Robert Shute

Transcriptional control, but not subcellular location, of PGC-1α is altered following exercise in a hot environment

The purpose of this study was to determine mitochondrial biogenesis-related mRNA expression, binding of transcription factors to the peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC-1α) promoter, and subcellular location of PGC-1α protein in human skeletal muscle following exercise in a hot environment compared with a room temperature environment. Recreationally trained males (n = 11) completed two trials in a temperature- and humidity-controlled environmental chamber. Each trial consisted of cycling in either a hot (H) or room temperature (C) environment (33 and 20°C, respectively) for 1 h at 60% of maximum wattage (Wmax) followed by 3 h of supine recovery at room temperature. Muscle biopsies were taken from the vastus lateralis pre-, post-, and 3 h postexercise. PGC-1α mRNA increased post (P = 0.039)- and 3 h postexercise in C (P = 0.002). PGC-1α, estrogen-related receptor-α (ERRα), and nuclear respiratory factor 1 (NRF-1) mRNA was all lower in H than C post (P = 0.038, P < 0.001, and P = 0.030, respectively)- and 3 h postexercise (P = 0.035, P = 0.007, and P < 0.001, respectively). Binding of cAMP response element-binding protein (CREB) (P = 0.005), myocyte enhancer factor 2 (MEF2) (P = 0.047), and FoxO forkhead box class-O1 (FoxO1) (P = 0.010) to the promoter region of the PGC-1α gene was lower in H than C. Nuclear PGC-1α protein increased postexercise in both H and C (P = 0.029) but was not different between trials (P = 0.602). These data indicate that acute exercise in a hot environment blunts expression of mitochondrial biogenesis-related mRNA, due to decreased binding of CREB, MEF2, and FoxO1 to the PGC-1α promoter.

Leptin, adiponectin, and ghrelin responses to endurance exercise in different ambient 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.

Local muscle cooling does not impact expression of mitochondrial-related genes

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.

Effects of exercise in a cold environment on transcriptional control of PGC-1α

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.

Irisin and Fibronectin Type III Domain-Containing 5 Responses to Exercise in Different Environmental Conditions: 1051 Board #230 May 31 3

Fibronectin type III domain-containing 5 (FNDC5) is a skeletal muscle membrane-bound precursor to the myokine irisin. Irisin is involved in stimulating adipose tissue to become more metabolically active in order to produce heat. The purpose of this study was to determine the effects of exercise in a hot (33 °C), cold (7 °C), and room temperature (RT, 20 °C) environment on the skeletal muscle gene expression of FNDC5 and the plasma concentrations of irisin. Twelve recreationally trained males completed three separate, 1 h cycling bouts at 60% of Wmax in a hot, cold, and RT environment followed by three hours of recovery at room temperature. Blood samples were taken from the antecubital vein and muscle biopsies were taken from the vastus lateralis pre-, post-, and 3 h post-exercise. Plasma concentrations of irisin did not change from pre- (9.23 ± 2.68 pg·mL−1) to post-exercise (9.6 ± 0.2 pg·mL−1, p = 0.068), but did decrease from post-exercise to 3 h post-exercise (8.9 ± 0.5 pg·mL−1, p = 0.047) regardless of temperature. However, when plasma volume shifts were considered, no differences were found in irisin (p = 0.086). There were no significant differences between trials for irisin plasma concentrations (p > 0.05). No significant differences in FNDC5 were observed between the hot, cold, or RT or pre-, post-, or 3 h post-exercise time points (p > 0.05). These data indicate that the temperature in which exercise takes place does not influence FNDC5 transcription or circulating irisin in a human model.

Exercise-Induced Interleukin-6 and Metabolic Responses in Hot, Temperate, and Cold Conditions

The purpose of this study was to determine the effects of exercise in hot, cold, and temperate environments on plasma interleukin-6 (IL-6). Eleven recreationally trained males (age 5 25 ¡ 4 years, height 5 178 ¡ 5 cm, weight 5 79.4 ¡ 13.5 kg, body fat 5 14.7 ¡ 3.6%, VO2 peak 5 54.6 ¡ 11.5 ml kg 21 min) performed a 1 hr cycling bout in hot (33 C̊), cold (7 C̊), and temperate (20 C̊) environments at 60% of Wmax followed by 3 hr of supine recovery in temperate conditions. Expired gases were measured every 15 min during exercise and once every hour during recovery. Heart rate was continuously measured throughout the trials. Blood samples were obtained from the antecubital vein pre-exercise, immediately post-exercise, and 3 hr post-exercise. Blood samples were analyzed for plasma concentrations of IL-6 using a commercial ELISA kit. Plasma IL-6 concentrations were significantly higher immediately post-exercise (14.8 ¡ 1.6 pg ml, p 5 0.008) and 3 hr post-exercise (14.8 ¡ 0.9 pg ml, p 5 0.018) compared to pre-exercise (11.4 ¡ 2.4 pg ml), across all trials. There were no differences in plasma IL-6 concentrations (p 5 0.207) between temperature conditions. Oxygen consumption and heart rate were higher and respiratory exchange ratio was lower in the hot compared to other conditions (p , 0.05). These data indicate that the temperature in which exercise occurs does not affect acute plasma IL-6 response despite differences in metabolic state.

Response of Appetite and Appetite Regulating Hormones to Acute Hypoxia

AIM: To determine the acute response of appetite and appetite regulating hormones after exposure to simulated altitude. METHODS: Seven males and five females (height: 178.9 ¡ 2.3 cm; weight: 77.3 ¡ 7.2 kg; body fat: 18.4 ¡ 1.7%) participated in two, three-hour trials in a hypoxic (5000 m) and normoxic (350 m) environment. Blood samples were collected prior to and immediately following three hours of exposure for the measurement of leptin, adiponectin, and acylated ghrelin. Appetite, acute mountain sickness, heart rate, blood oxygenation, tissue oxygenation, respiration rate, and whole body gases were also measured. RESULTS: Leptin was not different between hypoxic (5.8 ¡ 1.8 ng ml) and normoxic trials (6.2 ¡ 2.0 ng ml; p 5 0.603). Adiponectin was not different between hypoxic (9.0 ¡ 0.2 mg ml) and normoxic trials (8.4 ¡ 0.7 mg ml; p 5 0.216). Acylated ghrelin was not different between hypoxic (15.0 ¡ 3.8 pg ml) and normoxic trials (16.3 ¡ 4.6 pg ml; p 5 0.285). Appetite scores were not different between trials (p . 0.05) with the exception of fullness which was greater in the hypoxic condition (p 5 0.027). Heart rate and symptoms of acute mountain sickness were higher while blood and tissue oxygenation were lower in the hypoxic trial (p , 0.05). No differences were noted in other metabolic parameters (p . 0.05). CONCLUSION: Appetite and appetite regulating hormones are not affected by three hours of hypoxic exposure, and thus some of these negative consequences of hypoxic exposure may not be evident with short exposure times.