Final Exercise Bout Research Articles

Effects of ingestion of isomaltulose beverage on plasma volume and thermoregulatory responses during exercise in the heat.

Isomaltulose is a low glycemic and insulinaemic carbohydrate increasingly used as an alternative sweetener in commercial beverages. While isomaltulose beverages can improve hydration status compared to sucrose-based beverages, it remains unclear if ingestion of an isomaltulose beverage prior to exercise in the heat may improve plasma volume (PV) and thermoregulatory responses. Twelve endurance-trained men consumed a 1L carbohydrate beverage containing either 6.5%-sucrose (SUC) or 6.5%-isomaltulose (ISO) 60min prior to 5 successive, 15-min bouts of moderate-intensity (60% of their pre-determined maximum oxygen uptake) in the heat (32°C, 50% relative humidity), each separated by a 5min rest. A 6th bout was performed, wherein the participant adjusted running speed to maximize distance covered within the 15-min period. The change (Δ) in PV, heart rate (HR), body core (rectal and gastrointestinal) and skin temperatures, and whole-body sweat loss were assessed during each exercise bout. Ingestion of ISO induced a higher ΔPV at 4th bout only (P < 0.001) and lower HR (P = 0.032, main effect of beverage) during exercise compared to those of SUC. Body core and skin temperatures and whole-body sweat loss did not differ between conditions (all P ≥ 0.192, interaction effect). Running distance covered in final exercise bout tended to increase (~ 5%) in ISO versus SUC (P = 0.057, d = 0.64). Relative to a sucrose-based beverage, ISO ingestion prior to exercise in the heat reduced cardiovascular strain by preserving PV and attenuating HR, albeit with no corresponding benefit on thermoregulatory function. The former response may facilitate improvements in exercise performance.

1372-P: Hyperglycemia Impacts Mouse Skeletal Muscle in a Sex-Specific Manner

Functional Exercise Capacity (FEC) , a universal predictor of cardiovascular and all-cause mortality, is lower in adults and youth with diabetes for reasons that are poorly understood. Skeletal muscle is key determinant of FEC. We hypothesized that skeletal muscle capillary and mitochondrial density are lower with hyperglycemia and respond to exercise training. To test this hypothesis we generated a model of short-term hyperglycemia (HG) with inducible beta cell deletion of glucokinase (GKlox/lox;PdxCreER) . Male (M) and female (F) HG mice and euglycemic littermate controls (EG) completed 3 weeks of treadmill training (Ex) or remained sedentary (Sed) . The gastrocnemius was collected 24 hours after the final exercise bout. Expression of COX1 (mitochondrial marker) , Dystrophin (muscle fiber sarcolemma boundary marker) , and CD31 (capillary marker) was detected by immunofluorescence. Sirtuin 3 (SIRT3) , an NAD+ dependent deacetylase (mitochondrial homeostasis) was measured using the JESS system. (Fig 1) Mitochondrial density (mitochondria per fiber as quantified by fluorescence intensity units per fiber [FIU/fiber]) was significantly lower in HG vs. EG (p&amp;lt;0.0001) and differed by sex (p=0.0048 sex x glycemia interaction) . Ex resulted in greater mitochondrial density (p=0.0265) independent of sex and glycemia. Capillary density and SIRT3 were unchanged. Sex-differences in muscle response to HG warrant further investigation. Disclosure L.Knaub: None. G.Pott: None. N.A.Hulett: None. S.Hull: None. R.L.Scalzo: None. J.Reusch: Advisory Panel; Medtronic. Funding VA Merit (BX002046)

Effects of Amount, Intensity, and Mode of Exercise Training on Insulin Resistance and Type 2 Diabetes Risk in the STRRIDE Randomized Trials.

BackgroundLipoprotein Insulin Resistance Index (LP-IR) and Diabetes Risk Index are novel spectroscopic multimarkers of insulin resistance and type 2 diabetes risk. As the Studies of a Targeted Risk Reduction Intervention through Defined Exercise (STRRIDE) randomized trials have previously demonstrated the ability of exercise training to improve traditional markers of insulin action, the aim of this study was to examine the effects of exercise amount, intensity, and mode on LP-IR and the Diabetes Risk Index.MethodsA total of 503 adults with dyslipidemia [STRRIDE I (n = 194), STRRIDE AT/RT (n = 139)] or prediabetes [STRRIDE-PD (n = 170)] were randomized to control or one of 10 exercise interventions, ranging from doses of 8–23 kcal/kg/week; intensities of 50–75% V̇O2peak; and durations of 6–8 months. Two groups included resistance training and one included dietary intervention (7% weight loss goal). Fasting plasma samples were obtained at baseline and 16–24 h after the final exercise bout. LP-IR, the Diabetes Risk Index, and concentrations of the branched chain amino acids valine and leucine were determined using nuclear magnetic resonance spectroscopy. LP-IR and the Diabetes Risk Index scores range from 0–100 and 1–100, respectively (greater scores indicate greater risk). Paired t-tests determined significance within groups (p < 0.05).ResultsAfter training, six exercise groups significantly improved LP-IR (ranging from −4.4 ± 8.2 to −12.4 ± 14.1), and four exercise groups significantly improved the Diabetes Risk Index (ranging from −2.8 ± 8.2 to −8.3 ± 10.4). The most beneficial interventions for both LP-IR and the Diabetes Risk Index were low amount/moderate intensity aerobic, aerobic plus resistance, and aerobic plus diet.SummaryMultiple exercise interventions improved LP-IR and the Diabetes Risk Index. In those with dyslipidemia, adding resistance to aerobic training elicited a synergistic effect on insulin resistance and type 2 diabetes risk. In individuals with prediabetes, combining a dietary intervention and weight loss with aerobic training resulted in the most robust type 2 diabetes risk improvement.

Effects Of Amount, Intensity, And Mode Of Exercise Training On HOMA - The Strride Clinical Trials

PURPOSE: To examine the effects of amount, intensity, and mode of exercise training on HOMA (a marker of fasting insulin resistance) across 10 exercise-only interventions from the three STRRIDE (Studies of Targeted Risk Reduction Interventions through Defined Exercise) clinical trials. METHODS: A total of 518 subjects completed the three trials with pre and post intervention HOMA values. Subjects with dyslipidemia [STRRIDE I (n=224) and STRRIDE AT/RT (n=144)] or prediabetes [STRRIDE-PD (n=150)] were randomized to either control group or one of 10 interventions, ranging from doses of 8-22 kcal/kg/week (KKW); intensities of 50-75% V̇O2peak; and durations of 6-9 months. Two groups included resistance training and one group included diet intervention (weight loss of 7%). Fasting blood samples were obtained at baseline and 16-24 h after the final exercise bout. Paired t-tests determined within group change score significance (p<0.05). RESULTS: In the inactive controls. HOMA increased significantly —became more insulin resistant. After training, all intervention groups became more insulin sensitive; 6 of these 10 groups had significant improvements in HOMA. In non-statistical comparisons across the trials, the diet + exercise group had the greatest improvement (-0.90 ± 0.9); resistance training alone experienced the least improvement in HOMA. The 14 KKW moderate intensity (STRRIDE I) and the aerobic + resistance training (STRRIDE AT/RT) groups obtained 77% and 55% of the improvement observed in the diet + exercise group from STRRIDE-PD. Only 4 of the 7 aerobic exercise groups had significant improvements. CONCLUSION: On average, STRRIDE interventions improved fasting insulin resistance. Adding resistance to aerobic training elicits an additive training effect on insulin resistance. In individuals with prediabetes, incorporating dietary intervention with aerobic training results in the most robust improvement in fasting insulin resistance.

Abstract P177: Effects of Gender, Race, and Glucose Tolerance on Lipoprotein Insulin Resistance Index Responses to Exercise Training

Introduction: Lipoprotein Insulin Resistance Index (LP-IR) is a novel spectroscopic multimarker linked to future diabetes risk. We recently assessed changes in LP-IR across the three STRRIDE trials, where on average, STRRIDE exercise interventions improved LP-IR. In the present study, we sought to determine if there were effects of gender, race, and glucose tolerance on LP-IR responses across the STRRIDE trials. Methods: A total of 461 adults with dyslipidemia (STRRIDE I and STRRIDE AT/RT) or prediabetes (STRRIDE-PD) were randomized to one of 7 exercise interventions, ranging from doses of 8-22 kcal/kg/week (KKW); intensities of 50-75% VO 2peak ; and durations of 6-9 months. Six groups included aerobic exercise, two groups included resistance training, and one group included dietary intervention (weight loss goal of 7%). Fasting blood samples were obtained at both baseline and 16-24 h after the final exercise bout. In STRRIDE-PD only (n=165), subjects completed oral glucose tolerance tests and were categorized into normal (NGT) and impaired glucose tolerance (IGT) groups at baseline. NMR spectroscopy was performed at LabCorp to determine LP-IR score (comprised of six lipoprotein subclass and size parameters). LP-IR score ranges from 0 (most insulin sensitive) to 100 (most insulin resistant). Irrespective of intervention group, we assessed change in LP-IR in three stratified analyses: by gender, race, and baseline glucose tolerance category. Paired t-tests determined whether the post- minus pre- intervention change scores within each group were significant (p&lt;0.05). Analysis of covariance accounting for baseline values determined difference among groups. Results: At baseline, women had lower LP-IR scores compared to men (47.8 ± 22.3 vs 62.6 ± 21.5; p&lt;0.0001). Both women and men significantly improved LP-IR following exercise training by -4.3 ± 15.0 and -8.0 ± 15.6 points, respectively. There were also significant baseline differences when stratified by race. Black subjects had lower baseline LP-IR scores compared to White subjects (43.2 ± 20.7 vs 56.3 ± 23.0; p&lt;0.0001). After exercise training, Black subjects significantly improved their LP-IR score by -4.0 ± 14.6 points; White subjects significantly improved their LP-IR score by -6.2 ± 15.5 points. As expected, those with NGT had lower baseline LP-IR scores compared to those with IGT in STRRIDE-PD (49.0 ± 20.0 vs 64.4 ± 19.9; p&lt;0.0001). Both NGT and IGT groups significantly improved LP-IR by -4.3 ± 14.6 and -7.6 ± 12.9 points, respectively. In all three stratified analyses, change in LP-IR was not significantly different among groups after controlling for baseline values. Conclusion: There were significant baseline differences in LP-IR among gender, racial, and glucose tolerance groups. However, after adjusting for these baseline differences, there were similar beneficial responses to exercise in this marker of insulin resistance.

Impact of High-intensity Interval Exercise and Moderate-Intensity Continuous Exercise on the Cardiac Troponin T Level at an Early Stage of Training.

An elevation in cardiac troponin T (cTnT), as a highly specific biomarker of cardiomyocyte damage, after moderate-intensity continuous exercise (MCE) has been described. The exercise-induced cTnT response distorts the diagnostic role of the cTnT assay. Although high-intensity interval exercise (HIE) is growing in popularity and concerns remain about its safety, available data related to cTnT release after HIE is limited, which hampers the use of HIE as a health intervention. Here, we present three representative HIE protocols [traditional HIE (repeated 4 min cycling at 90% V̇O2max interspersed with 3 min rest, 200 kJ/session); sprint interval exercise (SIE, repeated 1 min cycling at 120% V̇O2max interspersed with 1.5 min rest, 200 kJ/session); and repeated sprint exercise (RSE, 40 x 6 s all-out sprints interspersed with 9 s rest)] and one representative MCE protocol (continuous cycling exercise at an intensity of 60% V̇O2max, 200 kJ/session). Forty-seven sedentary, overweight young women were randomly assigned to one of four groups (HIE, SIE, RSE, and MCE). Six bouts of respective exercise were performed by every single group, with each being 48 h apart. Meanwhile, for four groups, the duration of the entire testing period was identical, being 10 days. Before and after the first and final exercise bouts, an assessment was conducted of cTnT. The current study provides a frame of reference giving a clear picture of how a specific exercise session affects the circulating cTnT concentration at the early stage of training. The information may assist with clinical interpretations of post-exercise cTnT elevation and guide the prescription of exercise, especially for HIE.

The Differential Effects Of Amount, Intensity, And Mode Of Exercise Training On A Novel Lipoprotein Multimarker Of Insulin Resistance

PURPOSE: To examine the effects of amount, intensity, and mode of exercise training on Lipoprotein Insulin Resistance Index (LP-IR; a relatively new spectroscopic multimarker of insulin resistance) across 10 exercise interventions from the STRRIDE studies. METHODS: A total of 531 men and women with dyslipidemia [STRRIDE I (n=222) and STRRIDE AT/RT (n=142)] or prediabetes [STRRIDE-PD (n=167)] were randomized to either control group or one of 10 exercise interventions, which ranged from doses of 8-22 kcal/kg/week (KKW); intensities of 50-75% V̇O2peak; and durations of 6-9 months. Two groups included resistance training and one group included dietary intervention (weight loss goal of 7%). Fasting blood samples were obtained at both baseline and 16-24 hr after the final exercise bout. NMR spectroscopy was performed at LabCorp to determine LP-IR score, which is comprised of six lipoprotein subclass and size parameters. LP-IR score ranges from 0 (most insulin sensitive) to 100 (most insulin resistant). Paired t-tests determined post- minus pre-intervention change score significance within groups (p<0.05). Study-specific ANCOVA determined differences between groups. RESULTS: The inactive control group did not significantly change LP-IR. After training, seven of the 10 exercise groups significantly improved LP-IR, ranging from -4.0 ± 7.6 to -12.5 ± 14.2. The figure displays change scores across all groups. The Aerobic plus Resistance group resulted in significantly greater change than the Resistance only group in STRRIDE AT/RT. The Moderate plus Diet group had significantly greater LP-IR change than all other groups in STRRIDE-PD. CONCLUSION: On average, STRRIDE interventions improved LP-IR. Our results provide compelling evidence that adding resistance to aerobic training elicits a synergistic training effect on LP-IR. In individuals with prediabetes, incorporating dietary intervention with aerobic training results in the most robust LP-IR improvement.

The cTnT response to acute exercise at the onset of an endurance training program: evidence of exercise preconditioning?

Exercise induces a cardioprotective effect referred to as "preconditioning". Whether the preconditioning impacts upon the cardiac troponin T (cTnT) response to subsequent exercise bouts is unclear. This study investigated the effects of an initial exercise bout, a second exercise bout 48h later, as well as subsequent exercise every 48h for 4 days or a single identical exercise bout after 8 days of inactivity gap on cTnT response to acute exercise. Twenty-eight sedentary overweight young women were randomly assigned to either six bouts of exercise each separated by 48h or three bouts of exercise with 48h between the first two bouts and 8 days between the second and third bouts. All exercise bouts were identical (60% [Formula: see text], 200kJ) and the total testing period (10 days) was the same for both groups. cTnT was assessed before and after the 1st, 2nd, and final exercise bouts. cTnT increased (129%, P < 0.05) after the first bout of exercise in both groups (peak post-exercise cTnT, median [range], ngl-1: 3.43[< 3.00-27.26]) with no between-group differences in the response. The second exercise bout had no significant (P > 0.05) effect on post-exercise cTnT (< 3.00[< 3.00-21.96]). The final exercise bout resulted in an increase (190%, P < 0.05) in cTnT (4.35[< 3.00-13.05]) in both groups. A single bout exercise resulted in a temporary blunting of cTnT response to acute exercise 48h later. The effect of exercise preconditioning was not preserved, regardless of whether followed by repeated exercise every 48h or a cessation of exercise for 8 days.

TREADMILL EXERCISE TRAINING PROTECTS AGAINST METABOLIC DYSFUNCTION AND DIAPHRAGM WEAKNESS IN OBESE DIABETIC RATS

Excessive weight gain is a serious public health issue, as nearly one‐third of the population worldwide is obese or overweight. Obesity is a major risk factor in the development of various metabolic disorders, including type 2 diabetes. Furthermore, obesity and diabetes results in many physical disabilities, including inspiratory muscle weakness (i.e., diaphragm dysfunction) which can lower the quality of life and increase the risk of respiratory failure. Increased physical activity (i.e., exercise training) has been shown to be a critical intervention to attenuate the metabolic derangements associated with obese diabetics. Furthermore, endurance exercise training alters the diaphragmatic phenotype to protect against various stressors; however, whether endurance exercise training can attenuate obesity/diabetes‐induced diaphragm dysfunction is unclear. Therefore, we investigated the effects of exercise training on obesity/diabetes‐induced diaphragm dysfunction. Male Otsuka Long‐Evans Tokushima Fatty (OLETF) rats, a rodent model of obesity/diabetes, were randomly assigned to either sedentary (SED: n=7) or exercise groups (Ex: n=6). Dependent measures were compared to lean long‐Evans Tokushima Otsuka rats that were sedentary (LETO: n=6). Treadmill running was conducted 5 days/week for 20 weeks from 5 weeks of age for Ex group. An intraperitoneal glucose tolerance test was performed following overnight fasting, and blood and diaphragm samples were obtained 48 h after the final exercise bout. Exercise training positively impacted whole‐body metabolic function of OLETF rats, as indicated by improved glucose tolerance, and reductions in body weight, serum triglyceride, total cholesterol, and insulin that were comparable to LETO rats. A trend (p=0.0511) for decreased blood levels of free fatty acids was also observed in exercise trained OLETF rats. Diaphragm force production in OLETF rats was lower compared to LETO controls, but was rescued by exercise training. Mechanistically, OLETF rats presented increases in myocellular markers associated with diaphragmatic weakness, including increases in angiotensin II type 1 receptor (AT1R) and tumor necrosis factor‐like weak inducer of apoptosis receptor (TWEAKR). Interestingly, in conjunction with improved diaphragm function, the rise in diaphragmatic AT1R and TWEAKR were attenuated by exercise training in OLETF rats. Additionally, increased protein acetylation was prevented in OLETF rats that were exercise trained, potentially due to restoration in the protein abundance of the deacetylase sirtuin 1 (Sirt1) by exercise training (p&lt;0.05). These findings reveal that endurance exercise training protects against metabolic dysfunction and diaphragm weakness observed with obese diabetic rats. These data suggest exercise training is a potential intervention to prevent respiratory muscle weakness associated with obese diabetic individuals.Support or Funding InformationThis work was supported by JSPS KAKENHI 15KK0131 (NIS), MEXT‐Supported Program for the Private University Research Branding Project (HN) and NIH R01, R01AR064189 (SKP)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Distinct protein and mRNA kinetics of skeletal muscle proton transporters following exercise can influence interpretation of adaptations to training.

What is the central question of this study? Following a training intervention, how is the interpretation of adaptations in skeletal muscle H+ transporters influenced by biopsy timing in the context of individual protein and mRNA kinetics after the final exercise bout? What is the main finding and its importance? We show that distinct postexercise protein and mRNA kinetics for monocarboxylate transporter1/4 and sodium-hydrogen exchanger1 indicate that timing of a single end-point biopsy after a training intervention can influence the inferences made. Furthermore, we found the intrasubject, intersample variability of the muscle buffer capacity titration assay to be greater than the typical training effect. In order to gain a better understanding of training-induced adaptations in skeletal muscle pH regulation, in this study we measured protein and mRNA kinetics of proton (H+ ) transporters for 72h following a bout of high-intensity interval exercise (HIIE), conducted after 4 weeks of similar training. We also assayed muscle buffer capacity (βm) by a titration technique (βmin vitro ) over the same period. Sixteen active men cycled for seven bouts of 2min at ∼80% of peak aerobic power, interspersed with 1min rest. Compared with the first 9h postexercise, monocarboxylate transporter (MCT)1 protein content was ∼1.3-fold greater 24-72h post-HIIE, whereas there was no such change in MCT4 protein content. Conversely, MCT1 and MCT4 mRNA expression progressively decreased 9-72h post-HIIE. Sodium-hydrogen exchanger1 (NHE1) protein content was lower 9h post-HIIE (∼0.8-fold) compared with every other postexercise time point, but NHE1 mRNA expression was 2.2 to 2.9-fold greater 24-72h post-HIIE, compared with the first 24h post-HIIE. Furthermore, we determined the intrasubject, intersample variability (11.5%) of βmin vitro for resting samples taken on consecutive days to be greater than the typical training effect (mean 6%; 95% confidence limits ±4%). In conclusion, the delay in steady-state protein turnover should inform biopsy timing in studies investigating the response to training of the H+ transport proteins, whereas the temporal resolution provided by single time points has been shown to be of limited epistemological value for their corresponding mRNA expression. Finally, our data cast doubt on the ecological validity of the βmin vitro assay for measuring true changes in βm.

Exercise in personal protective equipment in a hot, humid environment does not affect risk propensity

ABSTRACTWe tested the hypothesis that heat stress created by light exertion in encapsulating personal protective equipment (PPE) in a hot, humid environment increases risk propensity. Ten healthy subjects (29 ± 7 y) completed 2 trials presented in a counter-balanced manner. Subjects donned encapsulating PPE, and in one trial they wore a tube-lined shirt underneath that was perfused with 5°C water. Subjects completed 2 15 min bouts of walking exercise on a treadmill at ˜50% maximal heart rate in a 32°C, 81% RH environment. Subjects completed the Balloon Analog Risk Task (BART), an objective measure of risk-taking, before, between the 2 exercise bouts, and following the final exercise bout. Personal cooling lowered (P < 0.01) mean skin temperature by 8.0 ± 1.6°C. Intestinal temperature rose (P < 0.01) in both trials, but was lower (P < 0.01) at the end of exercise in the cooling trial (38.0 ± 0.3°C vs. 37.6 ± 0.3°C). BART derived indices of risk propensity were not affected by trial or time (trial × time interaction: P ≥ 0.33). These data indicate that 60 min of exposure to mild heat stress created by light exertion in encapsulating PPE does not affect risk-taking behavior.

Intermittent bout exercise training down-regulates age-associated inflammation in skeletal muscles

Aging is characterized by the progressive decline in mass and function of the skeletal muscle along with increased susceptibility to inflammation, oxidative stress, and atrophy. In this study, we investigate the effect of intermittent bout and single bout exercise training on inflammatory molecules in young (3months) and old (22months) male Sprague–Dawley rats. The rats were divided into 6 groups. Young and old rats were randomly assigned for control and two exercise training groups, single bout (S type): 30min/day, 5days/week for 6weeks and intermittent bout (I type): three times for 10min/day, 5days/week for 6weeks respectively. The exercise training was carried out by a treadmill at a speed of 15m/min (young) or 10m/min (old) with a slope of 5°. After 48h of the final exercise bout, muscle samples were collected for biochemical assay. I type exercise training reduced the serum levels of inflammatory molecules such as interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and malondialdehyde (MDA) in old rats. By contrast, interleukin-4 (IL-4) and superoxide dismutase (SOD) were elevated. Consequently in skeletal muscles, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were decreased significantly in the old group of I type. However, the matrix metalloproteinase-2 (MMP-2) level had no positive effects. Also, phosphorylation of mammalian target of rapamycin (p-mTOR) and myogenic differentiation (MyoD) were increased markedly in S and I types of old rats. These results suggest that I type exercise training appears more effective to reduce age-associated inflammatory molecules, and may recommend in regulating against chronic complicated disease induced by aging.

CETP Expression Protects Female Mice from Obesity-Induced Decline in Exercise Capacity.

Pharmacological approaches to reduce obesity have not resulted in dramatic reductions in the risk of coronary heart disease (CHD). Exercise, in contrast, reduces CHD risk even in the setting of obesity. Cholesteryl Ester Transfer Protein (CETP) is a lipid transfer protein that shuttles lipids between serum lipoproteins and tissues. There are sexual-dimorphisms in the effects of CETP in humans. Mice naturally lack CETP, but we previously reported that transgenic expression of CETP increases muscle glycolysis in fasting and protects against insulin resistance with high-fat diet (HFD) feeding in female but not male mice. Since glycolysis provides an important energy source for working muscle, we aimed to define if CETP expression protects against the decline in exercise capacity associated with obesity. We measured exercise capacity in female mice that were fed a chow diet and then switched to a HFD. There was no difference in exercise capacity between lean, chow-fed CETP female mice and their non-transgenic littermates. Female CETP transgenic mice were relatively protected against the decline in exercise capacity caused by obesity compared to WT. Despite gaining similar fat mass after 6 weeks of HFD-feeding, female CETP mice showed a nearly two-fold increase in run distance compared to WT. After an additional 6 weeks of HFD-feeding, mice were subjected to a final exercise bout and muscle mitochondria were isolated. We found that improved exercise capacity in CETP mice corresponded with increased muscle mitochondrial oxidative capacity, and increased expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). These results suggest that CETP can protect against the obesity-induced impairment in exercise capacity and may be a target to improve exercise capacity in the context of obesity.

Hyperthermia, but not muscle water deficit, increases glycogen use during intense exercise.

We determined if dehydration alone or in combination with hyperthermia accelerates muscle glycogen use during intense exercise. Seven endurance-trained cyclists (VO2max = 54.4 ± 1.05 mL/kg/min) dehydrated 4.6% of body mass (BM) during exercise in the heat (150 min at 33 ± 1 °C, 25 ± 2% humidity). During recovery (4 h), subjects remained dehydrated (HYPO trial) or recovered all fluid losses (REH trials). Finally, subjects exercised intensely (75% VO2max ) for 40 min in a neutral (25 ± 1 °C; HYPO and REH trials) or in a hot environment (36 ± 1 °C; REHHOT ). Before the final exercise bout vastus lateralis glycogen concentration was similar in all three trials (434 ± 57 mmol/kg of dry muscle (dm)) but muscle water content was lower in the HYPO (357 ± 14 mL/100 g dm) than in REH trials (389 ± 25 and 386 ± 25 mL/100 g dm; P < 0.05). After 40 min of intense exercise, intestinal temperature was similar between the HYPO and REHHOT trials (39.2 ± 0.5 and 39.2 ± 0.4 °C, respectively) and glycogen use was similar (172 ± 86 and 185 ± 97 mmol/kg dm, respectively) despite large differences in muscle water content. In contrast, during REH, intestinal temperature (38.5 ± 0.4 °C) and glycogen use (117 ± 52 mmol/kg dm) were significantly lower than during HYPO and REHHOT . Our data suggest that hyperthermia stimulates glycogen use during intense exercise while muscle water deficit has a minor role.

Systemic cytokine response to three bouts of eccentric exercise

This research examined the changes in inflammatory cytokines interleukin 6 (IL-6), IL-1β, IL-10, as well as muscle force, muscle soreness, thigh circumference, and range of motion in response to 3 bouts of eccentric knee extension. Ten males were recruited to participate. The participants performed eccentric exercise on 3 consecutive days on the knee extensors on the right leg separated by 24h. Participants performed 6 sets of 10 repetitions of isokinetic eccentric knee extension at 120° per second. Blood was sampled before and after each exercise bout and 24h after the final exercise bout. Muscle isometric force, delayed onset muscle soreness (DOMS), thigh circumference, and range of motion were evaluated before and after each exercise bout and 24h after the final exercise bout. There were no statistically significant differences noted for the changes in isometric strength, thigh circumference, and range of motion, or IL-6 over the 4 days (all p > 0.05). On the second day and third day there was a significant increase noted in DOMS as compared with baseline (p < 0.05). These results suggest that 3 consecutive days of eccentric exercise results in DOMS but does not produce a sustained systemic inflammatory reaction or changes in muscle function.

Age-Related Decrements in Heat Dissipation during Physical Activity Occur as Early as the Age of 40

Older adults typically experience greater levels of thermal strain during physical efforts in the heat compared to young individuals. While this may be related to an age-dependent reduction in whole-body sweating, no study has clearly delineated at what age this occurs. In the present study, we report direct measurements of human heat dissipation during physical activity in the heat in males ranging in age from 20–70 years. Eighty-five males performed four 15-min bouts of cycling separated by 15-min rest periods, in a calorimeter regulated to 35°C and 20% relative humidity. Direct calorimetry was used to measure total heat loss (whole-body evaporative heat loss and dry heat exchange). We also used indirect calorimetry as a continuous measure of metabolic heat production. Body heat storage was calculated as the temporal summation of heat production and total heat loss over the experimental session. Whole-body sweat rate (WBSR) was calculated from measurements of evaporative heat loss. Males were divided into five age categories for the analysis of WBSR and body heat storage: 20–31 years (n = 18), 40–44 years (n = 15), 45–49 years (n = 15), 50–55 years (n = 21) and 56–70 years (n = 16). Relative to young males, WBSR was reduced in males aged 56–70 during each exercise (all P<0.05), in males aged 50–55 during the second (P = 0.031) and third exercises (P = 0.028) and in males aged 45–49 during the final exercise bout (P = 0.046). Although not significantly different, 40–44 years old males also had a lower rate of heat loss compared to younger males. Over the sum of two hours, the change in body heat content was greater in males 40–70 years compared to young males (all P<0.05). Our findings suggest that middle-aged and older adults have impairments in heat dissipation when doing physical activity in the heat, thus possibly increasing their risk of heat-related illness under such conditions.

The effect of progressive heat acclimation on change in body heat content in young males

Heat acclimation improves the physiological capacity to dissipate heat. As previous studies have only relied upon core temperature and local heat loss measurements, it remains unclear the extent to which whole‐body heat loss, and therefore body heat storage is altered during heat acclimation. Using direct calorimetry, we examined whole‐body heat exchange during progressive increases in the requirement for heat loss during and following a 14‐day heat acclimation protocol. Six young males (Mean±SD, age: 23±3yrs) performed intermittent exercise (3×30‐min bouts of cycling at 300, 350, and 400 W·m−2separated by 10 min rest period) in dry heat (35°C, 20% relative humidity [RH]) prior to (day 0), during (day 7), and at the end (day 14) of a 14‐day heat acclimation. On days 1–6 and 8–13, subjects cycled for 90 min (~50% VO2max) in the heat (40°C, 20% RH). Despite a similar requirement between test days, significantly lower increases in evaporative heat loss were observed for the final exercise bout in days 0 (P=0.01) and 7 (P=0.02) relative to day 14. After 7 days of acclimation, the ΔHb following the exercise did not significantly decrease from day 0 (673±165 vs. 449±109 kJ, p=0.112). However, on day 14 the ΔHb was significantly reduced compared to day 0 (363±64 vs. 673±165 kJ, p=0.04). These data suggest that 14 days is necessary to achieve sufficient heat acclimation to significantly reduce heat storage during exercise in the heat. Support: Deep Mining Research Consortium (Dr. Glen P. Kenny)

Exercise promotes bone marrow cell survival and recipient reconstitution post-bone marrow transplantation, which is associated with increased survival

Bone marrow transplantation (BMT) is associated with a high risk of mortality, partially because of the harmful effects of the preconditioning myeloablative regimens. We have recently demonstrated increased bone marrow cell survival and proliferation in response to exercise training, which may be attributable to increased quality of the niche. The purpose of the present study was to determine the extent to which exercise preconditioning of recipients could increase the success of BMT. Recipient mice remained sedentary (SED) or were exercise-trained (EX) on a treadmill (3 d/wk for 8 weeks) before reconstitution with green fluorescent protein (GFP)-labeled donor marrow. Recipient survival, both donor-derived and total (donor- and recipient-derived) blood reconstitution were measured by flow cytometry. The first and fourth day after BMT apoptosis, cellularity and donor cell homing were determined in the recipients' bone marrow cavity by flow cytometry. Whereas only 25% of SED mice survived, 82% of EX recipients survived the BMT. Homing of donor-derived marrow cells to the recipients' marrow cavity acutely after BMT was not altered in EX, but EX mice displayed decreased levels (10%; p < 0.05) of activated caspase-3/-7 one day after BMT, leading to a maintenance of marrow cellularity in mice preconditioned with exercise. The acute inhibition of marrow cell apoptosis in EX mice resulted in increased total blood cell reconstitution at 1 and 3.5 months after BMT in EX mice (42% and 43%, respectively; both p < 0.05). Short- and long-term donor-derived engraftment was not different between EX and SED recipients. Exercise training increases recipient survival after BMT with increased total blood cell reconstitution.

Exercise induced cardioprotection is mediated via delta opioid receptors

Acute exercise exposure dramatically reduces cellular death that results during ischemic reperfusion (IR). Existing evidence indicates endogenous opioids are a critical component of this protection; however the specific opioid receptor subtype responsible for these effects is unknown. The role of the delta opioid receptor in exercise induced cardioprotection was examined. Rats were randomly assigned into Sham, Sedentary (S) or Exercise (Ex) groups. A selective delta‐opioid receptor antagonist, Naltrindole, was administered 15 minutes prior to exercise in a subset of animals (ExD), and at a corresponding time in a subset of S animals (SD). 24hr following the final exercise bout animals received surgically induced IR in vivo. Significant between group differences existed for tissue necrosis, p &lt; 0.0001. Compared to Sham, S, SD, and ExD animals exhibited significant tissue necrosis post IR, while Ex hearts were protected. S increased necrosis compared to Ex, but was not different from SD. Significant between group differences existed for tissue apoptosis, p = 0.013 following IR. Apoptosis levels were elevated in S and SD compared to Sham while Ex and ExD were protected. These data provide evidence that the delta opioid receptor mediates exercise induced cardioprotection against necrosis but not apoptotic tissue death. Supported by JCQ Auburn University Intramural Grant Program.

Ten Days of Aerobic Exercise Enhances Aortic Endothelium Dependent Relaxation through Depressed NADPH-oxidase Activity

Tetrahydrobiopterin (BH4) is an essential co-factor of endothelial nitric oxide synthase (eNOS). BH4 can be depleted by oxidation, which leads to "uncoupling" of eNOS, where eNOS produces superoxide (O2-) rather than nitric oxide. In addition, enhanced O2- production by NADPH oxidase in the vasculature may create an oxidative environment that promotes eNOS uncoupling, thereby impairing endothelial function. PURPOSE: The purpose of this study was to investigate if 10 days of aerobic exercise can enhance aortic endothelium dependent relaxation (EDR) by BH4 preservation and/or alteration of NADPH oxidase activity. METHODS: Young, female Sprague-Dawley rats were assigned to either an exercise (Ex) or sedentary (Sed) group. Ex rats performed 10 consecutive days of exercise for 15/30/15 min on a treadmill at speeds of 15/30/15 m/min, respectively (6% grade). Rats were sacrificed 24 hrs following the final exercise bout and the aorta was excised and cut into ∼2 mm rings. Individual rings were mounted between 2 pins on a myograph system and bathed with physiological saline. EDR was assessed in rings pre-constricted with 0.3 μM phenylephrine (PE) by cumulative doses of acetylcholine (ACh) in the 0.001 - 10.0 μM range to generate a concentration-dependent response. The experiment was then repeated in each ring following a 30 min incubation in either 10.0 μM BH4 (Ex: n = 9; Sed: n = 2) or 1.0 mM apocynin (Ex: n = 4; Sed: n = 2), an NADPH oxidase inhibitor. The relaxation response was normalized to surface area and expressed as % of PE induced constriction. EDR was assessed as the EC50 value of the ACh dose-response curve. RESULTS: Exercise decreased the EC50 17% (0.171 ± 0.044 vs. 0.206 ± 0.051 μM; Ex vs. Sed). BH4 increased the EC50 35% in Ex (0.232 ± 0.047 vs. 0.171 ± 0.044 μM) and 25% in Sed (0.257 ± 0.074 vs. 0.206 ± 0.051 μM). Apocynin decreased the EC50 37% in Ex (0.158 ± 0.047 vs. 0.244 ± 0.085 μM) and 72% in Sed (0.041 ± 0.020 vs. 0.147 ± 0.039 μM). CONCLUSION: There is a trend toward enhanced EDR following 10 days of exercise. The trend of a greater improvement in ACh-sensitivity upon apocynin incubation in the Sed rings suggests that exercise training increases endothelium dependent relaxation at least partially via a suppression of NADPH oxidase activity. BH4 did not improve relaxation demonstrating a lack of detectable eNOS uncoupling.