Abstract The objective of this study was to determine metabolic and physiological differences between males with low testosterone (LT) versus those with normal testosterone (NT) following a period of severe energy deficit. In this secondary analysis, 68 male US Marines (mean ± SD, 24.6 ± 2.4 y) were dichotomized by testosterone concentration (< or ≥ 10.5 nmol/L as determined from a single blood sample collected between 0600–0630 after an 8–10 h overnight fast by automated immunoassay) following 7 days of near complete starvation (~300 kcal consumed/d, ~85% energy deficit) during Survival, Evasion, Resistance, and Escape (SERE) training. Dietary intake was assessed before (PRE) SERE. Body composition (dual‐energy x‐ray absorptiometry and peripheral quantitative computed tomography) and whole‐body protein turnover (15N alanine) were assessed before (PRE) and after (POST) SERE. Mean testosterone concentrations decreased PRE (17.5 ± 4.7 nmol/L) to POST (9.8 ± 4.0 nmol/L, p
Military and/or emergency services personnel may be required to perform high-intensity physical activity during exposure to elevated inspired carbon dioxide (CO 2 ). Although many of the physiological consequences of hypercapnia are well characterized, the effects of graded increases in inspired CO 2 on self-paced endurance performance have not been determined. The aim of this study was to compare the effects of 0%, 2%, and 4% inspired CO 2 on two-mile run performance as well as physiological and perceptual responses during time trial exercise. Twelve physically active volunteers (peak oxygen uptake = 49±5 mL kg ⁻¹ min ⁻¹ ; 3 women) performed three experimental trials in a randomized, single-blind, crossover manner, breathing 21% oxygen with either 0%, 2%, or 4% CO 2 . During each trial, participants completed 10 minutes of walking at ~40% peak oxygen uptake followed by a self-paced two-mile treadmill time trial. One participant was unable to complete the 4% CO 2 trial due to lightheadedness during the run. Compared to the 0% CO 2 trial, run performance was 5±3% and 7±3% slower in the 2% and 4% CO 2 trials, respectively (both p<0.001). Run performance was significantly slower with 4% vs. 2% CO 2 (p=0.046). The dose-dependent performance impairments were accompanied by stepwise increases in mean ventilation, despite significant reductions in running speed. Dyspnea and headache were significantly elevated during the 4% CO 2 trial compared to both the 0% and 2% trials. Overall, our findings show that graded increases in inspired CO 2 impair endurance performance in a stepwise manner in healthy humans.
The National Institute for Occupational Safety and Health recommendations for work in the heat suggest workers consume 237 mL of water every 15-20 min and allow for continuous work at heavy intensities in hot environments up to 34 °C and 30% relative humidity. The goal was to determine whether the National Institute for Occupational Safety and Health recommendations prevented core temperature from exceeding 38.0 °C and greater than 2% body mass loss during heavy-intensity work in the heat. Eight males consumed 237 mL of water every 20 min during 2 hours of continuous heavy-intensity walking (6.4 kph, 1% grade) in a 34 °C/30% relative humidity environment, in accordance with the National Institute for Occupational Safety and Health recommendations. Projected core temperature and percent body mass loss were calculated for 4 and 8 hr of continuous work. Core temperature rose from baseline (36.8 ± 0.3 °C) to completion of 2 hr of work (38.1 ± 0.6 °C, p < 0.01), with two participants reaching the 38.0 °C threshold. Projected core temperatures remained elevated from baseline (p < 0.01), did not change from 2 to 4 hr (38.1 ± 0.7 °C, p > 0.99) and 4 to 8 hr (38.1 ± 0.8 °C, p > 0.99), respectively, and one participant exceeded 38.0 °C at 4 to 8 hr. There was no change in body mass loss over time (p > 0.99). During two hours of continuous heavy-intensity work in the heat, 75% of participants did not reach 38 °C core temperature and 88% did not reach 2% body mass loss when working in accordance with National Institute for Occupational Safety and Health recommendations.
The French chemist Michel Eugène Chevreul discovered creatine in meat two centuries ago. Extensive biochemical and physiological studies of this organic molecule followed with confirmation that creatine is found within the cytoplasm and mitochondria of human skeletal muscles. Two groups of investigators exploited these relationships five decades ago by first estimating the creatine pool size in vivo with 14C and 15N labelled isotopes. Skeletal muscle mass (kg) was then calculated by dividing the creatine pool size (g) by muscle creatine concentration (g/kg) measured on a single muscle biopsy or estimated from the literature. This approach for quantifying skeletal muscle mass is generating renewed interest with the recent introduction of a practical stable isotope (creatine‐(methyl‐d3)) dilution method for estimating the creatine pool size across the full human lifespan. The need for a muscle biopsy has been eliminated by assuming a constant value for whole‐body skeletal muscle creatine concentration of 4.3 g/kg wet weight. The current single compartment model of estimating creatine pool size and skeletal muscle mass rests on four main assumptions: tracer absorption is complete; tracer is all retained; tracer is distributed solely in skeletal muscle; and skeletal muscle creatine concentration is known and constant. Three of these assumptions are false to varying degrees. Not all tracer is retained with urinary isotope losses ranging from 0% to 9%; an empirical equation requiring further validation is used to correct for spillage. Not all tracer is distributed in skeletal muscle with non‐muscle creatine sources ranging from 2% to 10% with a definitive value lacking. Lastly, skeletal muscle creatine concentration is not constant and varies between muscles (e.g. 3.89–4.62 g/kg), with diets (e.g. vegetarian and omnivore), across age groups (e.g. middle‐age, ~4.5 g/kg; old‐age, 4.0 g/kg), activity levels (e.g. athletes, ~5 g/kg) and in disease states (e.g. muscular dystrophies, <3 g/kg). Some of the variability in skeletal muscle creatine concentrations can be attributed to heterogeneity in the proportions of wet skeletal muscle as myofibres, connective tissues, and fat. These observations raise serious concerns regarding the accuracy of the deuterated‐creatine dilution method for estimating total body skeletal muscle mass as now defined by cadaver analyses of whole wet tissues and in vivo approaches such as magnetic resonance imaging. A new framework is needed in thinking about how this potentially valuable method for measuring the creatine pool size in vivo can be used in the future to study skeletal muscle biology in health and disease.
There are replicable inter-individual differences in cognitive responsivity to sleep loss. Genetic allele variations have been linked with behavioral differences in cognitive performance under these conditions, yet less burdensome tests or screeners are not available. This study tested whether a survey can classify U.S. Army Soldiers as cognitively vulnerable or resilient to sleep loss and whether Soldiers in these differentiated groups have the expected allele variants. Six genetic targets were sequenced from 75 Soldiers. Cognition was tested after a night of total sleep deprivation during a military exercise. The Iowa Resilience to Sleeplessness Test (iREST) was administered. A Wilcoxon Rank Sum test showed the iREST score of 2.5/5 differentiated groups behaviorally on all cognitive tests. Chi-squared tests showed that for the Catechol-O-Methyltransferase (COMT) gene, 82% of behaviorally vulnerable soldiers had alleles linked with vulnerability, compared with 41% of behaviorally genetic soldiers. If these findings are replicated, the iREST could be used to help military leaders make decisions about personnel placement when sleep loss is unavoidable.
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