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.

Ventilatory Threshold Related to V̇O 2 reserve, Heart Rate Reserve, and Rating of Perceived Exertion in a Large Varied Sample.

PURPOSE: ACSM guidelines state that aerobic exercise intensity should be 30%/40% to 89% V̇O 2 reserve (V̇O 2 R) or heart rate reserve (HRR). Determining the proper intensity within this range is the "art" of exercise prescription, often relying on rating of perceived exertion (RPE) as the adjunctive intensity modulator. Current guidelines do not consider the use of ventilatory threshold (VT) due to the need for specialized equipment and methodological issues. The purpose of this investigation was to evaluate VT related to V̇O 2peak , V̇O 2 R, HRR, and RPE across the full spectrum of very low to very high V̇O 2peak values. METHODS: Eight hundred and sixty-three records of exercise tests were retrospectively examined. Data were stratified for V̇O 2peak , activity level, age, test modality, and sex. RESULTS: When stratified for V̇O 2peak , V̇O 2 at VT (V̇O 2 vt) had a lower mean value of ~14 mL·kg -1 ·min -1 in the lowest fit, rose gradually until median V̇O 2peak , and rose steeply thereafter. When graphed relative to V̇O 2peak , V̇O 2 vt as a percentage of V̇O 2 R (VT%V̇O 2 R) resembled a U-shaped curve, with a nadir ~43% V̇O 2 R at V̇O 2peak ~40 mL·kg -1 ·min -1 . Average VT%V̇O 2 R increased to ~75% in groups with the lowest or highest V̇O 2peak . There was a large variance in the value of VT at all V̇O 2peak levels. Mean RPE at VT was 12.5 ± 0.93, regardless of V̇O 2peak . CONCLUSIONS: Given the relationship of VT as the transition from moderate- to higher-intensity exercise, these data may help the understanding of aerobic exercise prescription in persons across the spectrum of V̇O 2peak values.

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.

Physiology of the Wildland Firefighter: Managing Extreme Energy Demands in Hostile, Smoky, Mountainous Environments.

Wildland firefighters (WLFFs) are inserted as the front-line defense to minimize loss of natural resources, property, and human life when fires erupt in forested regions of the world. The WLFF occupation is physically demanding as exemplified by total daily energy expenditures that can exceed 25 MJ/day (6000 calories). WLFFs must also cope with complex physical and environmental situations (i.e., heat, altitude, smoke, compromised sleep, elevated stress) which challenge thermoregulatory responses, impair recovery, and increase short- and long-term injury/health risks while presenting logistical obstacles to nutrient and fluid replenishment. The occupation also imposes emotional strain on both the firefighter and their families. The long-term implications of wildfire management and suppression on the physical and mental health of WLFFs are significant, as the frequency and intensity of wildland fire outbreaks as well as the duration of the fire season is lengthening and expected to continue to expand over the next three decades. This article details the physical demands and emerging health concerns facing WLFFs, in addition to the challenges that the U.S. Forest Service and other international agencies must address to protect the health and performance of WLFFs and their ability to endure the strain of an increasingly dangerous work environment. © 2023 American Physiological Society. Compr Physiol 13:4587-4615, 2023.

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.

Exercise-Induced Antisenescence and Autophagy Restoration Mitigate Metabolic Disorder-Induced Cardiac Disruption in Mice.

INTRODUCTION: Metabolic disorder promotes premature senescence and poses more severe cardiac dysfunction in females than males. Although endurance exercise (EXE) has been known to confer cardioprotection against metabolic diseases, whether EXE-induced cardioprotection is associated with mitigating senescence in females remains unknown. Thus, the aim of the present study was to examine metabolic disorder-induced cardiac anomalies (cellular senescence, metabolic signaling, and autophagy) using a mouse model of obese/type 2 diabetes induced by a high-fat/high-fructose (HFD/HF) diet. METHODS: Female C57BL/6 mice (10 wk old) were assigned to three groups ( n = 11/group): normal diet group (CON), HFD/HF group, and HFD/HF diet + endurance exercise (HFD/HF + EXE) group. Upon confirmation of hyperglycemia and overweight after 12 wk of HFD/HF diet, mice assigned to HFD/HF + EXE group started treadmill running exercise (60 min·d -1 , 5 d·wk -1 for 12 wk), with HFD/HF diet continued. RESULTS: EXE ameliorated HFD/HF-induced body weight gain and hyperglycemia, improved insulin signaling and glucose transporter 4 (GLUT4) levels, and counteracted cardiac disruption. EXE reversed HFD/HF-induced myocyte premature senescence (e.g., prevention of p53, p21, p16, and lipofuscin accumulation), resulting in suppression of a senescence-associated secretory phenotype such as inflammation (tumor necrosis factor α and interleukin-1ß) and oxidative stress (protein carbonylation). Moreover, EXE restored HFD/HF-induced autophagy flux deficiency, evidenced by increased LC3-II concomitant with p62 reduction and restoration of lysosome function-related proteins (LAMP2, CATHEPSIN L, TFEB, and SIRT1). More importantly, EXE retrieved HFD/HF-induced apoptosis arrest (e.g., increased cleaved CASPASE3, PARP, and TUNEL-positive cells). CONCLUSIONS: Our study demonstrated that EXE-induced antisenescence phenotypes, autophagy restoration, and promotion of propitiatory cell removal by apoptosis play a crucial role in cardiac protection against metabolic distress-induced cardiac disruption.

Physical activity, cardiorespiratory fitness, and cardiovascular health: A clinical practice statement of the ASPC Part I: Bioenergetics, contemporary physical activity recommendations, benefits, risks, extreme exercise regimens, potential maladaptations.

Regular moderate-to-vigorous physical activity (PA) and increased levels of cardiorespiratory fitness (CRF) or aerobic capacity are widely promoted as cardioprotective measures in the primary and secondary prevention of atherosclerotic cardiovascular (CV) disease (CVD). Nevertheless, physical inactivity and sedentary behaviors remain a worldwide concern. The continuing coronavirus (COVID-19) pandemic has been especially devastating to patients with known or occult CVD since sitting time and recreational PA have been reported to increase and decrease by 28% and 33%, respectively. Herein, in this first of a 2-part series, we discuss foundational factors in exercise programming, with specific reference to energy metabolism, contemporary PA recommendations, the dose-response relationship of exercise as medicine, the benefits of regular exercise training, including the exercise preconditioning cardioprotective phenotype, as well as the CV risks of PA. Finally, we discuss the 'extreme exercise hypothesis,' specifically the potential maladaptations resulting from high-volume, high-intensity training programs, including accelerated coronary artery calcification and incident atrial fibrillation. The latter is commonly depicted by a reverse J-shaped or U-shaped curve. On the other hand, longevity data argue against this relationship, as elite endurance athletes live 3-6 years longer than the general population.

Physical activity, cardiorespiratory fitness, and cardiovascular health: A clinical practice statement of the American Society for Preventive Cardiology Part II: Physical activity, cardiorespiratory fitness, minimum and goal intensities for exercise training, prescriptive methods, and special patient populations.

The prescription of exercise for individuals with and without cardiovascular disease (CVD) should be scientifically-based yet adapted to the patient. This scientific statement reviews the clinical and physiologic basis for the prescription of exercise, with specific reference to the volume of physical activity (PA) and level of cardiorespiratory fitness (CRF) that confer significant and optimal cardioprotective benefits. Recommendations are provided regarding the appropriate intensity, frequency, and duration of training; the concept of MET-minutes per week; critical components of the exercise session (warm-up, conditioning phase, cool-down); methodologies for establishing the training intensity, including oxygen uptake reserve (V̇O2R), target heart rate derivation and rating perceived exertion; minimum and goal intensities for exercise training; and, types of training activities, including resistance training, adjunctive lifestyle PA, marathon/triathlon training, and high-intensity interval training. In addition, we discuss the rationale for and value of exercise training programs for patients with peripheral artery disease, diabetes mellitus, and heart failure.

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.

High level physical activity in cardiac rehabilitation: Implications for exercise training and leisure-time pursuits.

IMPORTANCE: Regular moderate-to-vigorous physical activity and increased levels of cardiorespiratory fitness (CRF) are widely promoted as cardioprotective measures in secondary prevention interventions. OBSERVATIONS: A low level of CRF increases the risk of cardiovascular disease (CVD) to a greater extent than merely being physically inactive. An exercise capacity <5 metabolic equivalents (METs), generally corresponding to the bottom 20% of the fitness continuum, indicates a higher mortality group. Accordingly, a key objective in early cardiac rehabilitation (CR) is to increase the intensity of training to >3 METs, to empower patients to vacate this "high risk" group. Moreover, a "good" exercise capacity, expressed as peak METs, identifies individuals with a favorable long-term prognosis, regardless of the underlying extent of coronary disease. On the other hand, vigorous-to-high intensity physical activity, particularly when unaccustomed, and some competitive sports are associated with a greater incidence of acute cardiovascular events. Marathon and triathlon training/competition also have limited applicability and value in CR, are associated with acute cardiac events each year, and do not necessarily provide immunity to the development of or the progression of CVD. Furthermore, extreme endurance exercise regimens are associated with an increased incidence of atrial fibrillation and accelerated coronary artery calcification. CONCLUSIONS AND RELEVANCE: High-intensity training offers a time-saving alternative to moderate intensity continuous training, as well as other potential advantages. Additional long-term studies assessing safety, adherence, and morbidity and mortality are required before high-intensity CR training can be more widely recommended, especially in previously sedentary patients with known or suspected CVD exercising in non-medically supervised settings.

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.