Performance enhancement in rally car drivers via heat acclimation and race simulation

To investigate the combined use of an interactive racecar simulator and heat acclimation on psychomotor (driving) performance, eight rally drivers underwent 4 days of repeated heat (50 degrees C) exposure (1 h x day(-1)) during which they performed a simulated rally drive (3x12-min stages each separated by a 2-min break), after first cycling for 15 min at 125 W to induce some degree of fatigue and heat storage prior to beginning the rally. During the rally stages, a generic set of pace notes were read to the subject by a co-driver. In each simulation, sweat loss, heart rate, core (rectal) and skin temperatures were recorded and driving and psychomotor performance were assessed by recording stage times and time to complete a psychomotor test. Levels of physiological and perceived thermal strain were also recorded. Significant decreases in rally stage times (88 s; P<0.005), psychomotor test time (18 s; P<0.01), final core (0.25 degrees C; P<0.001) and skin (0.44 degrees C; P<0.005) temperatures, heart rate (16 beats x min(-1); P<0.05) and physiological (15 W x m(-2); P<0.005) and perceived thermal (3.7 units; P<0.01) strain were evident by the end of the final simulation, and a significant (P<0.05) increase in sweat sensitivity (+0.33 g x h(-1) x degrees C(-1)) was also recorded. These results suggest that both heat acclimation and race simulation can improve the psychomotor performance of rally drivers, although the relative contribution of each factor was not determined here. However, in a practical setting, these factors would not be used in isolation. After performing the acclimation and simulation protocol prior to an actual rally, drivers subjectively reported improvements in tolerating a high thermal load and in their ability to control the rally vehicle.     

Superior performance of African runners in warm humid but not in cool environmental conditions.

The purpose of this study was to examine the running performances and associated thermoregulatory responses of African and Caucasian runners in cool and warm conditions. On two separate occasions, 12 (n = 6 African, n = 6 Caucasian) well-trained men ran on a motorized treadmill at 70% of peak treadmill running velocity for 30 min followed by an 8-km self-paced performance run (PR) in cool (15 degrees C) or warm (35 degrees C) humid (60% relative humidity) conditions. Time to complete the PR in the cool condition was not different between groups ( approximately 27 min) but was significantly longer in warm conditions for Caucasian (33.0 +/- 1.6 min) vs. African (29.7 +/- 2.3 min, P < 0.01) runners. Rectal temperatures were not different between groups but were higher during warm compared with cool conditions. During the 8-km PR, sweat rates for Africans (25.3 +/- 2.3 ml/min) were lower compared with Caucasians (32.2 +/- 4.1 ml/min; P < 0.01). Relative rates of heat production were less for Africans than Caucasians in the heat. The finding that African runners ran faster only in the heat despite similar thermoregulatory responses as Caucasian runners suggests that the larger Caucasians reduce their running speed to ensure an optimal rate of heat storage without developing dangerous hyperthermia. According to this model, the superior running performance in the heat of these African runners can be partly attributed to their smaller size and hence their capacity to run faster in the heat while storing heat at the same rate as heavier Caucasian runners.     

Ventilation and acid-base balance in awake dogs exposed to heat and CO2

Some awake quiet dogs pant at cool ambient temperature (Ta) and some do not pant even when acutely exposed to heat. The purpose of the study was to determine whether this puzzling variability in respiratory behavior diminished during prolonged heat. The contributions of thermal and CO2 drives to respiratory adaptations were also examined. Five awake dogs acclimated to 20 degrees C were studied before and 2 and 48 h following exposure to 30-31 degrees C. Rectal temperature did not change; the important thermal stimulus, even at 48 h, appeared to be the increase in peripheral temperature. Variability between nonpanting and panting persisted over 48 h. On the average, ventilation (VE) doubled during heat, largely due to increased dead space ventilation. Nonpanting dogs at cool Ta decreased the threshold of the ventilatory response to CO2. A panting dog at cool Ta changed its slope of the ventilatory response from negative to positive. During hypercapnia in acute heat, ventilatory pattern changed so that frequency increased and tidal volume decreased for a given VE. By 48 h of heat, the ventilatory response to CO2 returned to control in only two dogs, but the ventilatory pattern during hypercapnia returned to control in four dogs. Since thermal stimuli remained unchanged at 48 h, adaptations of respiratory control may have been related to progressive adjustments of strong ions and acid-base balance.     

Thermal effects of whole head submersion in cold water on nonshivering humans.

This study isolated the effect of whole head submersion in cold water, on surface heat loss and body core cooling, when the confounding effect of shivering heat production was pharmacologically eliminated. Eight healthy male subjects were studied in 17 degrees C water under four conditions: the body was either insulated or uninsulated, with the head either above the water or completely submersed in each body-insulation subcondition. Shivering was abolished with buspirone (30 mg) and meperidine (2.5 mg/kg), and subjects breathed compressed air throughout all trials. Over the first 30 min of immersion, exposure of the head increased core cooling both in the body-insulated conditions (head out: 0.47 +/- 0.2 degrees C, head in: 0.77 +/- 0.2 degrees C; P < 0.05) and the body-exposed conditions (head out: 0.84 +/- 0.2 degrees C and head in: 1.17 +/- 0.5 degrees C; P < 0.02). Submersion of the head (7% of the body surface area) in the body-exposed conditions increased total heat loss by only 10%. In both body-exposed and body-insulated conditions, head submersion increased core cooling rate much more (average of 42%) than it increased total heat loss. This may be explained by a redistribution of blood flow in response to stimulation of thermosensitive and/or trigeminal receptors in the scalp, neck and face, where a given amount of heat loss would have a greater cooling effect on a smaller perfused body mass. In 17 degrees C water, the head does not contribute relatively more than the rest of the body to surface heat loss; however, a cold-induced reduction of perfused body mass may allow this small increase in heat loss to cause a relatively larger cooling of the body core.     

Body cooling between two bouts of exercise in the heat enhances subsequent performance

The purpose was to assess whether body cooling between 2 bouts of exercise in the heat enhances performance during the second exercise session. Using a random, crossover design, 15 subjects (3 women, 12 men; 28 +/- 2 years, 180 +/- 2 cm, 69 +/- 2.3 kg) participated in all 3 trials. Subjects ran 90 minutes on hilly trails in a hot environment (approximately 27 degrees C) before 12 minutes of either cold water immersion (CWI; 13.98 degrees C), ice water immersion (IWI; 5.23 degrees C), or a mock treatment (MT) of sitting in a tub with no water (29.50 degrees C). After immersion, subjects ran a 2-mile race. CWI had faster (p < 0.05) performance time (725 seconds) than MT (769 seconds). CWI and IWI had significantly (p < 0.05) lower rectal temperatures postimmersion than MT as well as postrace (p < 0.05). Heart rate also remained significantly lower (p < 0.05) during the CWI and IWI trials for the first half of the race. In conclusion, CWI enhances performance (6% improvement in race time) in the second bout of exercise, supporting its potential role as an ergogenic aid in athletic performance.     

Influence of training on sweating responses during submaximal exercise in horses.

Sweating responses were examined in five horses during a standardized exercise test (SET) in hot conditions (32-34 degrees C, 45-55% relative humidity) during 8 wk of exercise training (5 days/wk) in moderate conditions (19-21 degrees C, 45-55% relative humidity). SETs consisting of 7 km at 50% maximal O(2) consumption, determined 1 wk before training day (TD) 0, were completed on a treadmill set at a 6 degrees incline on TD0, 14, 28, 42, and 56. Mean maximal O(2) consumption, measured 2 days before each SET, increased 19% [TD0 to 42: 135 +/- 5 (SE) to 161 +/- 4 ml. kg(-1). min(-1)]. Peak sweating rate (SR) during exercise increased on TD14, 28, 42, and 56 compared with TD0, whereas SRs and sweat losses in recovery decreased by TD28. By TD56, end-exercise rectal and pulmonary artery temperature decreased by 0.9 +/- 0.1 and 1.2 +/- 0.1 degrees C, respectively, and mean change in body mass during the SET decreased by 23% (TD0: 10.1 +/- 0.9; TD56: 7.7 +/- 0.3 kg). Sweat Na(+) concentration during exercise decreased, whereas sweat K(+) concentration increased, and values for Cl(-) concentration in sweat were unchanged. Moderate-intensity training in cool conditions resulted in a 1.6-fold increase in sweating sensitivity evident by 4 wk and a 0.7 +/- 0.1 degrees C decrease in sweating threshold after 8 wk during exercise in hot, dry conditions. Altered sweating responses contributed to improved heat dissipation during exercise and a lower end-exercise core temperature. Despite higher SRs for a given core temperature during exercise, decreases in recovery SRs result in an overall reduction in sweat fluid losses but no change in total sweat ion losses after training.     

Heat stress increases muscle glycogen use but reduces the oxidation of ingested carbohydrates during exercise.

The aim of the present study was to test the hypothesis that the oxidation rate of ingested carbohydrate (CHO) is impaired during exercise in the heat compared with a cool environment. Nine trained cyclists (maximal oxygen consumption 65 +/- 1 ml x kg body wt(-1) x min(-1)) exercised on two different occasions for 90 min at 55% maximum power ouptput at an ambient temperature of either 16.4 +/- 0.2 degrees C (cool trial) or 35.4 +/- 0.1 degrees C (heat trial). Subjects received 8% glucose solutions that were enriched with [U-13C]glucose for measurements of exogenous glucose, plasma glucose, liver-derived glucose and muscle glycogen oxidation. Exogenous glucose oxidation during the final 30 min of exercise was significantly (P < 0.05) lower in the heat compared with the cool trial (0.76 +/- 0.06 vs. 0.84 +/- 0.05 g/min). Muscle glycogen oxidation during the final 30 min of exercise was increased by 25% in the heat (2.07 +/- 0.16 vs. 1.66 +/- 0.09 g/min; P < 0.05), and liver-derived glucose oxidation was not different. There was a trend toward a higher total CHO oxidation and a lower plasma glucose oxidation in the heat although this did not reach statistical significance (P = 0.087 and P = 0.082, respectively). These results demonstrate that the oxidation rate of ingested CHO is reduced and muscle glycogen utilization is increased during exercise in the heat compared with a cool environment.     

Thermoregulation in complex situations: combined heat exposure, infectious fever and water deprivation

Heat exposure, infectious fever and water deprivation are stressors that, individually, produce disturbances in more than one regulated system, calling for diverse compensatory responses. A potential conflict is created when these stimuli are combined and impose concurrent stressful loads on the body because the homeostatic defenses mobilized against one are also partly needed against the other stressors. To learn how the competing demands of combined stressors for shared regulatory systems are met, rabbits were exposed to 32°C and 37°C (heat), administered lipopolysaccharide (Salmonella enteritidis LPS, 2 μg/kg, i.v.) in temperatures of 22°C or 27°C, or water-deprived for 1 or 2 days in 22°C or 27°C, in separate experiments. The corresponding controls were exposed to 22°C or 27°C, administered pyrogen-free saline i.v. in 22°C or 27°C, or normally hydrated in 22°C or 27°C. In subsequent experiments, two or all three of these treatments were applied concurrently. Core and ear skin temperatures and respiratory rates were monitored continuously. The results indicated that the concomitant needs of moderate heat exposure, fever and 1 day of water deprivation were generally met by the regulatory systems involved, but different patterns of thermoeffector activities were evoked and the eventual body temperature changes produced were different under each condition. However, when the test conditions were severe, their combined needs were not met adequately and the eventual compensatory response depended not only on the particular stimulus intensity, but also on the immediate importance for survival of the functions being defended. Thus, dehydration was the most dangerous factor to the physiological integrity of the animals. In sum, conflicting physiological stimuli appear to result in responses that are different from the responses to a single perturbation, the eventual output representing the resultant of the inputs rather than a singular output dictated by one dominant drive to the exclusion of the others. Received: 20 August 1999 / Revised: 8 December 1999 / Accepted: 15 December 1999     

Lactate threshold predicting time-trial performance: impact of heat and acclimation

The relationship between exercise performance and lactate and ventilatory thresholds under two distinct environmental conditions is unknown. We examined the relationships between six lactate threshold methods (blood- and ventilation-based) and exercise performance in cyclists in hot and cool environments. Twelve cyclists performed a lactate threshold test, a maximal O(2) uptake (Vo(2max)) test, and a 1-h time trial in hot (38°C) and cool (13°C) conditions, before and after heat acclimation. Eight control subjects completed the same tests before and after 10 days of identical exercise in a cool environment. The highest correlations were observed with the blood-based lactate indexes; however, even the indirect ventilation-based indexes were well correlated with mean power during the time trial. Averaged bias was 15.4 ± 3.6 W higher for the ventilation- than the blood-based measures (P < 0.05). The bias of blood-based measures in the hot condition was increased: the time trial was overestimated by 37.7 ± 3.6 W compared with only 24.1 ± 3.2 W in the cool condition (P < 0.05). Acclimation had no effect on the bias of the blood-based indexes (P = 0.51) but exacerbated the overestimation by some ventilation-based indexes by an additional 34.5 ± 14.1 W (P < 0.05). Blood-based methods to determine lactate threshold show less bias and smaller variance than ventilation-based methods when predicting time-trial performance in cool environments. Of the blood-based methods, the inflection point between steady-state lactate and rising lactate (INFL) was the best method to predict time-trial performance. Lastly, in the hot condition, ventilation-based predictions are less accurate after heat acclimation, while blood-based predictions remain valid in both environments after heat acclimation.     

Individualized model of human thermoregulation for the simulation of heat stress response.

A population-based dynamic model of human thermoregulation was expanded with control equations incorporating the individual person's characteristics (body surface area, mass, fat%, maximal O(2) uptake, acclimation). These affect both the passive (heat capacity, insulation) and active systems (sweating and skin blood flow function). Model parameters were estimated from literature data. Other data, collected for the study of individual differences (working at relative or absolute workloads in hot-dry [45 degrees C, 20% relative humidity (rh)], warm-humid [35 degrees C, 80% rh], and cool [21 degrees C, 50% rh] environments), were used for validation. The individualized model provides an improved prediction [mean core temperature error, -0.21 --> -0.07 degrees C (P < 0.001); mean squared error, 0.40 --> 0.16 degrees C, (P < 0.001)]. The magnitude of improvement varies substantially with the climate and work type. Relative to an empirical multiple-regression model derived from these specific data sets, the analytical simulation model has between 54 and 89% of its predictive power, except for the cool climate, in which this ratio is zero. In conclusion, individualization of the model allows improved prediction of heat strain, although a substantial error remains.     

Muscle blood flow and muscle metabolism during exercise and heat stress

The effect of heat stress on blood flow and metabolism in an exercising leg was studied in seven subjects walking uphill (12-17%) at 5 km/h on a treadmill for 90 min or until exhaustion. The first 30 min of exercise were performed in a cool environment (18-21 degrees C); then subjects moved to an adjacent room at 40 degrees C and continued to exercise at the same speed and inclination for a further 60 min or to exhaustion, whichever occurred first. The rate of O2 consumption, 2.6 l/min (1.8-3.3) (average from cool and hot conditions), corresponded to 55-77% of their individual maximums. In the cool environment a steady state was reached at 30 min. When the subjects were shifted to the hot room, the core temperature and heart rate started to rise and reached values greater than 39 degrees C and near-maximal values, respectively, at the termination of the exercise. The leg blood flow (thermodilution method), femoral arteriovenous O2 difference, and consequently leg O2 consumption were unchanged in the hot compared with the cool condition. There was no increase in release of lactate and no reduction in glucose and free net fatty acid uptake in the exercising leg in the heat. Furthermore, the rate of glycogen utilization in the gastrocnemius muscle was not elevated in the hot environment. There was a tendency for cardiac output to increase in the heat (mean 15.2 to 18.4 l/min), which may have contributed to the increase in skin circulation, together with a possible further reduction in flow to other vascular beds, because muscle blood flow was not reduced.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improving the performance of Rosetta using multiple sequence alignment information and global measures of hydrophobic core formation

This study explores the use of multiple sequence alignment (MSA) information and global measures of hydrophobic core formation for improving the Rosetta ab initio protein structure prediction method. The most effective use of the MSA information is achieved by carrying out independent folding simulations for a subset of the homologous sequences in the MSA and then identifying the free energy minima common to all folded sequences via simultaneous clustering of the independent folding runs. Global measures of hydrophobic core formation, using ellipsoidal rather than spherical representations of the hydrophobic core, are found to be useful in removing non-native conformations before cluster analysis. Through this combination of MSA information and global measures of protein core formation, we significantly increase the performance of Rosetta on a challenging test set. Proteins 2001;43:1-11.     

Cold exposure during military operations: effects on anaerobic performance

This study examined the effects of military field operations (MFO) under different environmental conditions on anaerobic performance. US Marines were tested in the field under the following conditions: 1) noncold environment (NC; n = 30, 10-32 degrees C) and 2) cold environment (CO; n = 32, -2 to -22 degrees C). Subjects performed 30-s Wingate tests (WIN) pre- and immediately post-MFO to assess anaerobic performance. The MFO consisted of approximately 4.5 days of combat training maneuvers while carrying field equipment (packs and weapon, approximately 25 kg). WIN measures obtained were absolute and relative mean power (MP), 5-s peak power (PP), and fatigue index (% decline). Significant main effects (P less than 0.01) were observed for time (pre-post MFO). Reductions occurred in absolute MP [651.8 +/- 30.3 to 616.4 +/- 28.5 (SE) W] and PP (897.8 +/- 41.6 to 857.0 +/- 39.1 W); however, no effect on fatigue index was seen. Significant interaction effects (P less than 0.05) were observed in relative measures. Reductions (pre-post) in MP (NC = 8.64 +/- 0.16 to 8.37 +/- 0.14 W/kg; CO = 8.91 +/- 0.26 to 8.04 +/- 0.15 W/kg) and PP (NC = 11.80 +/- 0.24 to 11.61 +/- 0.33 W/kg; CO = 12.23 +/- 0.35 to 11.20 +/- 0.19 W/kg) were greater under CO than NC conditions. These changes were found despite significant (P less than 0.05) but comparable pre-post weight reductions in both CO and NC conditions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atropine, diazepam, and physostigmine: thermoregulatory effects in the heat-stressed rat

We have previously reported that administration of atropine (A) to unrestrained, sedentary, heat-stressed rats resulted in a dose-dependent increase in heating rate (rate of rise of core temperature, degree C/min). Additionally, we have demonstrated that the decrements in treadmill endurance and increments in heating rate of physostigmine (PH)-treated running rats can both be restored to control levels by pretreating the animals with A and diazepam (D). Our objective in the present work was to determine if the administration of D + PH to A-treated unrestrained, sedentary, heat-stressed rats (N = 16/group, 510-530 g) could improve their thermal tolerance. The following drugs were administered singly (at 10 min intervals) via lateral tail vein: vehicle-control (C), A (200 micrograms/kg), D (500 micrograms/kg), and PH (200 micrograms/kg). After drug administration, the rats were heat-stressed (Tamb = 41.5 degrees C) until a core temperature of 42.6 degrees C was attained when they were removed to a 26 degrees C chamber. The heating rates (degrees C/min) and tolerance times (min) of the respective groups were: C- 0.02, 235; A- 0.08, 58; A D- 0.06, 94; and A + D + PH- 0.04, 143. Administration of D with A significantly decreased heating rate, and D + PH more than doubled the thermal tolerance of A-treated rats. Thus, the combination of A + D + PH not only restores PH-induced performance and thermoregulatory decrements of rats exercised in a moderate environment, but also reduces A-induced heat intolerance.     

Variation in the k(cat) of Rubisco in C(3) and C(4) plants and some implications for photosynthetic performance at high and low temperature

The capacity of ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) to consume RuBP is a major limitation on the rate of net CO(2) assimilation (A) in C(3) and C(4) plants. The pattern of Rubisco limitation differs between the two photosynthetic types, as shown by comparisons of temperature and CO(2) responses of A and Rubisco activity from C(3) and C(4) species. In C(3) species, Rubisco capacity is the primary limitation on A at light saturation and CO(2) concentrations below the current atmospheric value of 37 Pa, particularly near the temperature optimum. Below 20 degrees C, C(3) photosynthesis at 37 and 68 Pa is often limited by the capacity to regenerate phosphate for photophosphorylation. In C(4) plants, the Rubisco capacity is equivalent to A below 18 degrees C, but exceeds the photosynthetic capacity above 25 degrees C, indicating that Rubisco is an important limitation at cool but not warm temperatures. A comparison of the catalytic efficiency of Rubisco (k(cat) in mol CO(2) mol(-1) Rubisco active sites s(-1)) from 17 C(3) and C(4) plants showed that Rubisco from C(4) species, and C(3) species originating in cool environments, had higher k(cat) than Rubisco from C(3) species originating in warm environments. This indicates that Rubisco evolved to improve performance in the environment that plants normally experience. In C(4) plants, and C(3) species from cool environments, Rubisco often operates near CO(2) saturation, so that increases in k(cat) would enhance A. In warm-habitat C(4) species, Rubisco often operates at CO(2) concentrations below the K(m) for CO(2). Because k(cat) and K(m) vary proportionally, the low k(cat) indicates that Rubisco has been modified in a manner that reduces K(m) and thus increases the affinity for CO(2) in C(3) species from warm climates.     

Thermal effects of dorsal head immersion in cold water on nonshivering humans.

Personal floatation devices maintain either a semirecumbent flotation posture with the head and upper chest out of the water or a horizontal flotation posture with the dorsal head and whole body immersed. The contribution of dorsal head and upper chest immersion to core cooling in cold water was isolated when the confounding effect of shivering heat production was inhibited with meperidine (Demerol, 2.5 mg/kg). Six male volunteers were immersed four times for up to 60 min, or until esophageal temperature = 34 degrees C. An insulated hoodless dry suit or two different personal floatation devices were used to create four conditions: 1) body insulated, head out; 2) body insulated, dorsal head immersed; 3) body exposed, head (and upper chest) out; and 4) body exposed, dorsal head (and upper chest) immersed. When the body was insulated, dorsal head immersion did not affect core cooling rate (1.1 degrees C/h) compared with head-out conditions (0.7 degrees C/h). When the body was exposed, however, the rate of core cooling increased by 40% from 3.6 degrees C/h with the head out to 5.0 degrees C/h with the dorsal head and upper chest immersed (P < 0.01). Heat loss from the dorsal head and upper chest was approximately proportional to the extra surface area that was immersed (approximately 10%). The exaggerated core cooling during dorsal head immersion (40% increase) may result from the extra heat loss affecting a smaller thermal core due to intense thermal stimulation of the body and head and resultant peripheral vasoconstriction. Dorsal head and upper chest immersion in cold water increases the rate of core cooling and decreases potential survival time.     

Effects of environmental cooling on force production in the quadriceps and hamstrings

The purpose of this study was to determine the effects of environmental cooling on force production in the quadriceps and hamstring muscles. Ten men (mean +/- SD: age = 21.4 +/- 2.2 years, height = 168.5 +/- 35.9 cm, body mass = 78.0 +/- 6.4 kg) participated in this study. Each subject completed 2 sets of 10 maximal effort repetitions on a Cybex II isokinetic dynamometer at 3.14 rad x s(-1). Between sets, subjects sat in environmental temperatures of 20, 15, 10, or 5 degrees C for 40 minutes. A significant decrease (p 相似文献   

C4 photosynthesis at low temperature. A study using transgenic plants with reduced amounts of Rubisco

C(4) plants are rare in the cool climates characteristic of high latitudes and elevations, but the reasons for this are unclear. We tested the hypothesis that CO(2) fixation by Rubisco is the rate-limiting step during C(4) photosynthesis at cool temperatures. We measured photosynthesis and chlorophyll fluorescence from 6 degrees C to 40 degrees C, and in vitro Rubisco and phosphoenolpyruvate carboxylase activity from 0 degrees C to 42 degrees C, in Flaveria bidentis modified by an antisense construct (targeted to the nuclear-encoded small subunit of Rubisco, anti-RbcS) to have 49% and 32% of the wild-type Rubisco content. Photosynthesis was reduced at all temperatures in the anti-Rbcs plants, but the thermal optimum for photosynthesis (35 degrees C) did not differ. The in vitro turnover rate (kcat) of fully carbamylated Rubisco was 3.8 mol mol(-)(1) s(-)(1) at 24 degrees C, regardless of genotype. The in vitro kcat (Rubisco Vcmax per catalytic site) and in vivo kcat (gross photosynthesis per Rubisco catalytic site) were the same below 20 degrees C, but at warmer temperatures, the in vitro capacity of the enzyme exceeded the realized rate of photosynthesis. The quantum requirement of CO(2) assimilation increased below 25 degrees C in all genotypes, suggesting greater leakage of CO(2) from the bundle sheath. The Rubisco flux control coefficient was 0.68 at the thermal optimum and increased to 0.99 at 6 degrees C. Our results thus demonstrate that Rubisco capacity is a principle control over the rate of C(4) photosynthesis at low temperatures. On the basis of these results, we propose that the lack of C(4) success in cool climates reflects a constraint imposed by having less Rubisco than their C(3) competitors.     

Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress.

This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO(2) (Pet(CO(2))). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease Pet(CO(2)) approximately 20 Torr) and normoxic hypercapnic (increase in Pet(CO(2)) approximately 9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and Pet(CO(2)) was used to evaluate cerebrovascular CO(2) responsiveness. Passive heat stress increased core temperature (1.1 +/- 0.2 degrees C, P < 0.001) and reduced middle cerebral artery blood velocity by 8 +/- 8 cm/s (P = 0.01), reduced CBVC by 0.09 +/- 0.09 CBVC units (P = 0.02), and decreased Pet(CO(2)) by 3 +/- 4 Torr (P = 0.07), while mean arterial blood pressure was well maintained (P = 0.36). The slope of the CBVC-Pet(CO(2)) relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 +/- 0.006 vs. 0.009 +/- 0.004 CBVC units/Torr, P = 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-Pet(CO(2)) relationship was not different between normothermia and heat stress conditions (0.028 +/- 0.020 vs. 0.023 +/- 0.008 CBVC units/Torr, P = 0.31). These results indicate that cerebrovascular CO(2) responsiveness, to the prescribed steady-state changes in Pet(CO(2)), is unchanged during passive heat stress.     

Skeletal muscle metabolism during exercise is influenced by heat acclimation

The influence of heat acclimation on skeletal muscle metabolism during submaximal exercise was studied in 13 healthy men. The subjects performed 30 min of cycle exercise (70% of individual maximal O2 uptake) in a cool [21 degrees C, 30% relative humidity (rh)] and a hot (49 degrees C, 20% rh) environment before and again after they were heat acclimated. Aerobic metabolic rate was lower (0.1 l X min-1; P less than 0.01) during exercise in the heat compared with the cool both before and after heat acclimation. Muscle and plasma lactate accumulation with exercise was greater (P less than 0.01) in the hot relative to the cool environment both before and after acclimation. Acclimation lowered (P less than 0.01) aerobic metabolic rate as well as muscle and plasma lactate accumulation in both environments. The amount of muscle glycogen utilized during exercise in the hot environment did not differ from that in the cool either before or after acclimation. These findings indicate that accumulation of muscle lactate is increased and aerobic metabolic rate is decreased during exercise in the heat before and after heat acclimation; increased muscle glycogen utilization does not account for the increased muscle lactate accumulation during exercise under extreme heat stress; and heat acclimation lowers the aerobic metabolic rate and muscle and blood lactate accumulation during exercise in a cool as well as a hot environment.