Effects of Acute Sleep Deprivation on the Physiological Response to Woodsmoke and Exercise.

OBJECTIVE: To evaluate sleep deprivation effects on the acute physiological response to a combined stressor of woodsmoke and exercise. METHODS: Ten participants completed two exercise trials (8 hours of sleep vs 4 hours) with woodsmoke. Trials were conducted in a crossover design. Key measures examined before and after each trial included heart rate variability, pulse wave velocity, blood pressure, pulmonary function testing, and oxidative stress. RESULTS: Acute sleep deprivation experienced before exercise and woodsmoke exposure did not impact metrics of heart rate variability, pulse wave velocity, pulmonary function testing, blood pressure, or oxidative stress. CONCLUSIONS: Acute sleep deprivation did not amplify physiologic metrics in response to moderate-intensity aerobic exercise with inhaled woodsmoke. Although findings do not eliminate the negative impacts of inhaling woodsmoke, more research is needed to understand the acute effects of woodsmoke exposure on the cardiovascular system. 1.

The Interaction of Duchenne Muscular Dystrophy and Insulin Resistance.

Duchenne muscular dystrophy (DMD), caused by deficiency of functional dystrophin protein, is a fatal, progressive muscle disease that frequently includes metabolic dysregulation. Herein, we explore the physiologic consequences of dystrophin deficiency within the context of obesity and insulin resistance. We hypothesized that dystrophin deficiency increases the frequency of insulin resistance, and insulin resistance potentiates muscle pathology caused by dystrophin deficiency.

Training in a Hot Environment Fails to Elicit Changes in the Blood Oxidative Stress Response.

Environmental temperature can impact exercise-induced blood oxidative stress; however, the effects of heat acclimation on this response have not been fully elucidated. The purpose of the study was to investigate the effects of hot (33°C) and room temperature (20°C) environments on post-exercise blood oxidative stress responses following 15 temperature acclimation sessions. Untrained participants (n = 38, 26 ± 7 years, VO2peak = 38.0 ± 7.2 years) completed 15 temperature acclimation sessions of a cycling bout at an intensity perceived as "hard" in either a hot (33°C) or room temperature (20°C) environment. Pre and post acclimation exercise tolerance trials were conducted, which involved cycling at 50% Wpeak for one hour. Blood sampling occurred before exercise, immediately after, two hours, and four hours after the exercise tolerance trials. Blood samples were analyzed for oxidative stress markers including lipid hydroperoxides, 8-isoprostanes, protein carbonyls, 3-nitrotyrosine, ferric-reducing ability of plasma, and Trolox-equivalent antioxidant capacity. Exercise-dependent increases were observed in lipid hydroperoxides, Trolox-equivalent antioxidant capacity, and ferric-reducing ability of plasma (p < 0.001). Considering exercise-induced elevations in markers of blood oxidative stress, there were no differences observed between environmental temperatures before or after the acclimation training period.

Indicators of increased ER stress and UPR in aged D2-mdx and human dystrophic skeletal muscles.

Duchenne muscular dystrophy (DMD) is a progressive muscle disease that results in muscle wasting, wheelchair dependence, and eventual death due to cardiac and respiratory complications. In addition to muscle fragility, dystrophin deficiency also results in multiple secondary dysfunctions, which may lead to the accumulation of unfolded proteins causing endoplasmic reticulum (ER) stress and the unfolded protein response (UPR). The purpose of this investigation was to understand how ER stress and the UPR are modified in muscle from D2-mdx mice, an emerging DMD model, and from humans with DMD. We hypothesized that markers of ER stress and the UPR are upregulated in D2-mdx and human dystrophic muscles compared to their healthy counterparts. Immunoblotting in diaphragms from 11-month-old D2-mdx and DBA mice indicated increased ER stress and UPR in dystrophic diaphragms compared to healthy, including increased relative abundance of ER stress chaperone CHOP, canonical ER stress transducers ATF6 and pIRE1α S724, and transcription factors that regulate the UPR such as ATF4, XBP1s, and peIF2α S51. The publicly available Affymetrix dataset (GSE38417) was used to analyze the expression of ER stress and UPR-related transcripts and processes. Fifty-eight upregulated genes related to ER stress and the UPR in human dystrophic muscles suggest pathway activation. Further, based on analyses using iRegulon, putative transcription factors that regulate this upregulation profile were identified, including ATF6, XBP1, ATF4, CREB3L2, and EIF2AK3. This study adds to and extends the emerging knowledge of ER stress and the UPR in dystrophin deficiency and identifies transcriptional regulators that may be responsible for these changes and be of therapeutic interest.

Hybrid and Traditional Cardiac Rehabilitation in a Rural Area: A RETROSPECTIVE STUDY.

PURPOSE: Cardiac rehabilitation is a prescribed exercise intervention that reduces cardiovascular mortality, secondary events, and hospitalizations. Hybrid cardiac rehabilitation (HBCR) is an alternative method that overcomes barriers to participation, such as travel distance and transportation issues. To date, comparisons of HBCR and traditional cardiac rehabilitation (TCR) are limited to randomized controlled trials, which may influence outcomes due to supervision associated with clinical research. Coincidental to the COVID-19 pandemic, we investigated HBCR effectiveness (peak metabolic equivalents [peak METs]), resting heart rate (RHR), resting systolic (SBP) and diastolic blood pressure (DBP), body mass index (BMI), and depression outcomes (Patient Health Questionnaire-9 [PHQ-9]). METHODS: Via retrospective analysis, TCR and HBCR were examined during the COVID-19 pandemic (October 1, 2020, and March 31, 2022). Key dependent variables were quantified at baseline (pre) and discharge (post). Completion was determined by participation in 18 monitored TCR exercise sessions and four monitored HBCR exercise sessions. RESULTS: Peak METs increased at post-TCR and HBCR ( P < .001); however, TCR resulted in greater improvements ( P = .034). The PHQ-9 scores were decreased in all groups ( P < .001), while post-SBP and BMI did not improve (SBP: P = .185, BMI: P = .355). Post-DBP and RHR increased (DBP: P = .003, RHR: P = .032), although associations between intervention and program completion were not observed ( P = .172). CONCLUSIONS: Peak METs and depression metric outcomes (PHQ-9) improved with TCR and HBCR. Improvements in exercise capacity were greater with TCR; however, HBCR did not produce inferior results by comparison, an outcome that may have been essential during the first 18 mo of the COVID-19 pandemic.

Application of a Novel Collection of Exhaled Breath Condensate to Exercise Settings.

The collection of exhaled breath condensate (EBC) is a non-invasive method for obtaining biosamples from the lower respiratory tract, an approach amenable to exercise, environmental, and work physiology applications. The purpose of this study was to develop a cost-effective, reproducible methodology for obtaining larger volume EBC samples. Participants (male: n = 10; female: n = 6; 26 ± 8 yrs.) completed a 10 min EBC collection using a novel device (N-EBC). After initial collection, a 45 min bout of cycling at 75% HRmax was performed, followed by another N-EBC collection. In a subset of individuals (n = 5), EBC was obtained using both the novel technique and a commercially available EBC collection device (R-EBC) in a randomized fashion. N-EBC volume-pre- and post-exercise (2.3 ± 0.8 and 2.6 ± 0.9 mL, respectively)-and pH (7.4 ± 0.5 and 7.4 ± 0.5, respectively) were not significantly different. When normalized for participant body height, device comparisons indicated N-EBC volumes were larger than R-EBC at pre-exercise (+12%) and post-exercise (+48%). Following moderate-intensity exercise, no changes in the pre- and post-trial values of Pentraxin 3 (0.25 ± 0.04 and 0.26 ± 0.06 pg/mL, respectively) and 8-Isoprostrane (0.43 ± 0.33 and 0.36 ± 0.24 pg/mL, respectively) concentrations were observed. In a cost-efficient fashion, the N-EBC method produced larger sample volumes, both pre- and post-exercise, facilitating more biomarker tests to be performed.

Cardiac Rehabilitation and Resting Blood Pressure: MONTANA OUTCOMES PROJECT CARDIAC REHABILITATION REGISTRY FINDINGS.

PURPOSE: Exercise-based cardiac rehabilitation (CR) is essential for treating cardiovascular disease, and modifying risk factor modification, including hypertension. Because the causes of hypertension and benefits of CR are faceted, we examined the influence of phase II CR on resting blood pressure (BP). METHODS: Outcomes straddle the release of the updated BP guidelines, and study emphases included CR session number, sex, race/ethnicity, insurance provider, and referring diagnosis. RESULTS: Patient files of 31 885 individuals uploaded to the Montana Outcomes Project registry indicated that lowered systolic and diastolic BP were further improved after the release of the revised BP guidelines. The CR session number was proportional to improvements in diastolic BP. Blood pressure improved independent of sex, although female patients exhibited lower diastolic BP before and after CR. Race/ethnicity analyses indicated that Asian and White patients experienced drops in systolic and diastolic BP, while diastolic BP was improved in Hispanic patients. Neither American Indian nor Black patients exhibited statistically altered BP. Medicare, Veterans Administration, and privately insured patients had lowered systolic and diastolic BP, while Medicaid patients had lower diastolic BP, and the uninsured had lower systolic BP. Blood pressure outcomes were generally improved independent of the primary referring diagnosis, while those with peripheral artery disease showed no improvements. CONCLUSIONS: Findings demonstrate that phase II CR is highly effective in the control of BP, although improvements are not equally distributed to all individuals according to differences in sex, race/ethnicity, and access to insurance-funded health care.

Deterioration of Lipid Metabolism Despite Fitness Improvements in Wildland Firefighters.

OBJECTIVE: Determine serum lipid and general health/fitness alterations following a 5-month wildfire suppression season. METHODS: We recruited 100 wildland firefighters (WLFFs) to a 5-month pre- to post-season observational study. Nude body mass, blood pressure (BP), grip strength, and steptest heart rate (HR) were recorded. Blood samples were collected for lipid panel analysis (total cholesterol, high density lipoproteins (HDL)-cholesterol, low density lipoproteins-cholesterol, very low density lipoproteinscholesterol, triglycerides, triglyceride:HDL-cholesterol ratio). Two-tailed dependent t tests determined statistical significance (P < 0.05). RESULTS: There were pre- to post-season changes in nude body mass (+2 ±â€Š4%, P  = 0.001), systolic BP (-2 ±â€Š10%, P  = 0.01), step-test HR (-5 ±â€Š10%, P  < 0.001), and all serum lipids (total cholesterol: +5 ±â€Š14%, P  = 0.02, HDL-cholesterol: = 1 ±â€Š17%, P  = 0.04, low density lipoproteins-cholesterol: +8 ±â€Š22%, P  = 0.02, very low density lipoproteins-cholesterol: +31 ±â€Š49%, P  < 0.001, triglycerides: +30 ±â€Š49%, P  < 0.001, triglyceride:HDL-cholesterol ratio: +37 ±â€Š58%, P  < 0.001). Pre- to post-season diastolic BP (P = 0.12) and grip strength (P = 0.60) remained stable. CONCLUSIONS: WLFFs demonstrate maladaptive serum lipids and body mass alterations despite subtle aerobic fitness improvements.

Cardiovascular and Blood Oxidative Stress Responses to Exercise and Acute Woodsmoke Exposure in Recreationally Active Individuals.

INTRODUCTION: Those who work and recreate outdoors experience woodsmoke exposure during fire season. Exercise during woodsmoke exposure harms the cardiovascular system, but the acute physiologic and biochemical responses are understudied. The purpose of this pilot laboratory-based study was to examine the effect of exercise during woodsmoke exposure on acute indicators of cardiovascular function, including heart rate variability (HRV), pulse wave velocity (PWV), blood pressure (BP), augmentation index (AIx), and blood oxidative stress. METHODS: Ten participants performed 2 moderate-intensity exercise (70% V˙O2 max) trials (clean air 0 µg·m-3, woodsmoke 250 µg·m-3) in a crossover design. HRV, PWV, BP, AIx, and blood oxidative stress were measured before, after, and 90 min after exercise for each trial. Blood oxidative stress was quantified through lipid damage (LOOH, 8-ISO), protein damage (3-NT, PC), and antioxidant capacity (TEAC). RESULTS: A 45-min woodsmoke exposure combined with moderate-intensity exercise did not result in a statistically significant difference in HRV, PWV, BP, AIx, or oxidative stress (P>0.05). CONCLUSIONS: Despite the known deleterious effects of smoke inhalation, moderate-intensity aerobic exercise while exposed to woodsmoke particulate matter (250 µg·m-3) did not result in a statistically significant difference in HRV, PWV, or blood oxidative stress in this methodologic context. Although findings do not negate the negative impact of woodsmoke inhalation, additional research approaches are needed to better understand the acute effects of smoke exposure on the cardiovascular system.

Indices of Defective Autophagy in Whole Muscle and Lysosome Enriched Fractions From Aged D2-mdx Mice.

Duchenne muscular dystrophy (DMD) is a fatal, progressive muscle disease caused by the absence of functional dystrophin protein. Previous studies in mdx mice, a common DMD model, identified impaired autophagy with lysosomal insufficiency and impaired autophagosomal degradation as consequences of dystrophin deficiency. Thus, we hypothesized that lysosomal abundance would be decreased and degradation of autophagosomes would be impaired in muscles of D2-mdx mice. To test this hypothesis, diaphragm and gastrocnemius muscles from 11 month-old D2-mdx and DBA/2J (healthy) mice were collected. Whole muscle protein from diaphragm and gastrocnemius muscles, and protein from a cytosolic fraction (CF) and a lysosome-enriched fraction (LEF) from gastrocnemius muscles, were isolated and used for western blotting. Initiation of autophagy was not robustly activated in whole muscle protein from diaphragm and gastrocnemius, however, autophagosome formation markers were elevated in dystrophic muscles. Autophagosome degradation was impaired in D2-mdx diaphragms but appeared to be maintained in gastrocnemius muscles. To better understand this muscle-specific distinction, we investigated autophagic signaling in CFs and LEFs from gastrocnemius muscles. Within the LEF we discovered that the degradation of autophagosomes was similar between groups. Further, our data suggest an expanded, though impaired, lysosomal pool in dystrophic muscle. Notably, these data indicate a degree of muscle specificity as well as model specificity with regard to autophagic dysfunction in dystrophic muscles. Stimulation of autophagy in dystrophic muscles may hold promise for DMD patients as a potential therapeutic, however, it will be critical to choose the appropriate model and muscles that most closely recapitulate findings from human patients to further develop these therapeutics.

Alterations in Metabolic and Cardiovascular Risk Factors During Critical Training in Wildland Firefighters.

OBJECTIVE: To identify physiologic stressors related to cardiovascular disease via changes in metabolic, inflammatory, and oxidative stress biomarkers during 2 weeks of preseason training in wildland firefighters (WLFFs). METHODS: Participants were recruited from a local hotshot crew and monitored during preseason training. Fitness was assessed via the Bureau of Land Management fitness challenge. Venipuncture blood was collected on days 1, 4, 8, and 11 and analyzed for changes in a lipid and glucose panel, C-reactive protein, and oxidative stress markers 8-isoprostane (8ISO), 3-nitrotyrosine (3NT), lipid hydroperoxides (LOOH), and protein carbonyls. RESULTS: The high physical demands of training resulted in significant (P < 0.05) reductions in total cholesterol, glucose, and hemoglobin A1c. A main effect for time was observed in 8ISO, 3NT, and LOOH. CONCLUSIONS: Alterations in metabolic and oxidative stress markers suggest an acute, high-intensity physical stress during WLFF preseason training.

Muscle Damage and Overreaching During Wildland Firefighter Critical Training.

OBJECTIVE: To document the effects of wildland firefighter (WLFF) critical training (CT) on physiologic markers of muscle damage and acute overreaching. METHODS: Eighteen male and three female WLFFs were studied during an 11-day CT. Upper-body (US), lower-body (LS) muscle soreness and body weight (BW) were collected daily. Blood was collected on days 1, 4, 8, and 11 to measure creatine kinase (CK), lactate dehydrogenase (LDH), cortisol, and testosterone. Skinfolds were taken on days 1 and 11 to estimate body fat (BF) and lean body weight (LBW). RESULTS: CT resulted in a significant depression in BF and elevation in LBW, while main effects of time were seen in US, LS, CK, LDH, cortisol, and testosterone/cortisol ratio (P < 0.05). CONCLUSION: These data suggest WLFFs undergo significant physiological stressors resulting in muscle soreness, damage, and possible overreaching during CT.

Exercise Preconditioning as a Cardioprotective Phenotype.

Cardiovascular disease (CVD) is potentiated by risk factors including physical inactivity and remains a leading cause of morbidity and mortality. Although regular physical activity does not reverse atherosclerotic coronary disease, precursory exercise improves clinical outcomes in those experiencing life-threatening CVD events. Exercise preconditioning describes the cardioprotective phenotype whereby even a few exercise bouts confer short-term multifaceted protection against acute myocardial infarction. First described decades ago in animal investigations, cardioprotective mechanisms responsible for exercise preconditioning have been identified through reductionist preclinical studies, including the upregulation of endogenous antioxidant enzymes, improved calcium handling, and enhanced bioenergetic regulation during a supply-demand mismatch. Until recently, translation of this research was only inferred from clinically-directed animal models of exercise involving ischemia-reperfusion injury, and reinforced by the gene products of exercise preconditioning that are common to mammalian species. However, recent clinical investigations confirm that exercise preconditions the human heart. This discovery means that simply the initiation of a remedial exercise regimen in those with abnormal CVD risk factor profiles will provide immediate cardioprotective benefits and improved clinical outcomes following acute cardiac events. In conclusion, the prophylactic biochemical adaptations to aerobic exercise are complemented by the long-term adaptive benefits of vascular and architectural remodeling in those who adopt a physically active lifestyle.

Blood oxidative stress and post-exercise recovery are unaffected byhypobaric and hypoxic environments.

Hypobaria and hypoxia exert independent effects on oxidative stress during exercise, while combined effectson the post-exercise recovery period remain unclear.Accordingly, this study examined the recovery period during lab-simulated hypoxic and hypobaric conditions following exercise-induced oxidative stress. Participants (n=13) performed 60-minutes of cycling (70% watts max) in a normobaric normoxic environment followed by a four-hour recovery under three conditions; 1000m normobaric normoxia (NN, 675mmHg), 4400m normobaric hypoxia (NH, 675mmHg), or 4400m hypobaric hypoxia (HH, 440mmHg). Blood samples collected at Pre, Post, 2-Hours (2-HR), and 4-Hours (4-HR) post-exercise were analyzed fora potential increase in biochemical modifications of proteins(protein carbonyls, PC; 3-nitrotyrosines, 3NT) lipids (lipid hydroperoxides, LOOH; 8-isoprostanes, 8-ISO), and antioxidant capacity (FRAP, TEAC). Gene transcripts (EPAS, HMOX1, SOD2, NFE2L2) were quantified by qRT-PCR from muscle biopsies taken Pre and Post exercise. Hypoxia and hypobaria had no effect throughout recovery. Post-exercise TEAC (p=0.041), FRAP (p=0.013), and 8-ISO (p=0.044) increased, while PC (p=0.002) and 3-NT (p=0.032) were decreased. LOOH was lower in Post (p=0.018) NH trial samples. Exercise-dependent increases occurred in NFE2L2 (p=0.003), HMXO1 (p<0.001), SOD2 (p=0.046), and EPAS (p=0.038). Exercise recovery under conditions of NH and HH did not impact blood oxidative stress or redox-sensitive gene transcripts.

Nutraceutical and pharmaceutical cocktails did not improve muscle function or reduce histological damage in D2-mdx mice.

Progressive muscle injury and weakness are hallmarks of Duchenne muscular dystrophy. We showed previously that quercetin (Q) partially protected dystrophic limb muscles from disease-related injury. As quercetin activates PGC-1α through Sirtuin-1, an NAD+-dependent deacetylase, the depleted NAD+ in dystrophic skeletal muscle may limit quercetin efficacy; hence, supplementation with the NAD+ donor, nicotinamide riboside (NR), may facilitate quercetin efficacy. Lisinopril (Lis) protects skeletal muscle and improves cardiac function in dystrophin-deficient mice; therefore, it was included in this study to evaluate the effects of lisinopril used with quercetin and NR. Our purpose was to determine the extent to which Q, NR, and Lis decreased dystrophic injury. We hypothesized that Q, NR, or Lis alone would improve muscle function and decrease histological injury and when used in combination would have additive effects. Muscle function of 11-mo-old DBA (healthy), D2-mdx (dystrophin-deficient), and D2-mdx mice was assessed after treatment with Q, NR, and/or Lis for 7 mo. To mimic typical pharmacology of patients with Duchenne muscular dystrophy, a group was treated with prednisolone (Pred) in combination with Q, NR, and Lis. At 11 mo of age, dystrophin deficiency decreased specific tension and tetanic force in the soleus and extensor digitorum longus muscles and was not corrected by any treatment. Dystrophic muscle was more sensitive to contraction-induced injury, which was partially offset in the QNRLisPred group, whereas fatigue was similar between all groups. Treatments did not decrease histological damage. These data suggest that treatment with Q, NR, Lis, and Pred failed to adequately maintain dystrophic limb muscle function or decrease histological damage.NEW & NOTEWORTHY Despite a compelling rationale and previous evidence to the contrary in short-term investigations, quercetin, nicotinamide riboside, or Lisinopril, alone or in combination, failed to restore muscle function or decrease histological injury in dystrophic limb muscle from D2-mdx mice after long-term administration. Importantly, we also found that in the D2-mdx model, an emerging and relatively understudied model of Duchenne muscular dystrophy dystrophin deficiency caused profound muscle dysfunction and histopathology in skeletal muscle.

Benefits and Risks of High-Intensity Interval Training in Patients With Coronary Artery Disease.

Exercise-based cardiac rehabilitation is integral to secondary prevention in patients with coronary artery disease. Recently, the effectiveness and "superiority" of high-intensity interval training (HIIT) is a purported time-saving alternative to "traditional" moderate-intensity continuous training (MICT) in cardiac rehabilitation. The rationale for HIIT adoption is, however, not fully substantiated in the scientific literature. Established guidelines for exercise testing and training, when carefully adhered to, reduce the likelihood of triggering a cardiac event or inducing musculoskeletal injury. Clinicians should likewise consider patient risk stratification and introduce HIIT as an alternative to MICT only after patients exhibit stable and asymptomatic responses to vigorous exercise training. Although HIIT adherence appears comparable with MICT during outpatient rehabilitation, compliance drops dramatically for unsupervised exercise. Despite the enthusiasm surrounding HIIT, its main advantage over MICT appears to be short-term exercise performance outcomes and indices of vascular function. Regarding benefits to cardiovascular disease risk factor modification, management of vital signs, and measures of cardiac performance, current evidence indicates that HIIT does not outperform MICT. Long-term outcomes to HIIT are currently uncertain and logistical constraints to HIIT incorporation need additional clarification. Based on these limited findings, derived from facilities and clinicians at the forefront of cardiac rehabilitation, the routine adoption of HIIT should be viewed cautiously. In conclusion, the current review highlights numerous specific research directives that are needed before the safety and effectiveness of HIIT can be confirmed and widely adopted in patients with known or suspected coronary artery disease, especially in unsupervised, nonmedical settings.

Experimental Woodsmoke Exposure During Exercise and Blood Oxidative Stress.

OBJECTIVES: The current laboratory study quantified blood oxidative stress to woodsmoke exposure. METHODS: Participants inhaled woodsmoke during three randomized crossover exercise trials (Clean Air [0 µg/m], Low Exposure [250 µg/m], and High Exposure [500 µg/m], Woodsmoke [particulate matter less than 2.5 µm, PM2.5]). Trolox equivalent antioxidant capacity (TEAC), uric acid (UA), 8-isoprostanes (8-ISO), lipid hydroperoxides (LOOH), protein carbonyls (PC), nitrotyrosine (3-NT), 8-isoprostane, and myeloperoxidase (MPO) were quantified in Pre, immediately Post, and 1- (1Hr) hour post blood samples. RESULTS: UA decreased following Low Exposure, while plasma TEAC levels increased Post and 1Hr. LOOH levels decreased 1Hr Post (High Exposure), while 8-Iso increased following both smoke trials. PC and MPO were unchanged following all trials, while 3-NT increased over Clean Air. CONCLUSION: Blood oxidative stress occurred largely independent of PM2.5 concentrations. Future studies should employ longer duration smoke and exercise combined with physiologic parameters.

Local Pressure Application Effects on Neurological and Circulatory Function.

BACKGROUND: Pain and discomfort reported during sitting is a significant problem for aviators during prolonged missions. Previous work has determined that areas of local pressure exist during prolonged sitting in UH-60 seat systems; however, no work has examined the effects of this local pressure on measures of neurological and circulatory function. METHODS: A total of 30 healthy subjects completed the study in which focal pressure was applied in three conditions (no pressure, pressure to the ischial tuberosity, and pressure to the posterior thigh). We applied pressure using a purpose-built pressure application system allowing subjects to sit in a position mimicking the sitting position in a UH-60 Black Hawk helicopter and measurements were taken before, during, and after pressure application. We measured neurological function with the soleus Hoffmann reflex and sural nerve conduction velocity, and circulatory function with dynamic infrared thermography. RESULTS: We found a decrease in soleus Hoffmann reflex by 0.87 V and 0.52 V during pressure application at the posterior thigh and ischial tuberosity, respectively. No changes in nerve conduction velocity were found among the conditions during or after pressure application. Limb temperature increased 0.42-0.44°C during pressure application, but began to return to baseline once pressure was removed. DISCUSSION: This study examined the development of neurological and circulatory alterations due to local pressure application in an aviation specific functional position. These results may be used in the development of future interventions to mitigate the negative effects of localized pressure in military aviators.Games KE, Lakin JM, Quindry JC, Weimar WH, Sefton JM. Local pressure application effects on neurological and circulatory function. Aerosp Med Hum Perform. 2018; 89(8):693-699.

Blood flow regulation and oxidative stress during submaximal cycling exercise in patients with cystic fibrosis.

BACKGROUND: The impact of blood flow regulation and oxidative stress during exercise in cystic fibrosis (CF) has yet to be investigated. METHODS: A maximal graded exercise test was conducted to determine exercise capacity (VO2 peak) and peak workload in 14 pediatric patients with mild CF (age 14±3y, FEV1 93±16 % predicted) and 14 demographically-matched controls. On a separate visit, participants performed submaximal cycling up to 60% of peak workload where brachial artery blood velocity was determined using Doppler ultrasound. Retrograde and antegrade components were further analyzed as indices of blood flow regulation. RESULTS: The cumulative AUC for retrograde velocity was lower in patients versus controls (1770±554 vs. 3440±522cm, P=0.038). In addition, an exaggerated oxidative stress response during exercise occurred in patients only (P=0.004). CONCLUSION: These data suggest that patients with mild CF exhibit impaired blood flow regulation and an exaggerated oxidative stress response to submaximal exercise.

Cardioprotective Exercise and Pharmacologic Interventions as Complementary Antidotes to Cardiovascular Disease.

Exercise and pharmacologic therapies to prevent and treat cardiovascular disease have advanced largely through independent efforts. Understanding of first-line drug therapies, findings from preclinical animal studies, and the need for research initiatives related to complementary cardioprotective exercise-pharma interventions are reviewed from the premise that contemporary cardioprotective therapies must include adjunctive exercise and lifestyle interventions in addition to pharmacologic agents.