Hr Of Exercise Research Articles

35 Effects of melatonin on inflammatory marker serum amyloid A in horses after exercise

Performance horses are regularly exposed to various stressors, such as training and exercise, that negatively impact their performance which may lead to increased oxidative stress (OS) and inflammation. Although important for the adaptive response, prolonged and unresolved OS and inflammation may decrease athletic performance or cause unnecessary cellular damage. Dietary supplements, such as antioxidants, have been shown to mitigate the negative effects of OS and inflammation and therefore may enhance performance. One such antioxidant that has been of interest is melatonin. The objectives of this study were to evaluate the potential of melatonin to reduce Serum Amyloid A (SAA), a sensitive inflammatory marker, in horses after exercise. Horses (n = 6) were randomly assigned to 2 groups (CON; n = 3, no supplement or MEL; n = 3, 20 g melatonin). Horses received diet based on BW (1% BW Nutrena Impact 12% Pellets and 2% BW bermudagrass hay/d). A switchback design was used, with 2 experimental trial periods lasting 14-d with a 30-d washout period in-between. Supplementation was given orally on exercise days during each trial period. Horses underwent 1.5hr of moderate-intensity exercise (avg >90 BPM), at 0700 3 d/wk. Blood was drawn before exercise (PRE), and at 30- and 90-min post-exercise. On exercise days (ED), horses received supplementation after PRE blood draw and before exercise (0630).After the washout period, the treatment groups were swapped, and the study was repeated, resulting in 12 ED total. Blood was collected via jugular venipuncture, immediately processed to separate plasma, and stored for analysis. SAA ELISA kits (Thermo Fisher Scientific Inc., Massachusetts) were used to determine blood SAA concentration. The first and last ED of each trial period were analyzed (ED1/ED6/ED7/ED12), and interactions of treatment, time, and day were analyzed with significance set at (P ≤ 0.05). PRE ED1 and 7 were set as baseline values, with no significant differences in baseline levels between treatments (P > 0.1862). There was a significant difference between treatments at 30- (P ≤ 0.01) and 90-min (P ≤ 0.01) post-exercise on ED1, 7, and 12, with average plasma SAA concentrations being lower for MEL group at all time points. There was also a treatment*day interaction for ED1 (P = 0.0005), ED7 (P = 0.0218), and ED12 (P = 0.0001), with MEL having lower SAA blood concentrations as compared with CON. Lower concentrations of SAA in MEL horses suggest melatonin supplementation may reduce inflammatory blood markers and, in turn, may suggest lower levels of inflammation in horses after exercise.

PRIOR SARS-COV-2 INFECTION DOES NOT INCREASE RISK OF EXERTIONAL HEAT STROKE OR CAUSE DETRIMENTAL CHANGES IN PLASMA CYTOKINES

BACKGROUND: SARS-CoV-2 is a viral infection that can cause systemic inflammation with fever symptoms and impaired respiration. Animal models suggest that some forms of viral infection can increase risk for exertional heatstroke (EHS), possibly via reductions in the cellular stress response. PURPOSE: To determine if persons with prior clinical diagnosis of SARS-CoV-2 infection exhibit any differences in thermoregulatory or cardiopulmonary responses to 60 min of cycling exercise in hot, dry conditions. METHODS: Nine participants (Age: 22 ± 2 years, Stature: 1.74 ± 0.02 m, Mass: 71.3 ± 3.9 kg, VO2max: 46 ± 2 mL/kg/min) completed 1 hr of cycling in an environmental chamber (35 °C / 35% RH) at an intensity that elicited 9.0 W/kg of metabolic heat production. Four participants had been previously diagnosed with SARS-CoV-2; the other five served as Control. Heart rate (HR), esophageal temperature (Tc), mean body temperature (Tb), physiological strain index (PSI), minute ventilation (Ve), and oxygen consumption (VO2) were examined throughout exercise. Interleukin 1 Receptor Antagonist (IL-1RA) and Interleukin 6 (IL-6) were assayed from plasma samples collected before (Pre), after (Post), and 1 h after (1-Post) exercise. Data were analyzed with RM-ANOVA and Tukey Post Hocs. RESULTS: As compared to Control, persons with prior SARS-CoV-2 infection did not exhibit greater elevations in HR (84 ± 4% of HRmax vs 87 ± 2% of HRmax), Tc (1.4 ± 0.3 °C vs 1.1 ± 0.2 °C), Tb (1.2 ± 0.3 °C vs 1.1 ± 0.2 °C), PSI (6.9 ± 1.0 vs 6.7 ± 0.6), Ve (38.8 ± 4.3 L/min vs 40.5 ± 0.3 L/min) or VO2 (23.8 ± 1.1 ml/kg/min vs 21.0 ± 1.4 ml/kg/min) during 1 hr of cycling exercise at a fixed rate of heat production in hot/dry ambient conditions [all P > 0.05]. There were no differences in plasma IL-1RA between the two groups at any time-point [all P > 0.05]. Despite having similar plasma IL-6 concentrations at baseline (0.5 ± 0.2 pg/ml vs 0.6 ± 0.3 pg/ml), the increase in IL-6 post-exercise was two-fold greater in Control (5.9 ± 1.6 pg/ml vs 2.8 ± 0.6 pg/ml; P = 0.04). CONCLUSIONS: Our data do not provide any evidence of an adverse response to exertional heat stress in persons with prior SARS-CoV-2 infection. Thermal and cardiovascular strain responses were not impaired. Plasma IL-6 was reduced following exercise, but the physiologic relevance of that change remains to be determined.

Select DNA Replication And Repair Genes Are Transcriptionally Modified By Acute Exercise In Hypoxia

DNA replication and repair in eukaryote cells are critical processes that ensures the correct transfer of DNA material through mitosis. Errors in the replication and repair of DNA during and following cell division may lead to genome instability. PURPOSE: To investigate the regulation of select gene transcripts aligned to DNA replication and repair following exercise in hypoxia. METHODS: Twenty-four (n = 24) apparently healthy male participants were recruited (age 28 ± 5 years; mass 74 ± 8 kg; stature 177 ± 6 cm; VO2max hypoxia 45 ± 2 ml·kg-1·min-1: normoxia 60 ± 9 ml·kg-1·min-1), and completed 1 hr of exercise at a workload corresponding to 75% of pre-determined VO2max in hypoxia (Fio2 = 0.16%), and repeated in normoxia (Fio2 = 0.21%). RNA was extracted from whole blood. Two-colour oligonucleotide microarrays [for DNA primase subunit 1 - PRIM1; Chromatin assembly factor 1 subunit B - CHAF1B; and Werner syndrome RecQ like helicase - WRN] were processed on an Agilent DNA microarray scanner, while mRNA analysis was conducted using GeneSpring software incorporating checks for data normalisation, quality control, filtering grouping (by experimental condition) and statistical analysis (paired t-test with Benjamini & Hochberg False Discovery Rate corrections for multiple comparisons). RESULTS: Exercise performed in hypoxia per se downregulated PRIM1 and CHAF1B (p = 0.03 and p = 0.01 respectively vs. pre-exercise), with no change observed in normoxia (p > 0.05). Compared with normoxia, CHAF1B and WRN were differentially downregulated following exercise in hypoxia (p = 0.05 and p = 0.05 respectively vs. pre-exercise). CONCLUSION: Acute exercise in moderate hypoxia interferes with gene transcription aligned to blood cell DNA replication and repair. Further work is necessary to ascertain the consequence of these select modifications on genome stability.

The Superoxide Scavenger And Antioxidant, L-Propionyl-carnitine, Is Metabolically Enhanced Following Exercise In Hypoxia

L-Propionyl-carnitine, a propionyl ester of L-carnitine, is known to scavenge the superoxide anion, inhibit lipid peroxidation, and protect against H2O2-induced DNA strand scission. While exogenous L-propionyl-carnitine supplementation modulates lipid peroxidation in humans, the endogenous metabolic response following exercise is currently unknown. PURPOSE: To investigate the metabolic profile of L-propionyl-carnitine following exercise in hypoxia. METHODS: Twenty-four (n=24) apparently healthy male participants were recruited (age 28 ± 5 years; mass 74 ± 8 kg; stature 177 ± 6 cm; 2max hypoxia 45 ± 2 ml·kg-1·min-1: normoxia 60 ± 9 ml·kg-1·min-1), and completed 1 hr of exercise at a workload corresponding to 75% of pre-determined 2max in hypoxia (Fio2 = 0.16%), and repeated in normoxia (Fio2 = 0.21%). Serum L-propionyl-carnitine was quantified using a LC ESI-qTOF-MS untargeted metabolomics approach at pre-, post-exercise and 3 h post-exercise (Recovery). RESULTS: Exercise performed in hypoxia and normoxia independently increased L-propionyl-carnitine metabolism (p<0.05, pre vs. post-exercise), and hypoxia per se did not induce a selective metabolic change when compared to normoxia (p>0.05). Recovery from exercise was similar for both hypoxia and normoxia (p<0.05, post vs. 3 hrs post-exercise). There was a main effect for time observed for pooled hypoxia and normoxia values (pre vs. post-exercise vs. 3 hrs post-exercise, p<0.05). CONCLUSION: This is the first data to show a metabolic response in L-propionyl-carnitine following exercise. As such, we propose the increased mobilisation of L-propionyl-carnitine may be beneficial to counteract deleterious free radical production and protect against vascular exercise-induced oxidative stress.

Gastrointestinal Effects of Exogenous Ketone Drinks are Infrequent, Mild, and Vary According to Ketone Compound and Dose.

Exogenous ketone drinks may improve athletic performance and recovery, but information on their gastrointestinal tolerability is limited. Studies to date have used a simplistic reporting methodology that inadequately represents symptom type, frequency, and severity. Herein, gastrointestinal symptoms were recorded during three studies of exogenous ketone monoester (KME) and salt (KS) drinks. Study 1 compared low- and high-dose KME and KS drinks consumed at rest. Study 2 compared KME with isocaloric carbohydrate (CHO) consumed at rest either when fasted or after a standard meal. Study 3 compared KME+CHO with isocaloric CHO consumed before and during 3.25hr of bicycle exercise. Participants reported symptom type and rated severity between 0 and 8 using a Likert scale at regular intervals. The number of visits with no symptoms reported after ketone drinks was n = 32/60 in Study 1, n = 9/32 in Study 2, and n = 20/42 in Study 3. Following KME and KS drinks, symptoms were acute but mild and were fully resolved by the end of the study. High-dose KS drinks caused greater total-visit symptom load than low-dose KS drinks (13.8 ± 4.3 vs. 2.0 ± 1.0; p < .05) and significantly greater time-point symptom load than KME drinks 1-2hr postdrink. At rest, KME drinks caused greater total-visit symptom load than CHO drinks (5.0 ± 1.6 vs. 0.6 ± 0.4; p < .05). However, during exercise, there was no significant difference in total-visit symptom load between KME+CHO (4.2 ± 1.0) and CHO (7.2 ± 1.9) drinks. In summary, exogenous ketone drinks cause mild gastrointestinal symptoms that depend on time, the type and amount of compound consumed, and exercise.

Dietary Behaviors of Amateur Endurance Athletes during Recovery from Exercise Training

PURPOSE: It is not known if amateur endurance athletes (runners, cyclists, triathletes, etc.) comply with nutrition guidelines for optimal recovery from exercise. We hypothesized that these athletes do not meet the recommendations from professional organizations for carbohydrate, protein, and fluid intake after exercise. METHODS: Data were collected by using an online questionnaire, 2-day food diaries and exercise logs. Specific post-exercise time periods in the food diaries were analyzed using computer software; nutrient intakes were compared to the published recommendations. RESULTS: Carbohydrate intake during the 30-min and 2-hr window immediately after exercise cessation was lower than recommended (24±7 vs. 70±2 g, p<0.001, 47±10 vs 70±2 g, p=0.012, respectively), as was carbohydrate intake between 2 and 4 hr after exercise (34±11 vs. 70±2 g, p=0.002) and between 4 and 6 hr (48±13 vs. 70±2 g, p=0.042); most subjects (75-88%) failed to meet the carbohydrate intake recommendations during these time periods. There was also a non-significant tendency for carbohydrate intake to be lower than recommendations in the 24 hours after exercise (390±24 vs. 419+15 g p=0.089). Protein intake within 1 hour of exercise and total daily protein intake met or exceeded the recommendations. Fluid intake within 1 hour of exercise met the recommendations. CONCLUSION: Amateur endurance athletes are not meeting the recommendations for post-exercise carbohydrate intake, specifically within 30 minutes, 2 hrs, 4 hours, and 6 hr of exercise, but they are meeting the recommendations for daily and post-exercise protein intake, and hydration status during exercise.

일회성 및 만성적 유산소운동이 초파리의 자가포식 관련 유전자 발현에 미치는 영향

자가포식은 자가포식소체에서 리소좀으로 이어지는 경로를 통해 세포내에서 일어나는 자가분해 시스템으로 다양한 질병과 관련된 운동의 효과를 설명하는데 있어 중요한 역할을 하는 것으로 알려져 있다. 하지만 현재까지 보고된 대부분의 연구는 일회성 운동 혹은 저항성 운동에 의한 자가포식만을 조사한 것으로 일회성 운동과 만성적 운동을 함께 조사한 연구는 전무하다. 따라서 본 연구의 목적은 일회성 및 만성적 유산소운동이 자가포식에 미치는 영향을 알아보는 것이다. White-eyed mutant Drosophila melanogaster를 대상으로 하여 이들을 통제집단, 일회성 운동 집단, 일주일간 하루 2시간 또는 3시간씩 운동을 실시한 집단에 무선배정 하였고, 운동은 일회성 운동과 만성적 운동으로 구성하여 실시하였다. 정량 실시간 연쇄반응을 통해 Atg1, Atg6, Atg8a 유전자의 발현을 관찰한 결과 일회성 운동은 Atg8a mRNA 발현을 유의하게 증가시켰다. 그러나 Atg1, Atg6 mRNA 발현은 일회성 운동으로 유도되지 않았다. 또한 2시간의 만성적 운동에 의해서 Atg6 mRNA 발현이 유의하게 증가되었으나 Atg1, Atg8a mRNA 발현에는 유의한 변화가 나타나지 않았다. 반면 3시간의 만성적 운동을 실시한 결과 Atg1, Atg6, Atg8a mRNA 발현이 각각 57%, 37%, 71%로 모두 유의하게 증가된 것을 관찰할 수 있었다. 본 연구의 결과를 통해서 일회성의 운동은 선별된 자가포식 관련 유전자를 모두 활성화시키지는 못하지만 선택적으로 유도한다는 사실을 확인할 수 있었고, 만성적 운동은 자가포식 관련 유전자의 발현을 증가시킨다는 사실을 확인할 수 있었다. 따라서 본 연구는 일회성 및 만성적 유산소운동이 자가포식에 미치는 영향을 규명하였으며, 자가포식 관련 유전자가 일회성 운동과 만성적 운동에 의해 차별적으로 증가한다는 사실을 확인하였다는데 의의가 있다. 향후 운동에 의한 자가포식 연구에 있어 운동 형태 및 지속시간 등을 고려한 보다 세부적이고 체계적인 연구가 수행될 필요가 있을 것이라 사료되는 바이다. Autophagy, the lysosomal degradation pathway, is an intracellular recycling system that is necessary for the metabolic benefits of exercise and for producing lasting beneficial effects of exercise in various diseases. However, the most recent studies have only examined the effect of a single bout of exercise or resistance exercise on autophagic responses. To determine the differential effects of acute and chronic exercise on the expression of autophagy-related genes in D. melanogaster, white-eyed mutant D. melanogaster were assigned randomly to four groups: control, acute exercise, 2 hr chronic exercise, and 3 hr chronic exercise. The flies were exercised using a mechanized platform known as the Power Tower. Our results revealed that a single bout of exercise resulted in increased mRNA levels of the Atg8a gene (~20%, p<0.05). However, Atg1 and Atg6 mRNA expression were not induced by acute exercise. Transcript levels of Atg6 (~29%, p<0.05) related to the nucleation of autophagosomes were significantly induced by 2 hr of chronic exercise. However, this chronic exercise was not enough to increase Atg1 and Atg8a mRNA expression. On the other hand, 3 hr of exercise for 7 days significantly increased Atg1, Atg6, and Atg8a gene expression-about 57%, 37%, and 71%, respectively (p<0.05). These results suggest that a single bout of exercise is not enough to induce full activation of selected autophagy-related genes in D. melanogaster. Our results demonstrated that chronic regular exercise induced autophagy-related gene expression, suggesting that chronic regular exercise training might be required to activate autophagic responses important for producing beneficial effects of exercise in various diseases.

F-20 Free Communication/Slide - Sex Differences in Mechanics

GXT was commonly used to evaluate aerobic fitness of athletes. However, GXT protocol was not specific to the characteristics of various racket sports such as table-tennis. Specific table-tennis test (STTT) maybe a suitable alternative assessment, although little is known regarding the difference between athletes of different performance levels. PURPOSE: The aims of this study were to validate the STTT for assessing the aerobic capability of table-tennis players, and to compare the difference between elite and non-elite players in terms of their physical fitness. METHODS: Eighteen table-tennis players participated in this study. Subjects were divided to either elite group (EG,F=3, M=3, 19.67 ± 1.03 yr; 168.83 ± 6.77 cm; 64.83 ± 11.18 kg; playing experience: 12.00 ± 1.26 yr) and non-elite group (NEG, F=3, M=9, 19.25 ± 0.97 yr; 170.08 ± 7.20 cm; 66.86 ± 10.34 kg; playing experience: 11.18 ± 0.98 yr) based on their current performance status. All subjects performed the GXT on treadmill. Indirect calorimetry was used to collect cardiopulmonary data and blood lactate concentration (LAC) was also determined throughout the test. The STTT was evaluated by using a mechanical ball thrower to control the exercise intensity. Each participant forehand topspin three position rally table-tennis trials at frequency of 60 balls/min. The test was ended when participants exhausted voluntary. The polar HR monitor was used to record HR and duration of exercise. RESULTS: For the STTT, exercise time in the EG was significantly higher than NEG. (EG: 492.00 ± 102.34 sec vs. NEG: 355.17 ± 98.41 sec, p =. 014). But there were no significant difference between two groups in the HRmax and LACpost during STTT (EG vs. NEG: 193.50 ± 9.89 vs. 186.58 ± 10.07 bpm; 8.17 ± 2.69 vs. 9.31 ± 2.02 mM). Furthermore, there were no significant difference between two groups in physiological parameters during the GXT, EG vs. NEG: VO2max = 54.60 ± 4.24 vs. 51.53 ± 8.57 ml·kg-1·min-1; HRmax= 198.33 ± 10.54 vs. 198.00 ± 11.90 bpm; LACpost = 10.12 ± 1.75 vs. 9.44 ± 3.56 mM, respectively (p > .05). CONCLUSION: The GXT can be used to assess the general fitness of athletes, but the results suggest that the STTT can be used to measure the sports related aerobic capacity of table-tennis players. This STTT can also differentiate athletes’ aerobic ability of different performance status.

Physical Activity and Cardiac Function in the Oldest Old

The relationship of physical activity (PA) and cardiac function in the oldest old remains unclear. The objective of this study was to evaluate the relationship between PA and cardiac structure and function, in the oldest old. Subjects were recruited from the Jerusalem Longitudinal Cohort Study that was initiated in 1990 and has followed an age homogeneous cohort of Jerusalem residents born in 1920-1921. A total of 496 of the subjects from the most recent set of data collection in 2005-2006 underwent echocardiography at their place of residence in addition to structured interviews and physical examination. Standard echocardiographic assessment of cardiac structure and function including ejection fraction (EF) and diastolic function as assessed by E:E' measurements was performed. PA was defined as a dichotomous (≥4 hr of light exercise weekly) and as a categorical variable (<4 hr weekly/4 hours weekly/at least 1 hr daily/sport at least twice weekly). On bivariate analysis, mean EF was lower among sedentary versus active women (55.5%±8.5% vs. 58.4%±8.3, p=0.021). No other significant differences were observed between sedentary and active subjects, for either systolic or diastolic function. After adjusting for sex, education, diabetes, ischemic heart disease, hypertension, dependence in activities of daily living, and body mass index (BMI), no significant associations were found between systolic or diastolic function, or left ventricular structure and PA. Gender-specific analyses yielded similar findings. Our study of the oldest old did not demonstrate an association between PA and cardiac structure or function.

Human Mitochondrial Biogenesis in Response to Exercise in Different Environmental Temperatures

Acute heat stress in animal and yeast models have demonstrated a down-regulation in mitochondrial function, while cold exposure in small mammal models has been linked to increased mitochondrial biogenesis in brown fat and skeletal muscle. However, evidence for temperature sensitivity of mitochondrial biogenesis in humans is lacking. PURPOSE: To determine the impact of environmental temperature in exercise induced mitochondrial biogenesis. METHODS: Twelve recreationally active males (27 ± 1 yrs, 78.1 ± 2.2 kg, 14.8 ± 1.6% fat, 4.40 ± 0.41 L/min VO2 max) completed 3 trials, each at different environmental temperatures, that included 1hr of cycling exercise at 60% workload max and 3 hrs recovery. The trials consisted of exercise and recovery in the cold (7°C, 40% humidity), room temperature (20°C, 40% humidity), and heat (33°C, 40% humidity). Muscle biopsies were obtained from the vastus lateralis before and after exercise and at the end of the three hour recovery period. Muscle was analyzed for muscle glycogen and mRNA related to mitochondrial development. Expired gases were collected during exercise and recovery to determine whole body substrate use. RESULTS: UCP3 mRNA increased with exercise (p<0.05), but was unaffected by temperature. PGC-1α increased to a greater degree (p<0.05) in the cold than in the heat. MFN2 demonstrated a trend (p=0.063) toward increasing with exercise while COX was unaffected by exercise and temperature in this protocol. Muscle glycogen decreased with exercise (p<0.05), but was no different between trials. Whole body carbohydrate oxidation was higher in the cold (p<0.05) trial during exercise and throughout recovery compared to both the hot and room temperature trials. Whole body fat oxidation was lower during exercise and higher during recovery (p<0.05) in the cold compared to both the hot and room temperature trials. CONCLUSIONS: This study reports mRNA evidence for the stimulation of mitochondrial biogenesis in response to cold exposure in humans. While additional confirmation of these results are needed, cold therapy may have potential as a novel stimulator for mitochondrial biogenesis. Sponsored by Air Force Surgeon General #FA7014-09-C-0010-P00001

Metabolic and Mitochondrial Response to Carbohydrate Feeding in the Heat

Heat stress research has demonstrated a down-regulation in mitochondrial function, while carbohydrate supplementation has been shown to attenuate the exercise induced stimulation of mitochondrial biogenesis. To date the concomitant effects of exogenous carbohydrate and exercise in the heat on metabolic mRNA has not been investigated. PURPOSE: To determine the impact of exercise induced mitochondrial biogenesis in a hot environment with and without carbohydrate supplementation. METHODS: Eight recreationally active males (23.5±1.4 yrs, 76.6±1.7 kg, 12.4±1.6% fat, 4.05±0.2 L.min-1) completed 2 trials that included 1hr of cycling exercise at 70% workload max and 3 hrs recovery. Both of these trials were conducted in a climate controlled environmental chamber (38°C and 40% RH). The trials differed by the delivery of a 6% carbohydrate containing beverage or placebo (4 ml.kg-1.hr-1). Muscle biopsies were obtained from the vastus lateralis before exercise, immediately post-exercise and at the end of the 3 hr recovery period. Muscle was analyzed for muscle glycogen and mRNA related to metabolic and mitochondrial development (PDK4, MFN2, PGC-1α, Glut4, UCP3). Expired gases were collected during exercise and recovery to determine whole body substrate use. RESULTS: Whole body substrate use and muscle glycogen utilization did not differ between trials. Carbohydrate attenuated the mRNA response in PDK4 and UCP3 (P>0.05). Exercise caused an increase in PGC-1α, and Glut4 (P>0.05) independent of exogenous carbohydrate availability. CONCLUSION: This study indicates that the provision of exogenous carbohydrate can attenuate the stimulation of mRNA expression of PDK4 and UCP3 while exercising in the heat. Similar responses have been demonstrated previously in the literature under ambient conditions. Together this suggests that heat does not modify the carbohydrate or exercise induced responses to metabolic and mitochondrial adaptations. Supported by the Office of Naval Research Grant Award N000140910850.

The Effect of Prolonged Exercise in the Heat and Subsequent Submaximal Exercise on Markers of Oxidative Stress

PURPOSE: To investigate the effect of a 3 hr exercise protocol performed in the heat followed by sub-max exercise at varying temperatures with and without fluid replacement on oxidative stress. METHODS: Thirty-two males (age; 22 ± 4 yrs, height; 1.80 ± 0.05 m, weight; 85.4 ± 10.8 kg)were divided into four cohorts (n=8) and tested in one environment (TEMP; 10, 20, 30, 40°C) while eu- and dehydrated (EUH, DEH). DEH was induced via 3 hr of intermittent exercise (< 30% VO2peak) in 50°C. In the EUH trials, fluid lost was replaced with a 0.05% NaCl-water solution (3.7 ± 0.6 liters). Volunteers recovered for 90 min (22°C), sat in their assigned TEMP for ∼30 min and then performed 30-min of cycling at 50% VO2peak (SUBMAX). Blood was drawn prior to 50°C heat exposure (PRE), after ∼30 min rest in TEMP (REST), and immediately following (SUBMAX). Plasma was stored and later assayed for lipid hydroperoxide (LOOH) and protein carbonyl (PC) concentrations. RESULTS: Subjects were euhydrated prior to each test (USG < 1.020, Posm <290 mOsm·kg-1) but lost -4% body mass in DEH trials. There was a significant main effect of exercise in the heat for both LOOH (p=0.003; EUH-PRE = 23.4±2.8; EUH-REST = 27.9±2.5; DEH-PRE = 23.4±2.3, DEH-REST = 25.9±2.7μM) and PC (p=0.009; EUH-PRE = 0.148±0.19, EUH-REST = 0.160±0.012; DEH-PRE = 0.148± 0.014, DEH-REST= 0.194±0.019 nmol/mg). There was no effect of TEMP on change in LOOH or PC following SUBMAX therefore data were collapsed across TEMP. Paired T-tests revealed no effect (p = 0.922) of EUH-SUBMAX on LOOH, however DEH-SUBMAX resulted in a significant increase in LOOH from REST (p = 0.034). There was no significant difference in PC between REST and SUBMAX in either EUH or DEH. CONCLUSIONS: In both EUH and DEH trials, prolonged intermittent exercise (3 hr) in 50°C increased two markers of oxidative stress. Despite environmental temp, subsequent submax exercise resulted in a further increase in LOOH when dehydrated. The opinions or assertions contained herein should not to be construed as official or reflecting the views of the Army or the DoD.

A Functional Murine Model of Hindlimb Demand Ischemia

To date, murine models of treadmill exercise have been used to study general exercise physiology and angiogenesis in ischemic hindlimbs. The purpose of these experiments was to develop a murine model of demand ischemia in an ischemic limb to mimic claudication in humans. The primary goal was to determine whether treadmill exercise reflected a hemodynamic picture which might be consistent with the hyperemic response observed in humans. Aged hypercholesterolemic ApoE null mice (ApoE(-/-), n = 13) were subjected to femoral artery ligation (FAL) and allowed to recover from the acute ischemic response. Peripheral perfusion of the hindlimbs at rest was determined by serial evaluation using laser Doppler imaging (LDI) on days 0, 7, and 14 following FAL. During the experiments, mice were also assessed on an established five-point clinical ischemic score, which assessed the degree of digital amputation, necrosis, and cyanosis compared to the nonischemic contralateral limb. After stabilization of the LDI ratio (ischemic limb flux/contralateral nonischemic limb flux) and clinical ischemic score, mice underwent 2 days of treadmill training (10 min at 10 m/min, incline of 10 degrees ) followed by 60 min of daily treadmill exercise (13 m/min, incline of 10 degrees ) through day 25. An evaluation of preexercise and postexercise perfusion using LDI was performed on two separate occasions following the onset of daily exercise. During the immediate 15 min postexercise evaluation, LDI scanning was obtained in quadruplicate, to allow identification of peak flux ratios. Statistical analysis included unpaired t-tests and analysis of variance. After FAL, the LDI flux ratio reached a nadir between days 1 and 2, then stabilized by day 14 and remained stable through day 25. The clinical ischemic score stabilized at day 7 and remained stable throughout the rest of the experiment. Based on stabilization of both the clinical ischemic score and LDI ratio, exercise training began on day 15. The peak 15 min postexercise LDI ratio increased significantly compared to the preexercise ratio on day 17 (0.48 +/- 0.04 vs. 0.34 +/- 0.04, p < 0.05) and day 25 (0.37 +/- 0.03 vs. 0.27 +/- 0.03, p < 0.01). Within 2 hr of exercise, the LDI ratio returned to preexercise levels on both days 17 and 25. Clinical and hemodynamic stabilization of limb perfusion is evident by 14 days after FAL. FAL followed by demand ischemia results in a reversible relative hyperemic response similar to that observed in exercising human claudicants. A murine model of FAL associated with demand ischemia may be useful to evaluate the metabolic, inflammatory, and flow-related changes associated with claudication in humans.

Development and Validation of a Food Pyramid for Swiss Athletes

Food-guide pyramids help translate nutrient goals into a visual representation of suggested food intake on a population level. No such guidance system has ever been specifically designed for athletes. Therefore, the authors developed a Food Pyramid for Swiss Athletes that illustrates the number of servings per food group needed in relation to the training volume of an athlete. As a first step, an average energy expenditure of 0.1 kcal . kg(-1) . min(-1) for exercise was defined, which then was translated into servings of different food groups per hour of exercise per day. Variable serving sizes were defined for athletes' different body-mass categories. The pyramid was validated by designing 168 daily meal plans according to the recommendations of the pyramid for male and female athletes of different body-mass categories and training volumes of up to 4 hr/d. The energy intake of the meal plans met the calculated reference energy requirement by 97% +/- 9%. The carbohydrate and protein intakes were linearly graded from 4.6 +/- 0.6-8.5 +/- 0.8 g . kg(-1) . d(-1) and 1.6 +/- 0.2-1.9 +/- 0.2 g . kg(-1) . d(-1), respectively, for training volumes of 1-4 hr of exercise per day. The average micronutrient intake depended particularly on the dietary energy intake level but was well above the dietary reference intake values for most micronutrients. No tolerable upper intake level was exceeded for any micronutrient. Therefore, this Food Pyramid for Swiss Athletes may be used as a new tool in sports nutrition education (e.g., teaching and counseling).

L-Cysteine’s Effect on Modulated Rat Brain Enzymes with Forced Swimming

Forced exercise is associated with oxidative stress, and L-cysteine (L-cys) administration reduces free-radical production. To investigate whether L-cys (5 mg/kg) intraperitoneal administration can ameliorate modulated total antioxidant status (TAS), protein concentration, and the activities of acetylcholinesterase (AChE), (Na+,K+)-ATPase, and Mg2+-ATPase in rat brain after 2 and 3 hr of forced swimming. TAS, protein, and enzyme activities were measured spectrophotometrically before and after 2 and 3 hr of exercise without or with L-cys administration. TAS concentration (55.6 +/- 1.5 vs. 42.1 +/- 1.0 vs. 37.4 +/- 1.2 micromol/L, p < .001), protein concentration (5.68 +/- 0.36 vs. 5.40 +/- 0.18 vs. 4.01 +/- 0.16 mg/ml, p < .01), and AChE activity (0.89 +/- 0.05 vs. 0.61 +/- 0.04 vs. 0.48 +/- 0.03 DeltaOD/min x mg protein, p < .001) were significantly reduced, whereas Na+,K+-ATPase (6.00 +/- 0.36 vs. 10.44 +/- 1.04 vs. 11.90 +/- 1.21 micromol phosphorus inorganic/hr x mg protein, p < .001) and Mg2+-ATPase activity (7.20 +/- 0.65 vs. 10.88 +/- 1.08 vs. 11.55 +/- 1.22 mmol phosphorus inorganic/hr x mg protein, p < .001) were statistically significantly increased after 2 and 3 hr of forced exercise. Post-L-cys administration, AChE activity was decreased (0.90 +/- 0.04 vs. 0.47 +/- 0.02 DeltaOD/min x mg protein, p < .001) and remained unaltered (0.64 +/- 0.04 vs. 0.67 +/- 0.04 DeltaOD/min x mg protein, p > .05) 2 and 3 hr postexercise (0.47 +/- 0.02 vs. 0.54 +/- 0.02 DeltaOD/min x mg protein, p > .05). Na+,K+-ATPase was decreased and remained unchanged (1.85 +/- 0.17 vs. 1.77 +/- 0.19 mumol phosphorus inorganic/hr x mg protein, p > .05) 2 and 3 hr postswimming (1.91 +/- 0.19 vs. 2.06 +/- 0.17 mumol phosphorus inorganic/hr x mg protein, p > .05). Mg2+-ATPase activity was similar with L-cys supplementation pre- vs. postswimming. L-cys administration might ameliorate modulated rat brain enzyme activities induced by free-radical production during forced swimming.

AMPK와 자식작용의 미토콘드리아 생합성 조절 기전

Increased oxidative stress by abnormal mitochondrial function can damage cell signal transduction and gene expression, and induce insulin resistance or diabetes. Autophagy, however, improve insulin resistance by clearance of malfunctioning mitochondria. Exercise also recovers the muscle dysfunction and degeneration by activating mitochondrial biogenesis. As it seems that exercise and autophagy might act as an orchestrated network to induce mitochondrial biogenesis, we investigated whether autophagy is involved in AMPK signal pathway stimulated by exercise or AICAR to increase mitochondrial biogenesis. And it showed that PGC-1 and mtTFA, but not autophagy marker LC3 mRNA expression were significantly increased by 6 hr of acute exercise. On the other hand, PGC-1 and mtTFA mRNA expression were upregulated by AICAR treatment to C2C12 myotube. However these genes were not inhibited by LC3 siRNA transfection. These results provide the evidence that autopahgy affects on mitochondrial biogenesis through different signal pathway from AMPK signal transduction.

Normobaric intermittent hypoxic exposure improves time‐trial performance in hypoxia but not in normoxia

Time-trial performance is impaired during initial exposure to normobaric hypoxia. This study determined if repeated intermittent hypoxic exposures (IHE) could ameliorate the performance impairment in hypoxia without affecting performance in normoxia. For 3 hrs a day for 6 consecutive days, 6 men (mean±SD; 21±2 yr, 178±6 cm, 76±8 kg) resided in a room at sea level (760 mmHg) where the partial pressure of inspired oxygen (PIO2) was reduced by nitrogen dilution. Daily IHE consisted of 2 hrs of rest at a PIO2 of 90 mmHg (4500 m equivalent) followed 1 hr of cycle exercise at ~55% of peak O2 uptake (VO2peak) at a PIO2 of 110 mmHg (3000 m equivalent). Before and after the 6 IHE, steady-state (SS) exercise was performed under conditions of normoxia (PIO2 = 159 mmHg) and hypoxia (PIO2 = 93 mmHg, 4300 m equivalent) for 20 min at 45% and then at 65% of VO2peak, followed by a peak effort 720 kJ time trial. From before to after IHE, SS exercise VO2, arterial oxygen saturation, and perceived exertion were not changed in either normoxia or hypoxia whereas heart rate was similarly lower (P<0.05) in both ambient conditions. Time-trial performance was improved after IHE in hypoxia (100±18 vs 89±15 min, P<0.01) but not in normoxia (71±10 vs 69±12 min, P>0.05). Because of the similarity of SS exercise responses in hypoxia and normoxia before and after IHE, the reason(s) for the time-trial performance improvement in hypoxia but not normoxia remains elusive.

Tracer Measured glucose uptake by the leg demonstrates dynamic kinetics across the working muscle

We compared two methods measuring glucose uptake, tracer measured (TMGU) and net balance (NGU). As part of a larger study, we examined the effects of exercise intensity and a 9-week leg cycle ergometer training program (5 d/w, 1 hr, 75% VO2peak) on glucose uptake by working muscles in 8 healthy male subjects (25.9±1.4 yr, 77.4±3.7 kg). Two pre-training trials (45% and 65% VO2peak, UT) and two post-training trials (same absolute workload as 65%UT VO2peak [ABT], and same relative-65% of post-training VO2peak [RLT]) were performed with the infusion of [6, 6D2] glucose. Subjects were studied 3-hr post-absorptive for 90 min at rest and during 1 hr of leg cycling exercise. Training increased VO2peak 15% (45.2±1.2 vs. 52.0±1.8 ml·kg−1·min−1, p<0.05). Glucose uptake in the leg increased from rest to exercise (P<0.05) regardless of method used (TMGU, rest=0.23 +/− 0.7, ex=2.1+/−2, NGU, rest=0.18+/−.4 ex=1.8+/−1mmol/kg/min). The methods were correlated (r=0.699, P<0.05) and TMGU is predicted 13% higher than NGU (TMGU = 1.13*NGU, P=0.01). The large between subject and time variability in measures demonstrates that glucose kinetics of working muscle is highly dynamic. Our results indicate that using TMGU is preferable when describing glucose flux across the working muscle, as the NGU method my underestimate glucose uptake. Supported by NIH, AR42906 to GAB.

AMPK regulates skeletal muscle capillarization and VEGF mRNA

AMP-activated protein kinase (AMPK) is a metabolic fuel gauge important in maintaining intracellular energy homeostasis. Vascular endothelial growth factor (VEGF) is essential in the maintenance and expansion of skeletal muscle capillarization. Both VEGF and AMPK are increased in skeletal muscle in response to acute hypoxia and exercise. Pharmacological activation of AMPK increases skeletal muscle VEGF in vitro and augments angiogenesis in response to limb ischemia in vivo. We hypothesized that AMPK regulates basal skeletal muscle capillarization and the VEGF mRNA responses to acute hypoxia and exercise. The gastrocnemius from mice overexpressing an inactive AMPK α2 isoform (AMPK DN) or wild type (WT) littermates was analyzed for capillarization and the VEGF mRNA response to 2 hr of acute systemic hypoxia (6% O2) or 1 hr of acute treadmill exercise (55% of maximum). Muscle was harvested immediately-post hypoxia or exercise. Skeletal muscle capillarization and resting VEGF mRNA were lower in AMPK DN compared to WT. Acute hypoxia increased VEGF mRNA in WT, but this response was abolished in AMPK DN. Interestingly, the increase in VEGF mRNA with acute exercise tended (p=0.07) to be greater in AMPK DN compared to WT. These data suggest that AMPK regulates skeletal muscle capillarization and VEGF mRNA expression, though the direction of VEGF mRNA regulation appears dependent upon the conditions under investigation. Supported by NIA AG-21891, AHA Mid-Atlantic 0465415U and Gatorade Sports Science Institute Student Grant

Adequacy of Fluid Ingestion in Adolescents and Adults during Moderate-Intensity Exercise

We compared ad libitum fluid consumption in adolescent (n = 15) and adult athletes (n = 34) exercising in similar environmental conditions (26.5°C, 27.3% relative humidity) and similar modes and intensities of exercise (80-85% of their age-predicted maximum heart rate). Throughout 1 hr of exercise, participants had access to sports bottles containing a sports drink (6% carbohydrate with electrolytes and identical flavoring). Sweat rate (SR) and percent dehydration were calculated from the change in body weight corrected for urine loss and fluid intake (FI). FI was significantly higher for the adults than for the adolescents. SR was also higher for the adults compared with that of the adolescents. Compared with adults, adolescents had significantly lower FI and SR, the combination of which allowed them to meet their fluid needs more closely during exercise. Minimal voluntary dehydration occurred in either group during exercise, possibly because of the nature of the exercise (noncompetitive) or the beverage characteristics (presence of sodium and sweetness) or availability of the beverage.