Immersion for approximately 9 minutes to a rectal temperature cooling limit of 38.6°C negated any risk associated with overcooling hyperthermic individuals when they were immersed in 2°C water.

Although females had a similar AD/M and greater body adiposity, they had approximately 1.7-fold greater rectal cooling rate. Because AD/M and body adiposity do not seem to influence rectal cooling rates in previously hyperthermic individuals, the greater cooling rates in females may be attributed to physical differences in lean body mass.

We evaluated the hypothesis that different rates of metabolic heat production between sexes, during exercise at the same percentage of maximum oxygen consumption [VO2 max] give proportional differences in evaporative heat loss. Seven males and seven females, exercised at 41.3 +/- 2.7% VO2 Max for 60-min at 40 degrees C and 30% relative humidity. Whole-body direct air calorimetry measured rate of whole-body evaporative heat loss (H e) while metabolic heat production (M - W) was measured by indirect calorimetry. M -W was greater in males (243 +/- 18 W m(-2)) relative to females (201 +/- 4 W m(-2)) (P

BackgroundImpaired skeletal muscle regeneration could contribute to the progression of muscle atrophy in patients with chronic obstructive pulmonary disease (COPD).MethodsSatellite cells and myogenesis-related proteins were compared between healthy subjects and patients with COPD, with or without muscle atrophy. Satellite cells were isolated and cultured to assess their proliferative and differentiation aptitudes.ResultsAlthough satellite cell numbers in muscle samples were similar between groups, the proportion of muscle fibers with central nuclei was increased in COPD. In muscle homogenates, increased expression of MyoD and decreased expression of myogenin and MRF4 were observed in COPD. In cultured satellite cells of patients with COPD, increased protein content was observed for Pax7, Myf5 (proliferation phase) and myogenin (differentiation phase) while myosin heavy chain protein content was significantly lower during differentiation.ConclusionIn COPD, the number of central nuclei was increased in muscle fibers suggesting a greater number of attempts to regenerate muscle tissue than in healthy subjects. Myogenesis signaling was also altered in muscle homogenates in patients with COPD and there was a profound reduction in the differentiation potential in this population as indicated by a reduced ability to incorporate myosin heavy chain into newly formed myotubes. Collectively, these results indicate that skeletal muscle regenerative capacity termination is impaired in COPD and could contribute to the progression of muscle atrophy progression in this population.

Context: The measurement of body temperature is crucial for the initial diagnosis of exertional heat injury and for monitoring purposes during a subsequent treatment strategy. However, little information is available about how different measurements of body temperature respond during and after exertional heat stress.Objective: To present the temporal responses of aural canal (T ac ), esophageal (T es ), and rectal (T re ) temperatures during 2 different scenarios (S1, S2) involving exertional heat stress and a subsequent recovery period.Design: Randomized controlled trial. Setting: University research laboratory.Patients or Other Participants: Twenty-four healthy volunteers, with 12 (5 men, 7 women) participating in S1 and 12 (7 men, 5 women) participating in S2.Intervention(s): The participants exercised in the heat (426C, 30% relative humidity) until they reached a 39.56C cutoff criterion, which was determined by T re in S1 and by T es in S2. As such, participants attained different levels of hyperthermia (as determined by T re ) at the end of exercise. Participants in S1 were subsequently immersed in cold water (26C) until T re reached 37.56C, and participants in S2 recovered in a temperate environment (306C, 30% relative humidity) for 60 minutes.Main Outcome Measure(s): We measured T ac , T es , and T re throughout both scenarios.Results: The T es (S1 5 40.19 6 0.416C, S2 5 39.50 6 0.026C) was higher at the end of exercise compared with both T ac (S1 5 39.74 6 0.426C, S2 5 38.89 6 0.326C) and T re (S1 5 39.41 6 0.046C, S2 5 38.74 6 0.286C) (for both comparisons in each scenario, P , .001). Conversely, T es (S1 5 36.26 6 0.746C, S2 5 37.36 6 0.346C) and T ac (S1 5 36.48 6 1.076C, S2 5 36.97 6 0.386C) were lower compared with T re (S1 5 37.54 6 0.046C, S2 5 37.78 6 0.316C) at the end of both scenarios (for both comparisons in each scenario, P , .001).Conclusions: We found that T ac , T es , and T re presented different temporal responses during and after both scenarios of exertional heat stress and a subsequent recovery period. Although these results may not have direct practical implications in the field monitoring and treatment of individuals with exertional heat injury, they do quantify the extent to which these body temperature measurements differ in such scenarios.Key Words: cold-water immersion, core temperature, exercise, hyperthermia Key Points N Aural canal, esophageal, and rectal temperatures presented different temporal responses during 2 scenarios of exertional heat stress and a subsequent recovery period.N Rectal temperature increased more slowly than esophageal and aural canal temperatures during exercise-induced hyperthermia.N Rectal temperature decreased more slowly than esophageal and aural canal temperatures after exercise-induced hyperthermia.N Rectal temperature is the only suitable and valid index for the monitoring of body temperature in a field setting; the use of esophageal temperature is not practical in such situations, and aural canal temperature is often influenced by external facto...

Impaired resting metabolism in peripheral muscles potentially contributes to exercise intolerance in chronic obstructive pulmonary disease (COPD). This study investigated the cytosolic energy metabolism of the quadriceps, from glycogen degradation to lactate accumulation, in exercising patients with COPD, in comparison to healthy controls. We measured, in 12 patients with COPD and 10 control subjects, resting and post-cycling exercise quadriceps levels of 1) energy substrates and end products of glycolysis (glycogen, glucose, pyruvate, and lactate) and intermediate markers of glycolysis (glucose-6-phosphate, glucose-1-phosphate, fructose-6-phosphate) and 2) the activity of key enzymes involved in the regulation of glycolysis (phosphofructokinase, lactate dehydrogenase). Exercise intensity (P < 0.01), duration (P = 0.049), and total work (P < 0.01) were reduced in patients with COPD. The variations in energy substrates and end products of glycolysis after cycling exercise were of similar magnitude in patients with COPD and controls. Glucose-6-phosphate (P = 0.036) and fructose-6-phosphate (P = 0.042) were significantly elevated in patients with COPD after exercise. Phosphofructokinase (P < 0.01) and lactate dehydrogenase (P = 0.02) activities were greater in COPD. Muscle glycogen utilization (P = 0.022) and lactate accumulation (P = 0.025) per unit of work were greater in COPD. We conclude that cycling exercise induced changes in quadriceps metabolism in patients with COPD that were of similar magnitude to those of healthy controls. These intramuscular events required a much lower exercise work load and time to occur in COPD. Our data suggest a greater reliance on glycolysis during exercise in COPD, which may contribute to exercise intolerance in COPD.

This study evaluated the effect of body adiposity on core cooling rates, as measured by decreases in rectal (T (re)), esophageal (T (es)) and aural canal (T (ac)) temperatures, of individuals rendered hyperthermic by dynamic exercise in the heat. Seventeen male participants were divided into two groups; low body fat (LF, 12.9 +/- 1.9%) and high body fat (HF, 22.3 +/- 4.3%). Participants exercised at 65% of their maximal oxygen uptake at an ambient air temperature of 40 degrees C until T (re) increased to 40 degrees C or until volitional fatigue. Following exercise, participants were immersed up to the clavicles in an 8 degrees C circulated water bath until T (re) returned to 37.5 degrees C. No significant differences were found between the LF and HF in the time to reach a T (re) of 39.5 degrees C (P = 0.205), 38.5 degrees C (P = 0.343) and 37.5 degrees C (P = 0.923) during the immersion. Overall cooling rate for T (re) was also similar between groups (0.23 +/- 0.09 degrees C/min (LF) vs. 0.20 +/- 0.09 degrees C/min (HF), P = 0.647) as well as those for T (es) (P = 0.502) and T (ac) (P = 0.940). Furthermore, mean rate of non-evaporative heat loss (702 +/- 217 W/m(2) (LF) vs. 612 +/- 141 W/m(2) (HF), P = 0.239) was not different between groups. These results suggest that a difference of approximately 10% of body adiposity does not affect core cooling rates in active individuals under 25% body fat rendered hyperthermic by exercise.

Muscle atrophy in chronic obstructive pulmonary disease (COPD) is associated with reduced exercise tolerance, muscle strength, and survival. The molecular mechanisms leading to muscle atrophy in COPD remain elusive. The mitogen-activated protein kinases (MAPKs) such as p38 MAPK and ERK 1/2 can increase levels of MAFbx/Atrogin and MuRF1, which are specifically involved in muscle protein degradation and atrophy. Our aim was to investigate the level of activation of p38 MAPK, ERK 1/2, and JNK in the quadriceps of patients with COPD. A biopsy of the quadriceps was obtained in 18 patients with COPD as well as in 9 healthy controls. We evaluated the phosphorylated as well as total protein levels of p38 MAPK, ERK 1/2, and JNK as well as MAFbx/Atrogin and MuRF1 in these muscle samples. The corresponding mRNA expression was also assessed by RT-PCR. Ratios of phosphorylated to total level of p38 MAPK (P = 0.02) and ERK 1/2 (P = 0.01) were significantly elevated in patients with COPD compared with controls. Moreover, protein levels of MAFbx/Atrogin showed a tendency to be greater in patients with COPD (P = 0.08). mRNA expression of p38 MAPK (P = 0.03), ERK 1/2 (P = 0.02), and MAFbx/Atrogin (P = 0.04) were significantly elevated in patients with COPD. In addition, phosphorylated-to-total p38 MAPK ratio (Pearson's r = -0.45; P < 0.05) and phosphorylated-to-total ERK 1/2 ratio (Pearson's r = -0.47; P < 0.05) were negatively associated with the mid-thigh muscle cross-sectional area. These data support the hypothesis that the MAPKs might play a role in the development of muscle atrophy in COPD.