Sedentary Males Research Articles

Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans

Hypoxic preconditioning prevents cerebrovascular/cardiovascular disorders by increasing resistance to acute ischemic stress, but severe hypoxic exposure disturbs vascular hemodynamics. This study compared how various exercise regimens with/without hypoxia affect hemodynamics and oxygenation in cardiac, muscle, and cerebral tissues during severe hypoxic exposure. Sixty sedentary males were randomly divided into five groups. Each group (n = 12) received one of five interventions: 1) normoxic (21% O(2)) resting control, 2) hypoxic (15% O(2)) resting control, 3) normoxic exercise (50% maximum work rate under 21% O(2); N-E group), 4) hypoxic-relative exercise (50% maximal heart rate reserve under 15% O(2); H-RE group), or 5) hypoxic-absolute exercise (50% maximum work rate under 15% O(2); H-AE group) for 30 min/day, 5 days/wk, for 4 wk. A recently developed noninvasive bioreactance device was used to measure cardiac hemodynamics, and near-infrared spectroscopy was used to assess perfusion and oxygenation in the vastus lateralis (VL)/gastrocnemius (GN) muscles and frontal cerebral lobe (FC). Our results demonstrated that the H-AE group had a larger improvement in aerobic capacity compared with the N-E group. Both H-RE and H-AE ameliorated the suppression of cardiac stroke volume and the GN hyperemic response (Delta total Hb/min) and reoxygenation rate by acute 12% O(2) exposure. Simultaneously, the two hypoxic interventions enhanced perfusion (Delta total Hb) and O(2) extraction [Delta deoxyHb] of the VL muscle during the 12% O(2) exercise. Although acute 12% O(2) exercise decreased oxygenation (Delta O(2)Hb) of the FC, none of the 4-wk interventions influenced the cerebral perfusion and oxygenation during normoxic/hypoxic exercise tests. Therefore, we conclude that moderate hypoxic exercise training improves cardiopulmonary fitness and increases resistance to disturbance of cardiac hemodynamics by severe hypoxia, concurrence with enhancing O(2) delivery/utilization in skeletal muscles but not cerebral tissues.

Hypoxic Exercise Training Improved Gardos Channel‐Mediated Erythrocyte Deformability

Erythrocyte deformability is an important player in blood rheology. Gardos channel (Ca2+‐activated K+ channel) regulates erythrocyte deformability by employing the ions‐mediated cytoskeleton proteins. This study investigated whether hypoxic exercise training affects Gardos channel‐mediated erythrocyte deformability and further explores its underlying mechanisms. Ten sedentary males were trained on a bicycle ergometer at 60%VO2max under 15%O2 air condition for 30 minutes per day, 5 days per week for 5 weeks. Erythrocyte deformability was determined by dynamic flow ektacytometer, whereas erythrocyte cell volume, Gardos channel performance, and cytoskeleton protein levels were evaluated by the flow cytometry. Our results demonstrated that at pre‐training stage, acute 12%O2 exercise declined erythrocyte deformability mediated by Gardos channel, which was accompanied by erythrocyte shrinkage and decreases in sprectrin and actin levels of erythrocytes. However, 5 weeks of 15%O2 exercise training enhanced Gardos channel‐mediated erythrocyte deformability and increased erythrocyte cytoskeleton protein levels at rest and following acute 12%O2 exercise. Therefore, we conclude that long‐term moderate‐intensity exercise at 15%O2 environment increases erythrocyte deformability under shear flow, possibly by improving performance of Gardos channel on erythrocyte.

Systemic hypoxia promotes the mobilization of senescent CD8+ T lymphocytes into the peripheral blood compartment during moderate‐intensity exercise

This study investigated how various regimens of exercise with/without hypoxia affected mobilization of T lymphocyte subsets into the peripheral blood compartment. Eighteen sedentary males randomly engaged in two normoxic exercise bouts [severe exercise (SE) (up to VO2max) and moderate‐intensity exercise (ME) (50%VO2max) while exposed to 21%O2], two hypoxic exercise bouts (ME while exposed to 12%O2 and 15%O2) and two hypoxic resting conditions (resting while exposed to 12%O2 and 15%O2) in a normobaric hypoxia chamber. Under normoxic conditions, SE, but not ME, increased the percentages of senescent (CD28− and CD57+)/activated (CD62L− and CD11a+)‐form CD8+T lymphocytes mobilized into the peripheral blood compartment. Although no significant change occurred in the distribution of various CD8+T lymphocyte subsets under resting 12%O2 or 15%O2 condition, the senescent/activated‐form CD8+T lymphocytes markedly released into the blood compartment following ME combined with 12%O2 or 15%O2 exposure. However, the distribution of CD4+T lymphocyte subsets in blood remained unchanged in response to various regimens of exercise with/without hypoxia. We conclude that the 12–15%O2 exposures promote the mobilization of senescent/activated CD8+ T lymphocytes into the peripheral blood compartment during ME.

Serum leptin, lipoprotein levels, and glucose homeostasis between national wrestlers and sedentary males

Leptin is an important controller of the size of fat stores by inhibiting appetite. In wrestling, fat metabolism is important not only for aerobic energy system, but also for weight control and weight loss before competition. The aim of this study was to measure and compare the serum leptin levels, glucose homeostasis, and serum lipoproteins between Turkish national wrestlers and sedentary males. Materials and methods: Forty-five Turkish national wrestlers at the end of Olympic training camp before Beijing 2008 Olympic Games and 43 sedentary students were selected as subjects. Post-exercise levels of serum leptin, HOMA (Homeostasis model assessment) values, triglycerides, total cholesterol, LDL-cholesterol, HDL-cholesterol, and VLDL-cholesterol were measured after overnight fasting. A Mann-Whitney U test was used to test the differences between 2 groups. Pearson Correlation was conducted between leptin and the other parameters. Results: No significant difference was observed among the means of leptin and total cholesterol levels of the 2 groups. Wrestlers had significantly higher fasting insulin, HDL-cholesterol, triglyceride, and HOMA levels, but a lower LDL-cholesterol level compared to the sedentary males. The positive correlation was only found between leptin and fasting insulin levels (r = 0.310, P = 0.043). Conclusion: This study indicated that wrestling training had no effect on resting leptin level after overnight fasting and wrestlers had also decreased insulin sensitivity with higher fasting insulin, HDL-cholesterol, triglyceride, and HOMA levels compared to sedentary males.

Effect of low-intensity aerobic exercise on insulin-like growth factor-I and insulin-like growth factor-binding proteins in healthy men.

Increased concentrations of circulating insulin-like growth factor-I (IGF-I) or IGF-I relative to IGF-binding proteins (IGFBPs) are associated with increased risk of developing several forms of cancer. Conversely, exercise is linked with reduced risk. This study aims to investigate the effect of a low-intensity exercise program on circulating levels of IGF-I, IGFBP-1, and IGFBP-3, in previously sedentary males. Fourteen healthy men participated in cycle ergometer training at lactate threshold intensity for 60 min/day, 5 days/week for 6 weeks. After aerobic training, insulin sensitivity improved by 20%, while fasting insulin levels decreased by 13%. Simultaneously, low-intensity aerobic training decreased the circulating levels of IGF-I by 9%, while IGFBP-1 levels increased by 16%. An interesting finding was that higher pretraining level of IGF-I was associated with greater decline in IGF-I with training. Insulin-sensitizing low-intensity aerobic exercise is thus considered to be an effective method for downregulating IGF-I and upregulating IGFBP-1 levels.

Comparison of Resistance and Concurrent Resistance and Endurance Training Regimes in the Development of Strength

Resistance and endurance training are often performed concurrently in most exercise programs and in rehabilitative settings in an attempt to acquire gains in more than 1 physiologic system. However, it has been proposed that by simultaneously performing these 2 modes of exercise training, the strength gains achieved by resistance training alone may be impaired. Thus, the aim of this study was to compare the effects of 16 weeks of resistance training and concurrent resistance and endurance training on muscular strength development in 38 sedentary, apparently healthy males (25 yr +/- 8 mo). Subjects were age-matched and randomly assigned to either a control (Con) group (n = 12), resistance training (Res) group (n = 13), or concurrent resistance and endurance training (Com) group (n = 13). After 16 weeks, no changes were found in the strength of the subjects in the Con group. Resistance training and concurrent resistance and endurance training significantly (p < or = 0.05) improved strength in all of the 8 prescribed exercises. The data also indicated that 16 weeks of concurrent resistance training and endurance training was as effective in eliciting improvements in strength as resistance training alone in previously sedentary males. As such, concurrent resistance and endurance training does not impede muscular strength gains and can be prescribed simultaneously for the development of strength in sedentary, apparently healthy males and thus may invoke all the physiologic adaptations of resistance and endurance training at once.

Endurance training enhances BDNF release from the human brain

The circulating level of brain-derived neurotrophic factor (BDNF) is reduced in patients with major depression and type-2 diabetes. Because acute exercise increases BDNF production in the hippocampus and cerebral cortex, we hypothesized that endurance training would enhance the release of BDNF from the human brain as detected from arterial and internal jugular venous blood samples. In a randomized controlled study, 12 healthy sedentary males carried out 3 mo of endurance training (n = 7) or served as controls (n = 5). Before and after the intervention, blood samples were obtained at rest and during exercise. At baseline, the training group (58 + or - 106 ng x 100 g(-1) x min(-1), means + or - SD) and the control group (12 + or - 17 ng x 100 g(-1) x min(-1)) had a similar release of BDNF from the brain at rest. Three months of endurance training enhanced the resting release of BDNF to 206 + or - 108 ng x 100 g(-1) x min(-1) (P < 0.05), with no significant change in the control subjects, but there was no training-induced increase in the release of BDNF during exercise. Additionally, eight mice completed a 5-wk treadmill running training protocol that increased the BDNF mRNA expression in the hippocampus (4.5 + or - 1.6 vs. 1.4 + or - 1.1 mRNA/ssDNA; P < 0.05), but not in the cerebral cortex (4.0 + or - 1.4 vs. 4.6 + or - 1.4 mRNA/ssDNA) compared with untrained mice. The increased BDNF expression in the hippocampus and the enhanced release of BDNF from the human brain following training suggest that endurance training promotes brain health.

Resistance training and predicted risk of coronary heart disease in sedentary males

The purpose of this study was to determine the impact of resistance training, designed to prevent the development of coronary heart disease (CHD) based on the Framingham Risk Assessment (FRA) score. Twenty-five healthy sedentary men with low CHD risk were assigned to participate in a 16-week (three days per week) resistance training programme (n = 13) or non-exercising control group (CG) (n = 12). Resistance training was performed using eight whole-body exercises for three sets of 15 repetitions at 60% of one-repetition maximum. Resistance training did not significantly (p > 0.05) reduce the number of cigarettes smoked daily (p > 0.133) or TC (p > 0.917), while significant improvements were found in SBP (p < 0.003), HDLC (p < 0.005) and FRA score (p < 0.021); thus improving absolute 10-year risks for CHD. The CG subjects were found to have had no significant changes in number of cigarettes smoked daily (p > 0.831), TC (p > 0.678), HDLC (p > 0.672) or FRA score (p > 0.504), but SBP increased significantly (p< 0.030). These data indicate that resistance training can effectively reduce the predicted risk of developing CHD, even in men with already low risk.

Systemic hypoxia promotes lymphocyte apoptosis induced by oxidative stress during moderate exercise

Blood undergoes oxidative stress during severe hypoxia or intense exercise. Excessive exposure to oxidative stress induces replicative senescence and apoptosis of lymphocytes. This study determines how various exercises with/without hypoxia affect lymphocyte subset mobilization and oxidative stress-induced lymphocyte apoptosis. Eighteen sedentary males randomly engaged in two normoxic exercise bouts [severe exercise (SE) (up to VO(2max)) and moderate-intensity exercise (ME) (50%VO(2max)) while exposed to 21%O(2)], two hypoxic exercise bouts (ME while exposed to 12%O(2) and 15%O(2)) and two hypoxic resting conditions (resting while exposed to 12%O(2) and 15%O(2)) in a normobaric hypoxia chamber. Under normoxic conditions, SE but not ME (1) increased the percentages of senescent (CD28(-) and CD57(+))/activated (CD62L(-) and CD11a(+))-form lymphocytes mobilized into the peripheral blood compartment; (2) decreased the levels of surface thiol and intracellular total (t-GSH) and reduced-form glutathione (r-GSH) of lymphocytes in blood; and (3) further enhanced the extents of H(2)O(2)-induced mitochondria trans-membrane potential diminishing, caspases 3/8/9 activation, poly(ADP-ribose) polymerase cleavage and phosphotidyl serine exposure in blood lymphocytes. However, no significant change occurred in the subset mobilization, antioxidant levels or apoptosis of lymphocytes following exposure to either 12%O(2) or 15%O(2). Although both 12%O(2) and 15%O(2) ME increased the mobilization of senescent/activated-form lymphocytes, only 12%O(2) ME enhanced H(2)O(2)-induced lymphocyte thiol, t-GSH and r-GSH consumption and apoptotic responses. Therefore, we conclude that the 12%O(2) exposure increases the mobilization of senescent/activated-form lymphocytes into the peripheral blood compartment and simultaneously enhances oxidative stress-induced lymphocyte apoptosis by diminishing cellular antioxidant levels during exercise.

Effect of resistance training on total, central and abdominal adiposity

Despite the clear benefits that resistance training might have in weight management the effects of resistance training on adiposity in sedentary individuals are unsubstantiated. As such, the aim of the study was to determine the effect of resistance training on anthropometric measures of total, central and abdominal adiposity. Twenty-five healthy, sedentary males not on an energy-restricted diet were assigned to a non-exercising control group (CON) (n = 12) or a resistance training group (RES) (n = 13) to determine the effect of 16 weeks of resistance training onanthropometric measures of total, centrally located and abdominal adiposity. Resistance training was prescribed three times weekly using eight exercises for three sets of 15 repetitions at 60% of one-repetition maximum. Resistance training decreased three of the six anthropometric measures of total adiposity and increased body mass and body mass index (BMI). Resistance training had no impact on the measures of centrally located and abdominal adiposity. Body mass and BMI shouldbe used with caution in risk calculations and measures of total adiposity inindividuals engaging in resistance training due to this mode of training increasing lean mass (and thus body mass and BMI). Resistance training reduced total adiposity but did not provide an effective stimulus to lower centrally located and abdominal adiposity.

Systemic hypoxia enhances exercise-mediated bactericidal and subsequent apoptotic responses in human neutrophils

Phagocytosis and oxidative burst are critical host defense mechanisms in which neutrophils clear invading pathogens. Clearing phagocytic neutrophils by triggering apoptosis is an essential process for controlling inflammation. This study elucidates how various exercise bouts with/without hypoxia affected neutrophil bactericidal activity and subsequent apoptosis in humans. Fifteen sedentary males performed six distinct experimental tests in an air-conditioned normobaric hypoxia chamber: two normoxic exercises [strenuous exercise (SE; up to maximal O2 consumption) and moderate exercise (ME; 50% maximal O2 consumption for 30 min) while exposed to 21% O2], two hypoxic exercises (ME for 30 min while exposed to 12% and 15% O2), and two hypoxic exposures (resting for 30 min while exposed to 12% and 15% O2). The results showed that 1) plasma complement-C3a desArg/C4a desArg/C5a concentrations were increased, 2) expressions of L-selectin/lymphocyte functin-associated antigen-1/Mac-1/C5aR on neutrophils were enhanced, 3) phagocytosis of neutrophils to Esherichia coli and release of neutrophil oxidant products by E. coli were elevated, and 4) E. coli-induced phosphotidylserine exposure or caspase-3 activation of neutrophils were promoted immediately and 2 h after both 12% O2 exposure at rest and with ME as well as normoxic SE. Although neither normoxic ME nor breathing 15% O2 at rest influenced these complement- and neutrophil-related immune responses, ME at both 12% and 15% O2 resulted in enhanced complement activation in the blood, expressions of opsonic/complement receptors on neutrophils, or the bactericidal activity and apoptosis of neutrophils. Moreover, the increased neutrophil oxidant production and apoptosis by normoxic SE and hypoxic ME were ameliorated by treating neutrophils with diphenylene iodonium (a NADPH oxidase inhibitor). Therefore, we conclude that ME at 12-15% O2 enhances bactericidal capacity and facilitates the subsequent apoptosis of neutrophils.

The Relationship Between Plasma Volume Changes Following Heat Acclimation And Thermotolerance During Uncompensable Heat Stress In Sedentary Males

Sedentary individuals can not tolerate the same increase in rectal temperature (Tre) during uncompensable heat stress (UHS) compared with endurance trained subjects, partially due to intestinal ischemia and endotoxin leakage that occurs with the redistribution of splanchnic blood flow. Heat acclimation (HA) may be an adaptive strategy for these individuals to increase plasma volume and delay endotoxin leakage, thus increasing thermotolerance during UHS. PURPOSE: The purpose was to examine the relationship between plasma volume (PV) changes and thermotolerance during UHS following 9 days of HA in sedentary males. METHODS: Seven sedentary males (mean±SD: 28±7 y, 75.3±8.0 kg, VO2peak= 42±6 mL·kg-1·min-1) walked to exhaustion on a treadmill (4.5 km·h-1, 2% grade) in 40°C and 30% R.H. wearing combat clothing and a protective hooded overgarment on 9 days (over 2 consecutive weeks). PV was determined prior to beginning HA using Indocyanine Green™ and resting hematocrit and hemoglobin values measured on subsequent days were used to calculate the change in PV. RESULTS: PV increased significantly over the 9 days from 49.6±9.0 to 53.3±10.3 mL·kg-1. The change in Tre from beginning to end of the UHS also increased significantly over the 9 days from 1.94±0.38 to 2.37±0.3°C owing to both a significant reduction in resting Tre from 36.83±0.32 to 36.59±0.26°C and a non-significant increase (p<0.08) in Tre at exhaustion (38.76±0.4 to 38.95±0.31°C). Total heat storage increased significantly from 6.7±1.3 to 8.0±1.2 kJ·kg-1. However, PV changes were not related to changes in heat storage or the changes in initial or final core temperatures during UHS. CONCLUSION: Although 9 days of HA induced an expansion of PV in these sedentary males, these changes were not directly related to the increase in heat storage that occurred. Funded by a Defence R&D Canada Technology Investment Fund and the US Navy Office of Naval Research.

Hypothalamic-pituitary-adrenal Axis And The Sympathetic-adrenomedullary System Responses During Heat Acclimation In Sedentary Males

Previous research suggests that the release of HPA and SAS stress hormones are functionally linked to the increase in core temperature during exercise and heat stress exposure. Yet, heat acclimation is known to increase tolerance time and the core temperature tolerated during uncompensable heat stress (UHS), and reduce physiological strain. It would be of interest, therefore, to know whether the HPA and SAS hormone response following heat acclimation is reduced at any given level of thermal strain. PURPOSE: To examine the HPA and SAS stress hormone responses in sedentary males during 9 days of exposure to UHS. METHODS: Nine sedentary males (Mean±SE: VO2peak= 51.7±1.9 mL·kgLBM-1·min-1, 17±2% fat) walked to exhaustion (EXH) on 9 days (over 2 consecutive weeks) on a treadmill (4.5 km·h-1, 2% incline) in 40°C and 30% R.H., wearing combat clothing and a protective hooded overgarment. At rest (PRE; prior to heat) and at a Tre of 38, 38.5, 39°C, and EXH venous blood samples were obtained. COR, GH, and ACTH were determined by chemiluminescence and NE and E by gas chromatography/mass spectrometry. RESULTS: Although Tre EXH was not different from Day 1 (38.8±0.1°C) to 9 (39.1±0.1°C), time to EXH increased from 95±8 to 145±13 min. Significant increases were observed from PRE to EXH for COR (357.0±8.5 to 491.3±18.8 nmol·L-1), ACTH (4.7±0.2 to 21.7±1.9 pmol·L-1), NE (1.9±0.0 to 4.7±0.0 nmol·L-1), and E (208.4±3.5 to 547.5±18.9 pmol·L-1) that were unaffected by heat acclimation. No differences also were observed between Day 1 and 9 from Pre to 39°C for COR, ACTH, NE, and E (p≤0.1). However, GH EXH on Day 1 (9.9±1.7 mIU·mL-1) was significantly greater than Days 5, 6, and 9 (6.5±0.9, 6.4±0.9, and 7.7±0.2 mIU·mL-1, respectively). CONCLUSION: Nine days of exertional heat acclimation improved the GH stress response, yet COR, ACTH, NE, and E remained temperature driven. Funded by a DRDC Technology Investment Fund.

Aerobic Vs. Resistance Exercise In Igfbp-3 In African American Males And Prostate Cancer Cells Growth

The value of aerobic exercise (ex) on health benefits have been well investigated while the benefits of resistance ex have been mostly minimized to that of building muscle and improving performance. Aerobic physical activity has been linked to reducing the growth of prostate tumors by altering function of the insulin-like growth factors. Prostate cancer affects blacks disproportionately, and whether aerobic and resistance ex affects the insulin-like growth factor system similarly is not known. PURPOSE: This pilot study investigated the influence of aerobic ex and resistance ex on the concentration of a substance (insulin-like growth factor binding protein-3 [IGFBP-3]) which attenuates the growth of prostate tumor cells. METHODS: Subjects were 14 sedentary black males 18-29 yrs. Subjects were assigned to groups of an aerobic ex (n = 7) and resistance ex (n = 7). The aerobic ex regime consisted of 7 consecutive days of treadmill jogging at 70% of peak oxygen uptake (VO2peak). The resistance ex regime consisted of 7 consecutive days of strength training the major muscle groups of the upper and lower extremity performing 3 sets of 10 repetitions corresponding to 70% 1 repetition maximum. At the beginning and end of 7 days of aerobic/resistance ex, serum samples of the subjects were incubated with cultures of prostate LNCaP tumor cells. The serum concentration of IGFBP-3 and the relative cell growth were measured. RESULTS: Characteristics of age, body weight and height, VO2peak, % body fat, and maximum leg strength were not significantly different across groups. Baseline serum concentration of IGFBP-3 was similar between the aerobic and resistance ex groups (.056 ±.03 vs..056 ±.01 ng/ml). Further, baseline serum growth rate of the tumor cells were similar between groups (.51 ±.09 vs..50 ±.14%). We observed the tumor cell growth rate after aerobic and resistance ex tended to be lower (11% and 21%), but the difference was not significant. There was a tendency for similar increases in IGFBP-3 after aerobic and resistance ex. CONCLUSION: Aerobic ex vs. resistance ex showed similar clinical directional findings for and increase in IGFBP-3 and decrement in prostate tumor cell growth rate. This study provides evidence suggesting aerobic ex and resistance ex are equally effective in possibly inhibiting the evolution of prostate cancer.

Exercise for sedentary males.

Exercise for sedentary males.

Hypoxic Exercise Training Suppresses Oxidative Stress‐induced Lymphocyte Apoptosis

This study investigates how hypoxic exercise training affects oxidative stress‐induced lymphocyte apoptosis and further explores its underlying mechanisms. Twelve sedentary males were trained on a bicycle ergometer at about 60%VO2max under 15% O2 air condition for 20 minutes per day, 5 days per week for 4 weeks. Sublethal oxidative stress was administered by treating the lymphocytes with 200μM H2O2, to closely approximate in vivo pro‐oxidative conditions. Our results demonstrated that before the training, strenuous exercise enhanced H2O2‐induced phosphotidyl serine exposure of lymphocyte, which was accompanied by a decline in mitochondrial transmembrane potential (MTP) and increases in active‐form caspase 3, 8 and 9 contents in lymphocyte. However, 4 weeks of hypoxic exercise training attenuated H2O2‐induced lymphocyte caspase activation and apoptotic response during strenuous exercise. We conclude that although strenuous exercise can promote oxidative stress‐induced lymphocyte apoptosis by declining MTP and activating intrinsic and extrinsic caspases, long‐term hypoxic exercise training suppresses the acute exercise effect on oxidative stress‐induced lymphocyte apoptosis.

Effects of hypoxic exercise training on exercise‐induced thrombin generation

Platelet‐derived microparticles (PDMP) are important players in thrombogenesis. This study investigates whether hypoxic exercise training affects PDMP‐mediated thrombin generation (TG) at performing strenuous exercise. Twelve sedentary males were trained on a bicycle ergometer at about 60%VO2max under 15% O2 air condition for 20 minutes per day, 5 days per week for 4 weeks. TG was determined by a novel calibrated, automated thrombinography assay, whereas PDMP count, procoagulant factor binding, and phosphatidylserine (PS) exposure were evaluated by a two‐color flow cytometry. Our results showed that strenuous exercise increased TG via enhancing circulating PDMP concentration. Pathological shear stress (108 dynes/cm2) increased the PS exposure of the PDMP, the binding of the PDMP to procoagulant factor V/Va and VIII, and PDMP‐induced TG peak and rate. However, 4 weeks of hypoxic exercise training remained unchanged in exercise‐induced PDMP secretion and TG. Therefore, we conclude that strenuous exercise magnifies shear stress‐induced TG by eliciting PDMP secretion and enriching procoagulant factors binding to PDMP, which remain unchanged after hypoxic exercise training.

Hypoxic Exercise Training Attenuated Bactericidal Activity of Neutrophil Enhanced by Strenuous Exercise

This study investigates how hypoxic exercise training affects acute exercise‐mediated bactericidal capacity of neutrophil and further explores its underlying mechanisms. Twelve sedentary males were trained on a bicycle ergometer at about 60%VO2max under 15% O2 air condition for 20 minutes per day, 5 days per week for 4 weeks. Our results showed that before the training, strenuous exercise enhanced the chemotaxis of neutrophil by exposure to N‐formyl‐Met‐Leu‐Phe, the phagocytosis of neutrophil to E.coli and the release of neutrophil oxidant products by E.coli, which was accompanied by the increases in expressions of CD62L, CD11a, CD16b and CD88 on neutrophil. However, 4 weeks of hypoxic exercise training attenuated the enhancements of chemotactic, phagocytic, and oxidative burst activities of neutrophil and opsonic/complement receptor expressions on neutrophil by acute strenuous exercise. Therefore, we conclude that although strenuous exercise promotes neutrophil bactericidal capacity by increasing the expressions of opsonic/complement receptors on neutrophil, 4 weeks of hypoxic exercise training suppresses the acute exercise effect on the neutrophil bactericidal cascades.

Hypoxic Exercise Training Enhances Vascular Hemodynamics and Oxygen Utilization in Skeletal Muscles

This study investigates how hypoxic exercise training impacts on vascular hemodynamic and O2 utilization in exercising skeletal muscles. Twelve sedentary males were trained on a bicycle ergometer at about 60%VO2max under 15% O2 air condition for 20 minutes per day, 5 days per week for 4 weeks. Vascular hemodynamics and O2 consumption and re‐oxygenation rate in gastrocnemius were determined by near infrared spectroscopy. Our results showed that 4 weeks of hypoxic exercise training improved subjects' aerobic fitness at ventilation threshold and maximal performance. Acute exposure to 12%O2 decreased arterial hyperemia and venous compliance, as well as, oxygen consumption and re‐oxygenation rate in gastrocnemius at pre‐training state. However, the suppressive effects in vascular hemodynamics and tissue O2 utilization in gastrocnemius by acute hypoxic exposure were ameliorated following the hypoxic exercise training. Therefore, we conclude that long‐term hypoxic exercise training can improve cardiopulmonary fitness and increase the tolerance to hypoxia‐limited O2 transport and utilization in skeletal muscles.

Vitamin E suppresses bactericidal activity of polymorphonuclear leukocyte enhanced by hypoxia

This investigation elucidates how various hypoxic interventions influence bactericidal activity of polymorphonuclear leukocyte (PMN) following treatment with an antioxidant vitamin E. Forty sedentary males were randomly assigned to vitamin E (n=20) and placebo (n=20) groups. Our results demonstrated that exposure to 12% O2 in the placebo group increased urinary 8‐isoprostane level and decreased plasma total antioxidant content. Moreover, this hypoxic exposure increased chemotactic, phagocytic, and oxidative burst activities of PMN, accompanied by increased expressions of L‐selectin, LFA‐1, Mac‐1, FcγIIIBR, C1qRp and C5aR on PMN. However, exposure to 12% O2 in the vitamin E group did not influence the opsonic/complement receptor expressions and bactericidal cascades of PMN. Additionally, the circulatory redox status, PMN‐mediated bactericidal activity and the opsonic/complement receptors on PMN were constant following exposure to 15%, 18% or 21% O2 in the two groups. We conclude that exposure to 12% O2 promotes PMN bactericidal activity, possibly by elevating lipid peroxidation. However, this hypoxic effect on PMN bactericidal activity is ameliorated by pretreatment with vitamin E.