVDP than WR + DOX (83 ± 12 vs. 109 ± 6 mm Hg baseline, 76 ± 11 vs. 100 ± 10 mm Hg recovery, P < 0.05). WR + DOX showed higher dP/dt max and lower dP/dt min when compared with SED + DOX during DOB infusion (7311 ± 1481 vs. 5167 ± 1436 mm Hg/s and -4059 ± 1114 vs.-3158 ± 1176 mm Hg/s, respectively). SED + DOX dP/dt max was significantly lower during baseline and during recovery when compared with all other groups ( P < 0.05). These data suggest that exercise preconditioning preserved cardiac function after DOX exposure even when the heart is challenged with DOB, and it appeared to preserve the heart's ability to recover from this functional challenge.

Regular moderate physical activity potentially accelerates and strengthens both the pro-inflammatory and pro-resolving lipid mediator response after acute exercise stress

The PUFA-derived lipid mediator response shifts from pro-inflammatory to inflammation resolution over time and may be modified by regular moderate exercise. This pre-post-test study aimed to compare the expression of PTGES2 (COX2) and ALOX15 in leucocytes and the plasma 5- and 15-HETE, 18-HEPE and 17-HDHA responses after unaccustomed resistance exercise between 18–35-year-old male recreational runners (n = 18) and less-active controls (n = 15). One repetition maximum (1RM) was determined for squats, 45° leg presses and leg extensions. Subsequently three sets of 8–10 repetitions were performed at 80 % 1RM and blood collected over 72 hours. PTGES2 and ALOX15 expression changed over time in runners (P = 0.016, P = 0.007) but not controls (P = 0.631, P = 0.539). 5- and 15-HETE changed over time in runners (P < 0.001, P = 0.022), but not controls (P = 0.457, P = 0.985). 18-HEPE changed in runners and controls (P < 0.001, P = 0.024), 17-HDHA changed borderline in runners (P = 0.076). In conclusion, pro-inflammatory and inflammation-resolving lipid mediators may respond sooner and more robust in recreational runners than less-active controls after strenuous resistance exercise.

THE IMPACT OF TWO GINSENG ADMINISTRATIONS ON STRESS FROM ACUTE PHYSICAL EFFORT

Panax Ginseng (GSG) may be a useful agent for treating depression and anxiety. The aim of the research was to evaluate two administrations of a product containing GSG (P-GSG) in intense acute physical stress. Healthy men were voluntarily enrolled into 4 groups: control (C) no treatment; who received placebo (P); who received P-GSG for one week (GSG1); who received P-GSG for 3 weeks (GSG3). All participants were subjected to the same type of stress: an acute and short-term intense physical effort on a cycle ergometer. The administered products were: placebo and P-GSG. The scans were: anxiety (A) and heart rate (HR). Parameters were significantly increased at C and P, for A and HR compared to GSG1 and GSG3. The greatest impact of P-GSG was on A. GSG1 compared to GSG3 had a greater impact on A and HR. In conclusion, through this study we found that Panax Ginseng, especially if taken for a longer period of time, reduces heart rate and anxiety in short-term acute intense exercise stress.

Preexercise Intermittent Passive Stretching and Vascular Function After Treadmill Exercise.

Acute aerobic exercise stress is associated with decreased endothelial function that may increase the likelihood of an acute cardiovascular event. Passive stretch (PS) elicits improvements in vascular function, but whether PS can be performed before exercise to prevent declines in vascular function remains unknown. This strategy could be directly applicable in populations that may not be able to perform dynamic exercise. We hypothesized that preexercise PS would provide better vascular resilience after treadmill exercise. Sixteen healthy college-aged males and females participated in a single laboratory visit and underwent testing to assess micro- and- macrovascular function. Participants were randomized into either PS or sham-control. Intermittent calf PS was performed by having the foot in a splinting device for a 5-minute stretch, 5-minute relaxation, repeated 4 times. Then, a staged O2 peak test was performed and 65% O2 peak calculated for subjects to run at for 30-minutes. Near-infrared spectroscopy derived microvascular responsiveness was preserved with the PS group (pre: 0.53±0.009%/s), (post: 0.56±0.012%/s; p=0.55). However, there was a significant reduction in the sham control group (pre: 0.67±0.010%/s), (post: 0.51±0.007%/s; p=0.05) after treadmill exercise. Flow mediated vasodilation (FMD) of the popliteal artery showed similar responses. In the PS group, FMD (pre: 7.23±0.74%), (post: 5.86±1.01%; p=0.27) did not significantly decline after exercise. In the sham-control group FMD (pre: 8.69±0.72), (post: 5.24±1.24%; p<0.001) was significantly reduced after treadmill exercise. Vascular function may be more resilient if intermittent PS is performed prior to moderate intensity exercise and, importantly, can be performed by most individuals.

Acute and chronic cardiovascular responses to concentric and eccentric exercise in older adults with knee osteoarthritis

PurposeMuscle contraction type in resistance exercise training may confer benefits besides strength in individuals with osteoarthritis and cardiovascular disease (CVD) risks. The purpose of the study was to explore whether Eccentric-resistance training (RT) improved hemodynamic responses to acute walking exercise stress compared to Concentric-RT among individuals with knee OA over four months.MethodsThis was a secondary analysis from a randomized, controlled, single-blinded study. Participants (N = 88; 68.3 ± 6.4 yrs; 67.4% female) were randomized to one of two work-matched resistance training (RT) programs against a non-RT control group. Pre-training and month four, participants completed a self-paced Six-Minute Walk Test (6MWT) and progressive treadmill exercise test. Heart rates, blood pressures and mean arterial pressures (MAP) were captured during each test. Antihypertensive medications use was documented at each time point.ResultsLeg strength improved in both training groups by month four (p < .05). Changes in 6MWT distance and progressive treadmill test time were not different across groups over four months. Neither Concentric or Eccentric RT produced different hemodyamic responses during the 6MWT compared to the control group post-training. However, Concentric RT was associated with 6.0%-7.4% reductions in systolic blood pressure during the graded treadmill walking test at 50%, 75% and 100% of the test time compared to Eccentric RT and the controls (p = .045). MAP values were lower at 75% and 100% of the treadmill test after Concentric RT (5.7%-6.0% reductions) compared to Eccentric RT (1.0%-2.4% reductions) and controls (1.5% and 4.0% elevations) post-training (p = .024). Antihypertensive medication use did not change in any group.ConclusionsThe repeated, progressive exposures of Concentric RT-induced blunted the hypertensive responses to acute exercise compared to Eccentric-RT. Among people with knee OA, Concentric-RT may confer strength benefits to manage OA and possibly reduce cardiovascular stress during exercise.

Lower extremity vascular responses to preexercise intermittent passive stretch and treadmill exercise

Intermittent passive stretch induces local tissue hypoxia with subsequent increases in micro- and- macrovascular shear-rate, a powerful stimulus for nitric oxide generation in endothelial cells. Acute aerobic exercise stress has been associated with decreased endothelial function of the active limb. Whether intermittent passive stretch can reduce endothelial injury and improve endothelial function if performed before exercise has yet to be shown. This work investigated the impact of preexercise intermittent passive stretch on popliteal artery flow-mediated vasodilation (FMD) and the post occlusive reactive hyperemic (PORH) response within the gastrocnemius after aerobic exercise. We hypothesized that preexercise intermittent passive stretch of the calf muscles would prevent a decline in micro- and- macrovascular function after treadmill exercise. Sixteen healthy college-aged males and females participated in a single laboratory visit and underwent a PORH test with near-infrared spectrometry and FMD test to assess micro- and- macrovascular function. Participants were split into a PS group and a sham-control group performing minimal stretch. Intermittent passive calf stretching was performed by having participants place their foot in a splinting device for a 5-minute stretch, 5-minute relaxation period, repeated four times. Pre, post treatment, and post exercise time points were used in this investigation for analysis with a two-way repeated measures ANOVA and significance set at (P≤0.05). Following the treatment protocol, participants completed a VO 2 peak test to calculate 65% VO 2 peak and ran at this intensity for 30-minutes with post measurements taking place after a brief 10–20-minute recovery period. PORH with the NIRS revealed that microvascular responsiveness was preserved with the passive stretch group (pre: 0.053±0.009 %/s -1 ), (post: 0.051±0.013 %/s -1 ). There was a significant reduction (p=0.05) in the sham control group (pre: 0.072± 0.015 %/s -1 ), (post: 0.051±0.007 %/s -1 ) after treadmill exercise. Flow mediated vasodilation of the popliteal artery showed similar responses. In the passive stretch group, %FMD (pre: 7.58±0.88 %), (post: 6.40±1.21 %; p=0.27) and shear normalized FMD did not significantly decline after exercise (pre: 7.24 E-04 ±1.50 E-04 ), (post: 5.05 E-04 ±1.25 E-04 ; p=0.83). In the sham-control group %FMD (pre: 9.31±0.72 %), (post: 4.73±1.24 %; p&lt;0.001) and normalized FMD were significantly reduced (pre: 1.06 E-03 ± 1.58 E-04 ), (post: 5.06 E-04 ±1.97 E-04 ; p&lt;0.001). Passive stretch prior to acute exercise preserved popliteal artery endothelial function and gastrocnemius microvascular reperfusion. This vasoprotection was not shown in the sham-control group after acute exercise. Passive stretch is an easy low-cost method to maintain vascular function in the face of an acute exercise stress. Future work investigating adaptations to long term training when combined with preexercise stretch would be a valuable next step. University of Wisconsin- La Crosse Start up funds This is the full abstract presented at the American Physiology Summit 2023 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.

The autonomic and nociceptive response to acute exercise is impaired in people with knee osteoarthritis

ObjectivesAn acute bout of exercise typically leads to short term exercise induced hypoalgesia (EIH), but this response is more variable in many chronic pain populations, including knee osteoarthritis (OA) and fibromyalgia (FM). There is evidence of autonomic nervous system (ANS) dysfunction in some chronic pain populations that may contribute to impaired EIH, but this has not been investigated in people with knee OA. The aim of this study was to assess the acute effects of isometric exercise on the nociceptive and autonomic nervous systems in people with knee OA and FM, compared to pain-free controls. MethodsA cross-sectional study was undertaken with 14 people with knee OA, 13 people with FM, and 15 pain free controls. Across two experimental sessions, baseline recordings and the response of the nociceptive and autonomic nervous systems to a 5-min submaximal isometric contraction of the quadriceps muscle was assessed. The nociceptive system was assessed using pressure pain thresholds at the knee and forearm. The ANS was assessed using high frequency heart rate variability, cardiac pre-ejection period, and electrodermal activity. Outcome measures were obtained before and during (ANS) or immediately after (nociceptive) the acute bout of exercise. ResultsSubmaximal isometric exercise led to EIH in the control group. EIH was absent in both chronic pain groups. Both chronic pain groups showed lower vagal activity at rest. Furthermore, people with knee OA demonstrated reduced vagal withdrawal in response to acute isometric exercise compared to controls. Sympathetic reactivity was similar across groups. DiscussionThe findings of reduced tonic vagal activity and reduced autonomic modulation in response to isometric exercise raise the potential of a blunted ability to adapt to acute exercise stress and modulate nociception in people with knee OA. The impairment of EIH in knee OA may, in part, be due to ANS dysfunction.

Molecular and physiological responses predict acclimation limits in juvenile brook trout (Salvelinus fontinalis).

Understanding the resilience of ectotherms to high temperatures is essential because of the influence of climate change on aquatic ecosystems. The ability of species to acclimate to high temperatures may determine whether populations can persist in their native ranges. We examined physiological and molecular responses of juvenile brook trout (Salvelinus fontinalis) to six acclimation temperatures (5, 10, 15, 20, 23 and 25°C) that span the thermal distribution of the species to predict acclimation limits. Brook trout exhibited an upregulation of stress-related mRNA transcripts (heat shock protein 90-beta, heat shock cognate 71 kDa protein, glutathione peroxidase 1) and downregulation of transcription factors and osmoregulation-related transcripts (nuclear protein 1, Na+/K+/2Cl- co-transporter-1-a) at temperatures ≥20°C. We then examined the effects of acclimation temperature on metabolic rate (MR) and physiological parameters in fish exposed to an acute exhaustive exercise and air exposure stress. Fish acclimated to temperatures ≥20°C exhibited elevated plasma cortisol and glucose, and muscle lactate after exposure to the acute stress. Fish exhibited longer MR recovery times at 15 and 20°C compared with the 5 and 10°C groups; however, cortisol levels remained elevated at temperatures ≥20°C after 24 h. Oxygen consumption in fish acclimated to 23°C recovered quickest after exposure to acute stress. Standard MR was highest and factorial aerobic scope was lowest for fish held at temperatures ≥20°C. Our findings demonstrate how molecular and physiological responses predict acclimation limits in a freshwater fish as the brook trout in the present study had a limited ability to acclimate to temperatures beyond 20°C.

Does Acute Exercise Stress Affect Postural Stability and Cognitive Function in Subjects with Chronic Ankle Instability?

Altered postural control in people with chronic ankle instability (CAI) may be attributed to deficits that are associated with neurocognitive function. Acute training is another factor that may negatively affect postural control and increase the risk of ankle sprain. The purpose of this investigation was to determine the effect of acute exercise on postural stability and cognitive function among patients with CAI. Fifteen patients with CAI (aged 21.5 ± 2.0 years) and 15 healthy controls (aged 20.3 ± 1.7 years) completed a single-limb stance postural control test and a battery of computer-based cognitive tests before and after acute exercise. The overall stability index (OSI) was used as a measure of postural stability. The cognitive domains tested were global cognitive score, executive function, attention, visual-spatial perception, information processing, and fine motor control. Subjects in both groups had similar OSI scores, with a trend for reduced stability in the CAI after the exercise protocol (p = 0.053). There were no differences between the groups in all cognitive domains before or after exercise. Following exercise, the domains of overall cognitive score, visual-spatial perception, and information processing speed improved in both groups (p = 0.003, p = 0.033, p = 0.001; respectively). These findings should be considered with caution due to the heterogeneity of the CAI population.

Combat and blast exposure blunt sympathetic response to acute exercise stress in specialised military men.

Electrodermal activity (EDA)-a measure of electrical skin conductance reflecting (exclusive) sympathetic control of the eccrine sweat gland-holds promise as an indicator of central sympathetic activation. The aim of this study was to determine whether combat and blast exposure modulate the EDA response to acute exercise stress in specialised military men. Fifty-one men (age M=36.1, SD=6.5) participated in this study as part of the Explosive Ordnance Disposal Operational Health Surveillance System. The EDA complex (i.e., tonic+phasic conductance) was continuously measured throughout a maximal effort, graded exercise test. As expected, exercise stress resulted in measurable, stepwise increases in EDA before tapering at higher exercise intensities. Individuals with more substantial combat exposure and those with blast exposure demonstrated blunted EDA patterns in comparison to their low/nonexposed counterparts. This blunted pattern might imply sub-optimal sympathetic nervous system function in the exposed cohorts and enhances our knowledge of factors influencing resilience in these men.

Withdrawal

Electrodermal activity (EDA) - a measure of electrical skin conductance reflecting (exclusive) sympathetic control of the eccrine sweat gland - holds promise as an indicator of central sympathetic activation. The aim of this study was to determine whether combat and blast exposure modulate the EDA response to acute exercise stress in specialized military men. Sixty-four men (Age M = 34.0, SD = 7.2) participated in this study as part of the Explosive Ordnance Disposal Operational Health Surveillance System. The EDA complex (i.e., tonic + phasic conductance) was continuously measured throughout a maximal effort, graded exercise test. As expected, exercise stress resulted in measurable, stepwise increases in EDA before tapering at higher exercise intensities. Individuals with more substantial combat exposure and those with blast exposure demonstrated blunted EDA patterns in comparison to their low/non-exposed counterparts. This blunted pattern might imply sub-optimal sympathetic nervous system function in the exposed cohorts and enhances our knowledge of factors influencing resilience in these men. This article is protected by copyright. All rights reserved.

Stress-related Genetic Variants Modulate Electrodermal Response To Maximal Exercise

Previous research from our lab established electrodermal activity (EDA) as a valid, surrogate marker of sympathetic nervous system activity during treadmill exercise. We have subsequently reported dose dependent effects of aerobic fitness, combat exposure and blast exposure on the electrodermal response to acute exercise stress. PURPOSE: As an extension of our prior work, this study evaluated the effect of stress related genetic variants on EDA during maximal exercise in specialized military men. METHODS: Sixty-four male (age = 34.2±7.0 yrs) Explosive Ordnance Disposal operators completed a graded exercise test to assess maximal oxygen consumption (VO2max). EDA was recorded at baseline, during exercise and recovery. Percent change from baseline was calculated for stages of 25, 50, 75 and 100% VO2max, and active and seated recovery. Genetic variants of catechol-o-methyltransferase (COMT), brain-derived neurotrophic factor (Val66Met) and serotonin transporter (5HTTLPR) were determined from saliva. Combination groups of 2 (COMT + Val66Met) or 3 (COMT + Val66Met + 5HTTLPR) variants (2 or 3GCOM) were created and divided into “low” and “high” EDA groups. A 2 or 3 (GCOM) x 6 (STAGE) repeated measures ANOVA evaluated EDA changes across stages for 2 or 3GCOM groups, separately. RESULTS: All GCOM groups showed linear increases in EDA percent change throughout exercise. Low 2GCOM response peaked at 75% VO2max and plateaued in recovery. High 2GCOM had a larger change, peaked at 100% VO2max then declined in recovery. There was a borderline main effect of 2GCOM (p=.06, ηp2=.108) and a main effect of STAGE (p<.001, ηp2=.183). Low 3GCOM had a similar pattern as low 2GCOM, but on a smaller scale. High 3GCOM demonstrated the largest change in magnitude, peaked at 100% VO2max and sharply declined in recovery. There was a 3GCOM x STAGE interaction effect (p<.001, ηp2=.352). CONCLUSION: When combined, genetic variants implicated in the human stress response modulate EDA during and after maximal exercise. Influence of COMT was expected, as EDA is a proxy of plasma catecholamine levels during exercise. Val66Met and 5HTTLPR have been shown to modulate exercise responses and cardiovascular reactivity, respectively. Future work will comprehensively evaluate biobehavioral characteristics and genetic variants in this sample.

Cell-free DNA release under psychosocial and physical stress conditions

The understanding of mechanisms linking psychological stress to disease risk depend on reliable stress biomarkers. Circulating cell-free DNA (cfDNA) has emerged as a potential biomarker of cellular stress, aging, inflammatory processes, and cell death. Recent studies indicated that psychosocial stress and physical exercise might also influence its release. We compared the effects of acute psychosocial and physical exercise stress on cfDNA release by exposing 20 young, healthy men to both an acute psychosocial laboratory stressor and an acute physical exercise stressor. Venous blood and saliva samples were collected before and after stress exposure. Cell-free DNA was extracted from plasma and quantified by qPCR. Furthermore, cfDNA fragment length was analyzed and cfDNA methylation patterns were assayed across time. In addition, release of stress hormones and subjective stress responses were measured. Results showed a twofold increase of cfDNA after TSST and fivefold increase after exhaustive treadmill exercise, with an overabundance of shorter cfDNA fragments after physical exhaustion. Interestingly, cell-free mitochondrial DNA showed similar increase after both stress paradigms. Furthermore, cfDNA methylation signatures—used here as a marker for diverse cellular origin—were significantly different post stress tests. While DNA methylation decreased immediately after psychosocial stress, it increased after physical stress, suggesting different cellular sources of active DNA release. In summary, our results suggest stimulus and cell-specific regulation of cfDNA release. Whereas the functional role of stress-associated cfDNA release remains elusive, it might serve as a valuable biomarker in molecular stress research as a part of the psychophysiological stress response.

Combat Exposure Blunts Sympathetic Response to Acute Exercise Stress in Explosive Ordnance Disposal Personnel

Electrodermal activity (EDA) is a valid proxy of sympathetic nervous system activity during exercise and thus possesses the translational potential for studying the effects of acute and chronic stress. PURPOSE: To evaluate the effect of combat exposure (CE) on the EDA response to acute exercise stress in chronically stressed military men. METHODS: Thirty-six healthy military men (mean age: 37.0±6.9 yr) completed a graded exercise test to assess maximal oxygen consumption (VO2max). EDA was recorded at baseline and during exercise (25, 50, 75, 100% VO2max) and recovery. A tertile split of CE levels established three exposure groups: low CE (n=12), medium CE (n=12), and high CE (n=12). A 3 (group) × 6 (stage) repeated-measures analysis of variance evaluated EDA changes across stages of exercise, as well as between CE levels. RESULTS: Baseline EDA values for high, medium, and low CE did not differ (p>0.05). From 25% to 100% VO2max, mean percent changes in EDA from baseline were +85.2 to +121.6%, with a subsequent decline in seated recovery (+105.8%) (p<0.001, ηp2 =0.28). An interaction between CE and exercise workload was observed (p=0.022, ηp2 =0.13). Specifically, low CE displayed a steep linear increase in EDA from 25% to 100% VO2max, followed by a steady decrease into recovery. In contrast, the high CE EDA response was blunted, with a peak occurring at 75% VO2max, after which it declined through 100% VO2max. The medium CE EDA response mirrored low CE until 75% VO2max, and then declined through seated recovery. CONCLUSION: Dose-dependent effects of CE were demonstrated on EDA response to exercise stress. The low-CE pattern is consistent with the literature characterizing healthy plasma catecholamine responses during exercise stress, as well as with our prior research illustrating EDA responses in aerobically fit individuals. High- CE individuals, by contrast, exhibit a less adaptive response. Collectively, these findings imply that CE disrupts the sympathetic response to acute exercise stress.

Aerobic Exercise and Environmental Heat Stress as Adjuvants to Seasonal Influenza Vaccine

Influenza strain diversity and variability and individual immune health contribute to reduced vaccine efficacy. Among adjuvants that enhance vaccine effectiveness, several studies have examined the relationship between acute exercise stress and influenza vaccination immune responses in humans. It is proposed that acute bouts of stress enhance immune response, but optimal intervention, timing of intervention, and mechanisms have yet to be identified. As Toll‐like receptor (TLR) agonists enhance innate immune responses and support development of chronic humoral responses, exercise induced release of the TLR4 ligand lipopolysaccharide (LPS) into circulation may be a mechanism for benefit of pre‐vaccine exercise. This study aimed to assess the effects of exercise and exercise‐heat stress completed before seasonal influenza vaccination (IV) on short‐ and long‐term immune responses. Thirty‐four males (body mass, 77.41±12.48kg; age, 21.5±4.4y; maximal aerobic capacity (VO2max), 43.53±8.24mL/kg/min) were randomized into 1 of 3 groups: no exercise (NE, n=12) or 60 minutes of 60%VO2max exercise with (MEH, n=11) or without (ME, n=11) environmental heat stress. Exercise and baseline blood samples were completed 25.11±5.92h before IV, and subsequent blood samples were collected 23.45±6.13h, 13.06±2.96d, and 29.54±3.73d following IV. Exercise environmental conditions were different between ME and MEH, respectively (average wet bulb globe temperature, 32.91±2.67°C, 41.21±2.88°C; p&lt;0.001), but physiological stress was similar (average rectal temperature, 37.30±0.48°C, 27.61±1.36°C, p=0.513; heart rate, 114±105bpm, 118±105bpm, p=0.103) due to controlled exercise intensity. On‐going research will utilize hemagglutinin inhibition, cortisol, and LPS assays to quantify virus‐specific antibody responses, stress, and TLR4 activation respectively. Understanding innate and humoral responses will elucidate the potential of exercise and exercise‐heat stressors as adjuvants for IV.Support or Funding InformationNew investigator start‐up, InCHIP Interdisciplinary Seed GrantThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effects of acute physical exercise on oxidative stress and inflammatory status in young, sedentary obese subjects.

Circulating oxidative stress and pro-inflammatory markers change after regular physical exercise; however, how a short session of acute physical activity affects the inflammatory status and redox balance in sedentary individuals is still unclear. Aim of this study is to assess antioxidant and inflammatory parameters, both at rest and after acute exercise, in sedentary young men with or without obesity. Thirty sedentary male volunteers, aged 20–45 (mean age 32 ± 7 years), were recruited, divided into 3 groups (normal weight: BMI < 25 kg/m2; overweight to moderate obesity: 25–35 kg/m2; severe obesity: 35–40 kg/m2), and their blood samples collected before and after a 20-min run at ~ 70% of their VO2max for the measurement of Glutathione Reductase, Glutathione Peroxidase, Superoxide Dismutase, Total Antioxidant Status (TAS) and cytokines (IL-2, IL-4, IL-6, IL-8, IL-10, IL-1α, IL-1β, TNFα, MCP-1, VEGF, IFNγ, EGF). Inter-group comparisons demonstrated significantly higher Glutathione Reductase activity in severely obese subjects in the post-exercise period (P = 0.036), and higher EGF levels in normal weight individuals, either before (P = 0.003) and after exercise (P = 0.05). Intra-group comparisons showed that the acute exercise stress induced a significant increase in Glutathione Reductase activity in severely obese subjects only (P = 0.007), a significant decrease in MCP-1 in the normal weight group (P = 0.02), and a decrease in EGF levels in all groups (normal weight: P = 0.025, overweight/moderate obesity: P = 0.04, severe obesity: P = 0.018). Altogether, these findings suggest that in sedentary individuals with different ranges of BMI, Glutathione Reductase and distinct cytokines are differentially involved into the adaptive metabolic changes and redox responses induced by physical exercise. Therefore, these biomarkers may have the potential to identify individuals at higher risk for developing diseases pathophysiologically linked to oxidative stress.

Exercise, Nrf2 and Antioxidant Signaling in Cardiac Aging.

Aging is represented by a progressive decline in cellular functions. The age-related deformities in cardiac behaviors are the loss of cardiac myocytes through apoptosis or programmed cell death. Oxidative stress (OS) and its deleterious consequence contribute to age-related mechanical remodeling, reduced regenerative capacity, and apoptosis in cardiac tissue. The pathogenesis of OS in the elderly can predispose the heart to other cardiac complications such as atherosclerosis, hypertension, ischemic heart disease, cardiac myopathy, and so on. At the molecular level, oxidant-induced activation of Nrf2 (Nuclear erythroid-2-p45-related factor-2), a transcription factor, regulates several genes containing AREs (Antioxidant Response Element) and bring the respective translates to counteract the reactive radicals and establish homeostasis. Myriad of Nrf2 gene knockout studies in various organs such as lung, liver, kidney, brain, etc. have shown that dysregulation of Nrf2 severely affects the oxidant/ROS sensitivity and predispose the system to several pathological changes with aberrant cellular lesions. On the other hand, its gain of function chemical interventions exhibited oxidant stress resistance and cytoprotection. However, thus far, only a few investigations have shown the potential role of Nrf2 and its non-pharmacological induction in cardiac aging. Therefore, here we review the involvement of Nrf2 signaling along with its responses and ramifications on the cascade of OS under acute exercise stress (AES), moderate exercise training (MET), and endurance exercise stress (EES) conditions in the aging heart.

Dexamethasone rapidly inhibits glucose uptake via non-genomic mechanisms in contracting myotubes

Glucocorticoids (GCs) are a class of steroid hormones that regulate multiple aspects of glucose homeostasis. In skeletal muscle, it is well established that prolonged GC excess inhibits glucose uptake and utilization through glucocorticoid receptor (GR)-mediated transcriptional changes. However, it remains obscure that whether the rapid non-genomic effects of GC on glucose uptake are involved in acute exercise stress. Therefore, we used electric pulse stimulation (EPS)-evoked contracting myotubes to determine whether the non-genomic actions of GC were involved and its underlying mechanism(s). Pretreatment with dexamethasone (Dex, 10 μM) significantly prevented contraction-stimulated glucose uptake and glucose transporter 4 (Glut4) translocation within 20 min in C2C12 myotubes. Neither GC nuclear receptor antagonist (RU486) nor protein synthesis inhibitor (cycloheximide, Chx) affected the rapid inhibition effects of Dex. AMPK and CaMKII-dependent signaling pathways were associated with the non-genomic effects of Dex. These results provide evidence that GC rapidly suppresses glucose uptake in contracting myotubes via GR-independent non-genomic mechanisms. AMPK and CaMKII-mediated Glut4 translocation may play a critical role in GC-induced rapid inhibition of glucose uptake.

The Influence of Different Training Programs on the Expression of Plasma Proenkephalin Peptide F in Women

To date there are no studies that have examined peptide F’s acute and chronic response to different exercise modalities in women in a single study. PURPOSE: To investigate the acute and chronic effects of resistance exercise (RE) and different exercise modalities on peptide F concentrations in women. METHODS: Fifty-nine healthy recreationally active women were recruited and matched for age, body mass, height, strength, and peak O2 consumption (VO2peak) and then randomly assigned to one of four training groups: control group (CN); endurance exercise only training group (EE), resistance exercise only training group (RT), and combined endurance and resistance exercise training group (CB). The treatment groups trained three days a week for eight weeks. The control group did not complete any training, but was tested at the same time points as the three treatment groups. Proenkephalin peptide F concentrations were measured prior to and following an intense acute resistance exercise test (ARET) both before and after training. A four (group) x two (time) block analysis of variance (ANOVA) was for analysis. Significance was set a priori at p≤0.05. RESULTS: Before training there were no significant differences in the concentration (pmol/ml) of plasma proenkephalin peptide F for any of the groups. For each treatment group, after training, peptide F concentration was significantly greater post- exercise than pre-exercise. In addition, peptide F in the EE and CB groups increased both pre-and post-exercise compared to their corresponding values before training. For the RT group peptide F increased post-exercise, but not pre-exercise compared to the before training values. Compared to the control group all of the treatment groups after training had a significantly greater concentration of peptide F post-exercise compared to the corresponding value for the control group. The CB group after training had a significantly greater concentration of peptide F than the other two (EE, RT) treatment groups. CONCLUSION: There are differential responses to different training programs from young, healthy, untrained women to acute and chronic resistance exercise stress after training. Training-induced adaptations appear to occur in the adrenal gland leading to changes in the circulating concentrations of proenkephalin Peptide F.