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.

Impact of local heating and cooling on skeletal muscle transcriptional response related to myogenesis and proteolysis.

PURPOSE: To determine the impact of local muscle heating and cooling on myogenic and proteolytic gene responses following resistance exercise. METHODS: Recreationally trained males (n = 12), age 25.3 ± 1.5, % body fat 13.6 ± 1.92, completed four sets of 8-12 repetitions of unilateral leg press and leg extension while heating one leg, and cooling the other. Muscle biopsies were taken from the vastus lateralis of each leg pre and 4 h post exercise. RESULTS: MyoD, FOXO1, and MuRF1 mRNA increased with exercise regardless of temperature (p < 0.05). Myostatin, MYF5, and atrogin-1 mRNA decreased with exercise regardless of temperature (p < 0.05). Myogenin, MRF4, and CASP3 mRNA were higher in the hot condition, compared to the cold (p < 0.05). PAX7 mRNA was lower in the hot compared to cold condition (p = 0.041). FOXO3 mRNA was higher in the cold compared to hot condition (p = 0.037). AKT1 and AKT2 were unaffected by either exercise or temperature. Femoral artery blood flow volume was higher in the hot (375.2 ± 41.2 ml min- 1), compared to the cold condition (263.5 ± 23.9 ml min- 1), p = 0.01. Tissue oxygen saturation was higher in the hot (71.7 ± 4.8%) than cold condition (55.3 ± 5.0%). CONCLUSION: These results suggest an impaired muscle growth response with local cold application compared to local heat application.

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

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.

Impact of hot and cold exposure on human skeletal muscle gene expression.

Many human diseases lead to a loss of skeletal muscle metabolic function and mass. Local and environmental temperature can modulate the exercise-stimulated response of several genes involved in mitochondrial biogenesis and skeletal muscle function in a human model. However, the impact of environmental temperature, independent of exercise, has not been addressed in a human model. Thus, the purpose of this study was to compare the effects of exposure to hot, cold, and room temperature conditions on skeletal muscle gene expression related to mitochondrial biogenesis and muscle mass. Recreationally trained male subjects (n = 12) had muscle biopsies taken from the vastus lateralis before and after 3 h of exposure to hot (33 °C), cold (7 °C), or room temperature (20 °C) conditions. Temperature had no effect on most of the genes related to mitochondrial biogenesis, myogenesis, or proteolysis (p > 0.05). Core temperature was significantly higher in hot and cold environments compared with room temperature (37.2 ± 0.1 °C, p = 0.001; 37.1 ± 0.1 °C, p = 0.013; 36.9 ± 0.1 °C, respectively). Whole-body oxygen consumption was also significantly higher in hot and cold compared with room temperature (0.38 ± 0.01 L·min-1, p < 0.001; 0.52 ± 0.03 L·min-1, p < 0.001; 0.35 ± 0.01 L·min-1, respectively). In conclusion, these data show that acute temperature exposure alone does not elicit significant changes in skeletal muscle gene expression. When considered in conjunction with previous research, exercise appears to be a necessary component to observe gene expression alterations between different environmental temperatures in humans.

Ingestion of an Amino Acid Electrolyte Beverage during Resistance Exercise Does Not Impact Fluid Shifts into Muscle or Performance.

The purpose of this study was to investigate the impact of ingesting an amino acid-electrolyte (AAE) beverage during upper body resistance exercise on transient muscle hypertrophy, exercise performance, markers of muscle damage, and recovery. Participants (n = 15) performed three sets of six repetitions-bench press, lat pull down, incline press, and seated row-followed by three sets of eight repetitions at 75% of the estimated 1 repetition maximum-triceps kickback, hammer curl, triceps push down, and preacher curl-with 90 s of rest between sets. The final set of the push down/preacher curl was performed to failure. Prior to and immediately post-exercise, as well as 24, 48, and 72 h post exercise, cross-sectional muscle thickness was measured. Blood samples were collected prior to exercise, as well as 24, 48, and 72 h post-exercise for serum creatine kinase (CK) analysis. No treatment effect was found for muscle cross-sectional area, repetitions to failure, or serum CK. A main effect (p < 0.001) was observed in the change in serum CK levels in the days following the resistance exercise session. The findings of this study suggest that the acute ingestion of a AAE beverage does not alter acute muscle thickness, performance, perceived soreness and weakness, or markers of muscle damage.

Acute effects of an arginine-based supplement on neuromuscular, ventilatory, and metabolic fatigue thresholds during cycle ergometry.

The purpose of the present study was to examine the effects of an acute dose of an arginine-based supplement on the physical working capacity at the fatigue threshold (PWCFT), lactate threshold (LT), ventilatory threshold (VT), and peak oxygen uptake during incremental cycle ergometry. This study used a double-blinded, placebo-controlled, within-subjects crossover design. Nineteen untrained men (mean age ± SD = 22.0 ± 1.7 years) were randomly assigned to ingest either the supplement (3.0 g of arginine, 300 mg of grape seed extract, and 300 mg of polyethylene glycol) or placebo (microcrystalline cellulose) and performed an incremental test on a cycle ergometer for determination of PWCFT, LT, VT, and peak oxygen uptake. Following a 1-week period, the subjects returned to the laboratory and ingested the opposite substance (either supplement or placebo) prior to completing another incremental test to be reassessed for PWCFT, LT, VT, and peak oxygen uptake. The paired-samples t tests indicated there were significant (P < 0.05) mean differences between the arginine and placebo conditions for the PWCFT (192 ± 42 vs. 168 ± 53 W, respectively) and VT (2546 ± 313 vs. 2452 ± 342 mL·min(-1)), but not the LT (135 ± 26 vs. 138 ± 22 W), absolute peak oxygen uptake (3663 ± 445 vs. 3645 ± 438 mL·min(-1)), or relative peak oxygen uptake (46.5 ± 6.0 vs. 46.2 ± 5.0 mL·kg(-1)·min(-1)). These findings suggested that the arginine-based supplement may be used on an acute basis for delaying the onset of neuromuscular fatigue (i.e., PWCFT) and improving the VT in untrained individuals.