PURPOSE: Decreased fraction of inspired oxygen (FiO2) is often used to simulate the atmospheric partial pressure of oxygen decreases experienced during high altitude sojourns. Therefore, we aimed to independently investigate hypoxia and altitude by isolating oxygen concentration and barometric pressure. METHODS: 18 subjects completed 3 trials (sea level, hypoxia, altitude). 90-minute duration and intensity matched hypoxic stimuli were induced via decreased FiO2 or 4,200 m ascent. Relative tissue oxygenation change and cardiovascular variables were measured during rest and a 3-minute step-test. RESULTS: Muscle oxygenated hemoglobin (O2Hb) and muscle deoxygenated hemoglobin (HHb) were not different across environments during rest or exercise (p > 0.339) with alterations noted during rest to exercise transitions (p < 0.001). Resting brain O2Hb at hypoxia and altitude were lower than sea level (p < 0.012), but not different than each other (p = 0.278). Exercising brain O2Hb was lower at altitude than sea level (p = 0.007) similarly trending compared to hypoxia (p = 0.066). Exercising brain O2Hb was not different between hypoxia and sea level (p = 0.158). Brain HHb at hypoxia and altitude were higher than sea level (p < 0.001), but not different than each other (p = 0.158). Exercise HR at hypoxia (141 ± 4 beats·min-1) and altitude (141 ± 3 beats·min-1) were lower than sea level (127 ± 44 beats·min-1, p < 0.002), but not different than each other (p > 0.208). Exercise stroke volume at altitude (109.6 ± 4.1 mL) was higher than hypoxia (97.8 ± 3.3 mL) and sea level (99.8 ± 3.9 mL, p < 0.010) with no differences between hypoxia and sea level (p = 0.481). Exercise cardiac output at hypoxia (13.8 ± 0.6 L) and altitude (15.5 ± 0.7 L) were greater than sea level (12.6 ± 0.5 L, p < 0.006) with altitude greater than hypoxia (p = 0.001). CONCLUSIONS: During acute hypoxic stimuli, skeletal muscle maintains oxygenation while the brain does not. Tissue oxygenation may be mediated by environmentally driven cardiovascular compensation. FiO2 decreases may not satisfactorily simulate all physiological outcomes experienced during altitude induced barometric pressure decreases. Funding: Department of Defense United States Army Medical Research and Materiel Command (DOD USAMRMC: W81XWH-15-2-0075).

The purpose of this study was to examine the effects of acute normobaric (NH, decreased FiO 2 ) and hypobaric (HH, 4200 m ascent) hypoxia exposures compared to sea level (normobaric normoxia, NN). Tissue oxygenation, cardiovascular, and body fluid variables measured during rest and a 3-min step-test following 90-min exposures (NH, HH, NN). Muscle oxygenated hemoglobin (O 2 Hb) decreased, and muscle deoxygenated hemoglobin (HHb) increased environmentally independent from rest to exercise ( p < 0.001). During exercise, brain O 2 Hb was lower at HH compared to NN ( p = 0.007), trending similarly with NH ( p = 0.066), but no difference between NN and NH ( p = 0.158). During exercise, HR at NH (141 ± 4 beats·min −1 ) and HH (141 ± 3 beats·min −1 ) were higher than NN (127 ± 44 beats·min −1 , p = 0.002), but not each other ( p = 0.208). During exercise, stroke volume at HH (109.6 ± 4.1 mL·beat −1 ) was higher than NH (97.8 ± 3.3 mL·beat −1 ) and NN (99.8 ± 3.9 mL·beat −1 , p ≤ 0.010) with no difference between NH and NN ( p = 0.481). During exercise, cardiac output at NH (13.8 ± 0.6 L) and HH (15.5 ± 0.7 L) were higher than NN (12.6 ± 0.5 L, p ≤ 0.006) with HH also higher than NH ( p = 0.001). During acute hypoxic stimuli, skeletal muscle maintains oxygenation whereas the brain does not. These differences may be mediated by environmentally specific cardiovascular compensation. Thus, caution is advised when equating NH and HH.

PGC-1a has been termed the master regulator of mitochondrial biogenesis. The exercise-induced rise in PGC-1a transcription is blunted when acute exercise takes place in the heat. However, it is unknown if this alteration has functional implications after heat acclimation and exercise training. To determine the impact of 3 weeks of aerobic exercise training in the heat (33 °C) compared to training in room temperature (20 °C) on thermoregulation, PGC-1a mRNA response, and aerobic power. Twenty-one untrained college aged males (age, 24 ± 4 years; height, 178 ± 6 cm) were randomly assigned to 3 weeks of aerobic exercise training in either 33 °C (n = 12) or 20 °C (n = 11) environmental temperatures. The 20 °C training group increased 20 °C $${{\dot{\text{V}}}}$$ ̇O2peak from 3.21 ± 0.77 to 3.66 ± 0.78 L·min−1 (p < 0.001) while the 33 °C training group did not improve (pre, 3.16 ± 0.48 L·min−1; post, 3.28 ± 0.63 L·min−1; p = 0.283). PGC-1a increased in response to acute aerobic exercise more in 20 °C (6.6 ± 0.7 fold) than 33 °C (4.6 ± 0.7 fold, p = 0.031) before training, but was no different after training in 20 °C (2.4 ± 0.3 fold) or 33 °C (2.4 ± 0.5 fold, p = 0.999). No quantitative alterations in mitochondrial DNA were detected with training or between temperatures (p > 0.05). This research indicates that exercise in the heat may limit the effectiveness of aerobic exercise at increasing aerobic power. Furthermore, this study demonstrates that heat induced blunting of the normal exercise induced PGC-1a response is eliminated after 3 weeks of heat acclimation.

A reduced mitochondrial DNA (mtDNA) copy number, the ratio of mitochondrial DNA to genomic DNA (mtDNA:gDNA), has been linked with dysfunctional mitochondria. Exercise can acutely induce mtDNA damage manifested as a reduced copy number. However, the influence of a paired (exercise and temperature) intervention on regional mtDNA (MINor Arc and MAJor Arc) are unknown. Thus, the purpose of this study was to determine the acute effects of exercise in cold (7 °C), room temperature (20 °C), and hot (33 °C) ambient temperatures, on regional mitochondrial copy number (MINcn and MAJcn). Thirty-four participants (24.4 ± 5.1 yrs, 87.1 ± 22.1 kg, 22.3 ± 8.5 %BF, and 3.20 ± 0.59 L·min−1 VO2peak) cycled for 1 h (261.1 ± 22.1 W) in either 7 °C, 20 °C, or 33 °C ambient conditions. Muscle biopsy samples were collected from the vastus lateralis to determine mtDNA regional copy numbers via RT-qPCR. mtDNA is sensitive to the stressors of exercise post-exercise (MIN fold change, −1.50 ± 0.11; MAJ fold change, −1.70 ± 0.12) and 4-h post-exercise (MIN fold change, −0.82 ± 0.13; MAJ fold change, −1.54 ± 0.11). The MAJ Arc seems to be more sensitive to heat, showing a temperature-trend (p = 0.056) for a reduced regional copy number ratio after exercise in the heat (fold change −2.81 ± 0.11; p = 0.019). These results expand upon our current knowledge of the influence of temperature and exercise on the acute remodeling of regional mtDNA.

The effects of exercise training in the heat have been well documented in men. However, the effects of exercise training in the heat in women have not received as much attention. We have previously reported a blunted rise in PGC1α in men after acute aerobic exercise in the heat. Purpose To determine the impact of three weeks of aerobic exercise training in the heat compared to training in room temperature on thermoregulation, PGC1αmRNA response, and aerobic capacity in women. Methods Twenty-three untrained college aged females (24±4 years old, 168±5 cm tall, and weighed 67.3±11.2 kg) were randomly assigned to 3 weeks of aerobic exercise training in either 20°C (n=12) or 33°C (n=11) environmental temperatures. Results VO2max in room temperature conditions increased with training (2.57±0.35 to 2.71±0.32 L·min-1, p=0.01), but was not different between 20°C or 33°C training conditions (p=0.821). HR decreased with training (152±16 to 140±0.13 bpm, p<0.001), but was not different between 20°C or 33°C training conditions (p=0.341). Sweat rate increased with training (0.655±0.192 to 0.775±0.212 L·hr-1, p=0.006) and was higher in 33°C (0.835±0.144 L·hr-1) than 20°C (0.605±0.132 L·hr-1, p<0.001). PGC1α mRNA increased with an acute exercise bout before (1.01±0.10 to 4.96±2.08 fold, p<0.001) and after training (1.07±0.10 to 3.21±1.39 fold, p<0.001) and had a smaller response after training than before training (p=0.005). There were no differences in PGC1α mRNAbetween groups (p=0.661). Conclusions Women can increase aerobic fitness and maintain their exercise induced PGC1α mRNA response in the heat equally to that of room temperature conditions. This response contrasts with the blunted PGC1α mRNA response and VO2 max alterations previously observed in men.

Our understanding of the molecular mechanisms underlying adaptations to resistance exercise remains elusive despite the significant biological and clinical relevance. We developed a novel voluntary mouse weightlifting model, which elicits squat-like activities against adjustable load during feeding, to investigate the resistance exercise-induced contractile and metabolic adaptations. RNAseq analysis revealed that a single bout of weightlifting induced significant transcriptome responses of genes that function in posttranslational modification, metabolism, and muscle differentiation in recruited skeletal muscles, which were confirmed by increased expression of fibroblast growth factor-inducible 14 (Fn14), Down syndrome critical region 1 (Dscr1) and Nuclear receptor subfamily 4, group A, member 3 (Nr4a3) genes. Long-term (8 weeks) voluntary weightlifting training resulted in significantly increases of muscle mass, protein synthesis (puromycin incorporation in SUnSET assay) and mTOR pathway protein expression (raptor, 4e-bp-1, and p70S6K proteins) along with enhanced muscle power (specific torque and contraction speed), but not endurance capacity, mitochondrial biogenesis, and fiber type transformation. Importantly, weightlifting training profound improved whole-body glucose clearance and skeletal muscle insulin sensitivity along with enhanced autophagy (increased LC3 and LC3-II/I ratio, and decreased p62/Sqstm1). These data suggest that resistance training in mice promotes muscle adaptation and insulin sensitivity with simultaneous enhancement of autophagy and mTOR pathway.

Cold environmental temperatures during exercise and recovery alter the acute response to cellular signaling and training adaptations. Approximately 3 wk is required for cold temperature acclimation to occur. To determine the impact of cold environmental temperature on training adaptations, fitness measurements, and aerobic performance, two groups of 12 untrained male subjects completed 1 h of cycling in 16 temperature acclimation sessions in either a 7°C or 20°C environmental temperature. Fitness assessments before and after acclimation occurred at standard room temperature. Muscle biopsies were taken from the vastus lateralis muscle before and after training to assess molecular markers related to mitochondrial development. Peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) mRNA was higher in 7°C than in 20°C in response to acute exercise before training (P = 0.012) but not after training (P = 0.813). PGC-1α mRNA was lower after training (P < 0.001). BNIP3 was lower after training in the 7°C than in the 20°C group (P = 0.017) but not before training (P = 0.549). No other differences occurred between temperature groups in VEGF, ERRα, NRF1, NRF2, TFAM, PINK1, Parkin, or BNIP3L mRNAs (P > 0.05). PGC-1α protein and mtDNA were not different before training, after training, or between temperatures (P > 0.05). Cycling power increased during the daily training (P < 0.001) but was not different between temperatures (P = 0.169). V̇o2peak increased with training (P < 0.001) but was not different between temperature groups (P = 0.460). These data indicate that a 3-wk period of acclimation/training in cold environmental temperatures alters PGC-1α gene expression acutely but this difference is not manifested in a greater increase in V̇o2peak and is dissipated as acclimation takes place.NEW & NOTEWORTHY This study examines the adaptive response of cellular signaling during exercise in cold environmental temperatures. We demonstrate that peroxisome proliferator-activated receptor-γ coactivator 1α mRNA is different between cold and room temperature environments before training but after training this difference no longer exists. This initial difference in transcriptional response between temperatures does not lead to differences in performance measures or increases in protein or mitochondria.

There has been recent debate on the potential difference in physiological response between exposure to simulated altitude (normobaric hypoxia) and terrestrial altitude (hypobaric hypoxia). Purpose: To determine the difference in the physiological response to normobaric and hypobaric hypoxia during exercise. Methods: Eight recreationally active subjects (27 ± 5 y old, 73.1 ± 7.4 kg body weight, 170.6 ± 6.7 cm height, and 19.3 ± 9.2 % body fat) completed incremental cycling exercise to volitional fatigue in three separate environments: normobaric normoxia (NN; 350 m), normobaric hypoxia (NH; simulated 3094 m), and hypobaric hypoxia (HH; 3094 m). Heart rate, blood oxygen saturation, and muscle tissue oxygenation were measured at rest and continuously throughout the exercise trials. Results: Blood oxygen saturation (SpO2) was ~10% higher in NN compared to the two hypoxic conditions (p < 0.001) at rest and all exercise stages, with no difference between NH and HH (p > 0.05). Heart rate was higher at rest in HH (98 ± 13 bpm) compared to NN (83 ± 15 bpm, p = 0.011) and NH (84 ± 14 bpm, p = 0.001) which persisted until 165 watts at which point no difference was observed (p > 0.05). Muscle tissue oxygenation was 17% higher in HH compared to NN and 19% higher than NH throughout exposure (p < 0.05). Conclusion: This data indicates that the hypoxic stress resulting from normobaric and hypobaric hypoxia are not the sameand that hypobaric hypoxia may not result in hypoxia at the level of the tissue.

Cold exposure during cycling and recovery enhances PGC-1α transcription, but aspects of mitophagy and a more intense cold exposure without recovery occurring in the cold have not been explored. PURPOSE:Determine the expression of genes related to mitochondrial biogenesis and mitophagy following an acute cycling bout at a temperature below freezing compared to that of room temperature. METHODS:Eleven male participants cycled at 65% Wmax for 1 h at -2 °C and 20 °C and then recovered at room temperature for 6 h. A muscle biopsy was taken from the vastus lateralis before exercise, 3 h, and 6 h post-exercise for gene expression analysis. RESULTS:Exercising heart rate and skin temperature were lower in the cold (p < 0.001; p = 0.004), while core temperature was higher (p = 0.016). Temperature had no effect on gene expression (p > 0.05). BNIP3 and BNIP3L mRNA were not influenced by exercise (p = 0.329; p 0.233). PGC-1α and VEGF were higher after cycling (p < 0.001), but the extent of PGC-1α upregulation was reduced 6 h post-exercise (p 0.006). TFAM increased 6 h post-exercise (p = 0.001). NRF2, ERRα, PINK1, and PARK2 decreased 3 h post-exercise (p 0.035; p = 0.005; p = 0.002; p = 0.001), but this downregulation was diminished after 6 h of recovery (p = 0.017; p 0.006; p = 0.043; p = 0.047). NRF1 was marginally attenuated with exercise (p = 0.001). CONCLUSIONS:Exercise induced alterations in gene expression for mitochondrial biogenesis and mitophagy, but these effects were independent of temperature.

Power meters are a training tool used to help cyclists improve performance by objectively monitoring intensity. Some power meters are well established and validated, whereas others are relatively new. Most power meters have been tested for validity and reliability in laboratory and field settings of similar conditions; however, the reproducibility of these power meters across different temperatures has not been established. To examine the potential differences of the CompuTrainer, PowerTap, Stages, and Vector power meters in hot and cold compared to a room temperature environment. Recreationally trained male (n=7) and female (n=3) participants each completed three incremental cycling trials in hot (33°C), cold (7°C), or room temperature (RT, 20°C) conditions. The power meters were placed on a standard road bicycle and power output was logged and recorded. The CompuTrainer was higher in the room temperature trial compared to the cold and the hot, but not between the hot and cold trial. The PowerTap was not different in RT and cold, but was lower in hot compared to RT and compared to cold. The Stages was not different between RT and cold, but was lower in the hot compared to RT and compared to cold. The Vector was not different between RT and cold but was lower in the hot compared to RT and compared to cold. These data indicate that environmental temperature may affect the reproducibility of power meters. It is important to recognize the potential differences between temperatures when choosing a power meter.

Background: The physiological effects of hypoxia may be influenced by how hypoxia is achieved. The purpose of this study was to determine the effects of recovery in hypobaric hypoxia (HH), normobaric hypoxia (NH), and normobaric normoxia (NN) after endurance exercise on gene expression related to mitochondrial biogenesis, myogenesis, and proteolysis. Methods: Fifteen recreationally trained subjects each cycled for 1 hour before recovering for 4 hours in NN (laboratory atmospheric conditions, 975 m), HH (depressurized to simulate 4420 m), and NH (fraction of O2 reduced to simulate 4420 m). Muscle biopsy samples were obtained before exercise and after 4 hours of recovery. Results: Blood oxygenation (SpO2) was lower in HH (76.02 ± 0.58%) than NH (79.45 ± 0.56, p < 0.001), which were both lower than in NN (96.3 ± 0.17, p < 0.001). Heart rate was higher in HH (82 ± 2 bpm) than NH (77 ± 1 bpm, p < 0.001), which were both higher than in NN (67 ± 1 bpm, p < 0.001). Mitochondrial transcription factor A (TFAM) mRNA was lower after NN than HH (p = 0.034) or NH (p = 0.005), but was not different between HH and NH (p = 0.460). Myostatin (MSTN) mRNA decreased from pre- to postexercise (p < 0.001) in all conditions and was lower in HH compared with NH (p = 0.035) and NN (p = 0.017). No other differences were noted in genes related to mitochondrial biogenesis, myogenesis, or proteolysis (p > 0.05). Conclusion:TFAM mRNA is lower with hypoxia exposure, but effected by the type of hypoxia. MSTN gene expression is lower after exposure to HH than NH or NN. These data support previous work and caution the translation of NH data obtained in a NH environment to a HH environment.

METHODS: The tibialis anterior (TA) of C57BL6 mice was injured with cardiotoxin (CTX) and collected 5, 7, 10, 14, and 21 post-injury for histological/ immunohistochemical (IHC) and gene expression analysis. To examine the function of senescent cells during muscle repair, mice were treated with a senolytic compound (ABT-263) following injury to selectively ablate senescent cells. RESULTS: Senescent cell number (as revealed using the senescence-associated beta-galactosidase (SA-β-gal) assay) increased significantly following injury (p <0.05) and returned to baseline by day 21 post-injury, a time-course that is coincident with the repair process. In agreement with this, qPCR analysis of putative senescence pathways including p16 and p21 and p53 as well as secreted factors commonly secreted by senescent cells such as IL1 and MMP13 were significantly upregulated in injured compared to control tissue (p <0.05). Preliminary IHC analysis demonstrated that at 5 days post-injury, 58% of senescent cells were positive for macrophage marker F480, while at 10 days post-injury, 43% of senescent cells were F480+ and 9% were CD31 positive; an endothelial cell marker. Identification of other cell types is under investigation. Senolytic treatment was effective at removing senescent cells as a significant 44% reduction in the number of SA-β-gal+ cells was observed, the consequences of which on muscle repair are currently under analysis. CONCLUSION: Senescent cells are a newly identified component of the muscle repair environment which may influence skeletal muscle repair and satellite cell function. Supported by NSERC discovery grant and The Canadian Foundation for Innovation and ACOA.

Peroxisome proliferator-activated receptor-α coactivator-1α (PGC-1α) mRNA is increased with both exercise and exposure to cold temperature. However, transcriptional control has yet to be examined during exercise in the cold. Additionally, the need for environmental cold exposure after exercise may not be a practical recovery modality. The purpose of this study was to determine mitochondrial-related gene expression and transcriptional control of PGC-1α following exercise in a cold compared with room temperature environment. Eleven recreationally trained males completed two 1-h cycling bouts in a cold (7°C) or room temperature (20°C) environment, followed by 3 h of supine recovery in standard room conditions. Muscle biopsies were taken from the vastus lateralis preexercise, postexercise, and after a 3-h recovery. Gene expression and transcription factor binding to the PGC-1α promoter were analyzed. PGC-1α mRNA increased from preexercise to 3 h of recovery, but there was no difference between trials. Estrogen-related receptor-α (ERRα), myocyte enhancer factor-2 (MEF2A), and nuclear respiratory factor-1 (NRF-1) mRNA were lower in cold than at room temperature. Forkhead box class-O (FOXO1) and cAMP response element-binding protein (CREB) binding to the PGC-1α promoter were increased postexercise and at 3 h of recovery. MEF2A binding increased postexercise, and activating transcription factor 2 (ATF2) binding increased at 3 h of recovery. These data indicate no difference in PGC-1α mRNA or transcriptional control after exercise in cold versus room temperature and 3 h of recovery. However, the observed reductions in the mRNA of select transcription factors downstream of PGC-1α indicate a potential influence of exercise in the cold on the transcriptional response related to mitochondrial biogenesis.

PURPOSE: Hypobaria and hypoxia exert independent effects on exercise-induced oxidative stress in blood, while the hypobaric and hypoxic influences are not well defined. The current study was undertaken to quantify exercise-induced oxidative stress recovery during lab-simulated hypoxic and hypobaric conditions following a common bout of exercise. METHODS: At a base elevation of 975m, physically active participants (n=16), ages 18-40, provided informed consent prior to performing 60 minutes of cycle ergometry at 70% watts max. Using a randomized counter-balanced crossover design participants recovered for 4 hours in 3 lab-simulated conditions; 1000m normobaric normoxia (NN, 675mmHg, 18.8%FiO2), 4400m normobaric hypoxia (NH, 675mmHg, 12% FiO2), or 4400m hypobaric hypoxia (HH, 440mmHg, 12% FiO2). O2 saturation was confirmed via pulse oximetry throughout the 3 exercise-recovery trials. Blood samples were collected in heparinized vacutainer tubes at time points Pre, Post, 2 Hours Post, and 4 Hours Post exercise. Blood plasma was analyzed for the quantification of oxidative stress to proteins (protein carbonyls, PC; 3-nitrotyrosines, 3NT), lipid (lipid hydroperoxides, LOOH; 8-isoprostanes, 8-ISO), and antioxidant capacity (ferric reducing ability of plasma, FRAP; trolox equivalent antioxidant capacity, TEAC). RESULTS: Plasma TEAC, FRAP, 3NT and PC were unaltered by exercise and recovery environments (p>0.05). Exercise-induced increases in LOOH and 8-ISO were observed, although time-by-trial differences were not present. CONCLUSIONS: These data indicate that exercise recovery in simulated conditions of NH and HH do not impact a common panel of blood oxidative stress measures.

PURPOSE: Altitude exposure and exercise provoke an acute oxidative stress response in muscle and blood tissues. Prior work indicates that redox-sensitive exercise recovery responses are attenuated above 1500 m, although the independent impact of hypobaria and hypoxia on these responses are unknown. Moreover, given that the wealth of existing exercise and altitude data are conducted primarily in males, the current study was designed to understand exercise recovery responses in males and females exposed to various hypoxia and hypobaria conditions following a common bout of aerobic exercise. METHODS: Sixteen active males (n=8) and females (n=8) between the ages of 18-40 performed cycle ergometer exercise for 60 minutes at 70% watts max at a base elevation of 975m. In a randomized counter-balanced crossover design subjects recovered in an environmental chamber for 4hours in three conditions; 1000m normobaric normoxia (NN, 675mmHg, 18.8%FiO2), a simulated 4400m normobaric hypoxia (NH, 675mmHg, 12% FiO2), or a simulated 4400 m hypobaric hypoxia (HH, 440mmHg, 12% FiO2). Pulse oximetry was used to measure O2 saturation throughout the exercise trials and to confirm hypoxia during recovery. Six muscle biopsies obtained from the vastus lateralis at baseline and following each exercise recovery were examined for hypoxia and redox sensitive transcripts including endothelial PAS domain protein-1 (EPAS-1), hemeoxygenase-1 (HMOX1), superoxide dismutase-2 (SOD2), and nuclear factor erythroid-derived 2-like 2 (NFE2L2). RESULTS: No sex-dependent differences in gene transcripts were observed for any markers examined (p>0.05). No differences were observed for EPAS-1 (variable 2 fold increase, p>0.05) or NFE2L2 (1.29 fold increase, p>0.05). Time-, but not trial-, dependent differences existed for HMOX1 (8.4 fold increase, p<0.000) and SOD2 (1.4 fold increase, p=0.017) and indicate a similar redox stimulus was present 4 hours post exercise in all three recovery condition. CONCLUSIONS: These data suggest exercise recovery in simulated conditions of NH and HH do not impact EPAS-1, HMOX1, SOD2 or NFE2L2. Additional redox-sensitive markers in blood and muscle should be examined to determine whether additional adaptive responses are impacted by NH and HH recovery conditions.

ABSTRACT Excessive positive energy balance is a major factor leading to obesity. The ability to alter the appetite-regulating hormones leptin, adiponectin, and ghrelin may help decrease excessive energy intake. Exercise and exposure to extreme temperatures can independently affect these appetite-regulating hormones. PURPOSE: To determine the effect of exercising in different environmental conditions on the circulating concentrations of leptin, adiponectin, and ghrelin. METHODS: Eleven recreationally-trained male participants completed 3 separate 1 h cycling bouts at 60% Wmax in hot, cold, and room temperature conditions (33°C, 7°C, 20°C), followed by a 3 h recovery at room temperature. Blood was drawn pre-exercise, post-exercise, and 3 h post-exercise. Hematocrit and hemoglobin were measured to account for change in plasma volume. RESULTS: Leptin concentrations were lower at post and 3 h post-exercise compared with pre-exercise, with and without correction for plasma volume shifts, regardless of temperature (p < 0.05). Adiponectin was higher post-exercise compared with pre-exercise (p = 0.021) but not 3 h post-exercise (p = 0.084) without correction for plasma volume shifts. However, adiponectin concentrations were not different at any time point when plasma volume shifts were accounted for (p > 0.05). Total ghrelin and acylated ghrelin concentrations were not affected at post and 3 h post-exercise compared with pre-exercise, with and without correcting for plasma volume shifts, regardless of ambient temperature (p > 0.05). No differences in leptin, adiponectin, or ghrelin were found between trials (p > 0.05). CONCLUSION: Temperature does not affect the circulating concentrations of appetite-regulating hormones during an acute bout of endurance exercise.

Markers for mitochondrial function in the skeletal muscle appear to be reduced after extended exposure to altitude. However, short term training at altitude enhances aerobic capacity. Further investigation is needed to determine the skeletal muscle response to altitude. PURPOSE: The purpose of this study was to determine the impact of exposure to normobaric hypoxia after exercise on the gene expression and subcellular location of PGC-1α protein compared to a normoxic environment. METHODS: Six male participants (age 25 ± 2, height 180 ± 4 cm, weight 82 ± 2 kg) completed two 90 min cycling trials in laboratory conditions followed by a 6 h recovery in either ambient conditions (975 m) or in a hypoxic environment (5000 m). Biopsies were taken from the vastus lateralis before exercise, after exercise, and following 6 h recovery. Samples were analyzed for PGC1-α gene expression using RT-qPCR and subcellular location using western blot on cytosolic and nuclear fractions. RESULTS: Exposure to hypoxia following exercise resulted in significantly lower expression of PGC-1α (p = 0.014) but no significant differences were found in protein translocation between the cytosolic (p = 0.225) and nuclear (p = 0.211) fractions. CONCLUSIONS: It appears that the post-translational events of PGC-1α are not altered by acute hypoxia after exercise, despite a reduced transcriptional response of PGC-1α.It is unclear if these cellular events would account for the deficit in mitochondrial function observed with extended exposure to a hypoxic environment. This project was funded by grants from the Department of Defense (W8IXWH-10-Z-0120) and NASA Nebraska Space Grant.

The American College of Sports Medicine (ACSM) recommends adults participate in weekly aerobic activity for a minimum of 30 minutes moderate intensity exercise 5 days per week or 20 minutes of vigorous activity 3 days per week. The electrically assisted bicycle may help individuals achieve the ACSM's aerobic recommendations and introduce inactive individuals to physical activity. To compare the physiological requirements of riding a bicycle with electric pedal assist versus non-assist among healthy active young adults. 6 males and 6 females completed two randomized cycling trials using electric pedal assist (PAB) and non-assist (NON). Cycling trials were completed over a 3.54 km course with varying terrain. Time to completion was faster in the PAB (12.5 ± 0.3 min) than the NON (13.8 ± 0.3 min, p=0.01). Rating of Perceived Exertion (RPE) was lower in the PAB (12.0 ± 0.4) than the NON (14.8 ± 0.5, p < 0.001). There was no difference in mean VO2 between PAB (2.3 ± 0.1 L·min-1) and NON (2.5 ± 0.1 L·min-1, p=0.45). There was no difference in mean power output when comparing PAB (115 ± 11 Watts) to NON (128 ± 11 Watts, p=0.38). There was no difference in heart rate between PAB (147 ± 5 bpm) and NON (149 ± 5 bpm, p=0.77). Recreationally active younger (college age) individuals may self-select a similar physiological intensity of physical activity regardless of mechanical assistance, resulting in quicker completion of a commuting task with PAB. Both the PAB and NON exercise bouts met ACSM criteria for vigorous exercise.

Recovery that takes place in a cold environment after endurance exercise elevates PGC-1α mRNA whereas ERRα and NRF2 mRNA expression are inhibited. However, the effect of local skeletal muscle cooling on mitochondrial-related gene expression is unknown. PURPOSE:To determine the impact of local skeletal muscle cooling during recovery from an acute bout of exercise on mitochondrial-related gene expression. METHODS:Recreationally-trained male cyclists (n=8, age 25±3 y, height 181±6cm, weight 79±8kg, 12.8±3.6% body fat, VO2peak 4.52±0.88L·min-1 protocol) completed a 90-min variable intensity cycling protocol followed by 4h of recovery. During recovery, ice was applied intermittently to one leg (ICE) while the other leg served as a control (CON). Intramuscular temperature was recorded continuously. Muscle biopsies were taken from each vastus lateralis at 4h post-exercise for the analysis of mitochondrial-related gene expression. RESULTS:Intramuscular temperature was colder in ICE (26.7±1.1°C) than CON (35.5±0.1°C) throughout the 4h recovery period (p<0.001). There were no differences in expression of PGC-1α, TFAM, NRF1, NRF2, or ERRα mRNA between ICE and CON after the 4h recovery period. CONCLUSION:Local muscle cooling after exercise does not impact the expression of mitochondrial biogenesis-related genes compared to recovery from exercise in control conditions. When these data are considered with previous research, the stimuli for cold-induced gene expression alterations may be related to factors other than local muscle temperature. Additionally, different intramuscular temperatures should be examined to determine dose-response of mitochondrial-related gene expression.

Obesity can result from a lack of energy expenditure or excessive energy intake. The appetite-regulating hormones leptin, adiponectin, and ghrelin may help decrease energy intake by affecting appetite. Exercise and exposure to extreme temperatures can independently affect these hormones. However, less is known on how exercise and temperature interact to affect appetite. PURPOSE: To determine the effect of exercise in different temperatures on the circulating concentrations of leptin, adiponectin, ghrelin, and acylated ghrelin. METHODS: Eleven recreationally-trained male participants completed three separate 1 h cycling bouts at 60% Wmax in different environmental temperatures (Hot 33 °C, Cold 7 °C, Room Temperature 20 °C), followed by 3 h recovery at room temperature. Blood was drawn pre-exercise, post-exercise, and 3 h post-exercise from the antecubital vein. Hematocrit and hemoglobin were measured to account for changes in plasma volume. RESULTS: Leptin concentrations were lower at post and 3 h post-exercise compared to pre-exercise, with and without correcting for plasma volume shifts, regardless of temperature (p < 0.05). Adiponectin was higher post-exercise than pre-exercise (p = 0.021) and then returned to pre-exercise levels by 3 h post-exercise (p = 0.084) without correction for plasma volume shifts. However, adiponectin concentrations were not different at any time point when plasma volume shifts were accounted for (p > 0.05). Ghrelin and acylated ghrelin concentrations were not affected at post and 3 h post-exercise compared to pre-exercise, with and without correcting for plasma volume shifts, regardless of temperature (p > 0.05). No differences in leptin, adiponectin, ghrelin or acylated ghrelin were found between trials (p > 0.05). CONCLUSION: Temperature does not effect the circulating concentrations of leptin, adiponectin, or ghrelin during an acute bout of endurance exercise. Supported by the University of Nebraska-Omaha University Committee on Research and Creative Activity and the National Institute for General Medical Science (5P20GM103427).