Effect of saline infusion during exercise on thermal and circulatory regulations

To quantify the effect of an acute increase in plasma volume (PV) on forearm blood flow (FBF), heart rate (HR), and esophageal temperature (Tes) during exercise, we studied six male volunteers who exercised on a cycle ergometer at 60% of maximal aerobic power for 50 min in a warm [(W), 30 degrees C, less than 30% relative humidity (rh)] or cool environment [(C), 22 degrees C, less than 30% rh] with isotonic saline infusion [Inf(+)] or without infusion [Inf(-)]. The infusion was performed at a constant rate of 0.29 ml.kg body wt-1.min-1 for 20-50 min of exercise to mimic fluid intake during exercise. PV decreased by approximately 5 ml/kg body wt within the first 10 min of exercise in all protocols. Therefore, PV in Inf(-) was maintained at the same reduced level by 50 min of exercise in both ambient temperatures, whereas PV in Inf(+) increased toward the preexercise level and recovered approximately 4.5 ml/kg body wt by 50 min in both temperatures. The restoration of PV during exercise suppressed the HR increase by 6 beats/min at 50 min of exercise in W; however, infusion had no effect on HR in C. In W, FBF in Inf(+) continued to increase linearly as Tes rose to 38.1 degrees C by the end of exercise, whereas FBF in Inf(-) plateaued when Tes reached approximately 37.7 degrees C. The infusion in C had only a minor effect on FBF.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thermoregulatory and blood responses during exercise at graded hypohydration levels

We studied the effects of graded hypohydration levels on thermoregulatory and blood responses during exercise in the heat. Eight heat-acclimated male subjects attempted four heat-stress tests (HSTs). One HST was attempted during euhydration, and three HSTs were attempted while the subjects were hypohydrated by 3, 5, and 7% of their body weight. Hypohydration was achieved by an exercise-heat regimen on the day prior to each HST. After 30 min of rest in a 20 degrees C antechamber the HST consisted of a 140-min exposure (4 repeats of 10 min rest and 25 min treadmill walking) in a hot-dry (49 degrees C, 20% relative humidity) environment. The following observations were made: 1) a low-to-moderate hypohydration level primarily reduced plasma volume with little effect on plasma osmolality, whereas a more severe hypohydration level resulted in no further plasma volume reduction but a large increment in plasma osmolality; 2) core temperature and heart rate responses increased with severity of hypohydration; 3) sweating rate responses for a given rectal temperature were systematically decreased with severity of hypohydration; and 4) the reduction in sweating rate was more strongly associated with plasma hyperosmolality than hypovolemia. In conclusion, an individual's thermal strain increases linearly with the severity of hypohydration during exercise in the heat, and plasma hyperosmolality influences the reduction in sweating more profoundly than hypovolemia.     

Temperature and sweating responses in one-legged and two-legged exercise.

In looking at the thermoregulatory responses resulting from symmetrical or asymmetrical exercise, this paper has focused on the effect of local skin temperature (Tsk,local) on local sweat rates (msw,local) during one-legged (W1) and two-legged (W2) exercise on an ergocycle. Five subjects underwent four 3-h tests at 36 degrees C, each consisting of six 25-min exercise periods alternating with 5-min rest periods. The subjects performed W1 and W2 at 45 and 90 W, respectively, either dehydrated or rehydrated. Body temperatures and total sweat rate were measured as well as four msw,local (on chest and thighs), assessed from sweat capsules under which Tsk,local was maintained at predetermined levels (37.0 degrees C and 35.5 degrees C). The combinations of Tsk,local levels, capsule locations, exercise intensity and hydration level chosen in our protocol led to the following results. The hydration level affected rectal temperature but not total or msw,local. No specific effect of muscle activity was found; msw,local on thighs of resting and working legs were similar. The msw,local were only influenced by exercise intensity, msw,local being more elevated during the higher intensity. No significant effect of Tsk,local on msw,local was found, whatever the experimental condition and/or the location. It was concluded that local thermal effects on msw,local could have been masked by the strong central drive for sweating which has been found to exist in subjects exercising in a warm environment.     

Thermal and circulatory responses during prolonged exercise at different levels of hydration

After a control experiment under initial normal hydration (N), five healthy unacclimated subjects were studied to investigate the effects of initial hypo- and hyperhydration on cardiovascular and thermo-regulatory responses to prolonged intermittent exercise in the heat (To = 36 degrees C; Tdp = 10 degrees C; Va = 0.6 m.s-1). Prior hydrohydration (O) was obtained by diuretics and prior hyperhydration (R) by ingestion of 0.5 L of isotonic (ISO) electrolyte sucrose solution 30 min before the experiments (4 h) started. Exercise (70 W) lasted 3 hours, and was periodically interrupted by resting periods (5-10 min). Three dehydration (D) runs were thus performed under the three initial hydration states (O,N,R) without fluid replacement during the exercise period. Four additional rehydration runs were carried out: 2 in each initial hydration level (O, R) included ingestion (at 36 degrees C) of water or ISO-solution during the first 3 hours. Physiological measurements were continuously recorded and hourly blood samples (15 ml) were obtained. Results showed that dehydration increased core temperature and heart rate and provoked blood hypovolemia and hyperosmolarity, the latter being somewhat prevented by prior ISO-ingestion. Dehydration reduced significantly the overall sweat rate only in hypohydrated subjects and the large hyperosmolarity seemed to be responsible for this. The significant Tcore rise during dehydration is unlikely to be the result of a decrease in evaporative heat transfer, which was found only in the case of initial hypohydration. Rehydration during exercise with water or ISO-solution induced different dynamic responses depending on the initial hydration level, but it never restored plasma volume.(ABSTRACT TRUNCATED AT 250 WORDS)     

Body temperature and plasma prolactin and norepinephrine relationships during exercise in a warm environment: effect of dehydration

The effects of euhydration (Eh) and light (Dh1) and moderate (Dh2) dehydrations on plasma prolactin (PRL) levels were studied in 5 young male volunteers at rest and during exercise to exhaustion (50% of VO2max) in a warm environment (Tdb = 35 degrees C, rh = 20-30%). Light and moderate dehydrations (loss of 1.1 and 1.8% body respectively) were obtained before exercise by controlled hyperthermia. Compared to Eh, time for exhaustion was reduced in Dh1 and Dh2 (p less than 0.01) and rectal temperature (Tre) rose faster in Dh2 (p less than 0.05). Both venous plasma PRL and norepinephrine (NE) increased during exercise at any hydration level (p less than 0.05). Plasma PRL reached higher values after 40 and 60 min in Dh2 and Dh1 (p less than 0.05). Plasma NE values were higher in Dh2 at rest and at the 40th min during exercise (p less than 0.05). Plasma PRL was linearly correlated to Tre and plasma NE (p less than 0.001) but unrelated to plasma volume variation and osmolality. Our results provide further evidence for the major effect of body temperature in exercise-induced PRL changes. Moreover, the plasma PRL-NE relationship suggests that these changes may result from central noradrenergic activation.     

Hydration and vascular fluid shifts during exercise in the heat

This study examined the effects of hypohydration on plasma volume and red cell volume during rest in a comfortable (20 degrees C, 40% relative humidity) and exercise in a hot-dry (49 degrees C, 20% relative humidity) environment. A group of six male and six female volunteers [matched for maximal O2 uptake (VO2 max)] completed two test sessions following a 10-day heat acclimation program. One test session was completed when subjects were euhydrated and the other when subjects were hypohydrated (-5% from base-line body wt). The test sessions consisted of rest for 30 min in a 20 degrees C antechamber, followed by two 25-min bouts of treadmill walking (approximately 30% of VO2 max) in the heat, interspersed by 10 min of rest. No significant differences were found between the genders for the examined variables. At rest, hypohydration elicited a 5% decrease in plasma volume with less than 1% change in red cell volume. During exercise, plasma volume increased by 4% when subjects were euhydrated and decreased by 4% when subjects were hypohydrated. These percent changes in plasma volume values were significantly (P less than 0.01) different between the euhydration and hypohydration tests. Although red cell volume remained fairly constant during the euhydration test, these values were significantly (P less than 0.01) lower when hypohydrated during exercise. We conclude that hydration level alters vascular fluid shifts during exercise in a hot environment; hemodilution occurs when euhydrated and hemoconcentration when hypohydrated during light intensity exercise for this group of fit men and women.     

Postexercise hypotension causes a prolonged perturbation in esophageal and active muscle temperature recovery

We examined the effect of two levels of exercise-induced hypotension on esophageal (Tes) and active and nonactive muscle temperatures during and following exercise. Seven males performed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their peak oxygen consumption during bilateral knee extensions (VO2sp). This was followed on separate days by 15-min of isolated bilateral knee extensions at moderate (60% VO2sp) (MEI) and high (80% VO2sp) (HEI) exercise intensities, followed by 90 min of recovery. Muscle temperature was measured with an intramuscular probe inserted in the left vastus medialis (Tvm) and triceps brachii (Ttb) muscles under ultrasound guidance. The deepest sensor (tip) was located approximately 10 mm from the femur and deep femoral artery and from the superior ulnar collateral artery and humerus for the Tvm and Ttb, respectively. Additional sensors were located 15 and 30 mm from the tip with an additional sensor located at 45 mm for the Tvm measurements only. Following exercise, mean arterial pressure (MAP) remained significantly below preexercise rest for the initial 60 min of recovery after MEI and for the duration of the postexercise recovery period after HEI (P< or =0.05). After HEI, significantly greater elevations from preexercise rest were recorded for Tes and all muscle temperatures paralleled a greater decrease in MAP compared with MEI (P< or =0.05). By the end of 90-min postexercise recovery, MAP, Tes, and all muscle temperatures remained significantly greater after HEI than MEI. Furthermore, a significantly shallower muscle temperature profile across Tvm, relative to preexercise rest, was observed at the end of exercise for both HEI and MEI (P< or=0.05), and for 30 min of recovery for MEI and throughout 90 min of recovery for HEI. No significant differences in muscle temperature profile were observed for Ttb. Thus we conclude that the increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was paralleled by an increase in the magnitude and recovery time of the postexercise esophageal and active muscle temperatures.     

The effect of exercise in cool, control and hot environments on cardioprotective HSP70 induction

A number of environmental and metabolic stimuli rapidly induce the expression of several highly conserved proteins such as heat shock proteins (HSPs) or stress proteins. The purpose of this study was to investigate the effects of a single bout of submaximal exercise in varying ambient temperatures on cardiac and skeletal muscle. Adult male Sprague-Dawley rats were randomly placed in one of three ambient temperature groups; control (23 degrees C), hot (41 degrees C) and cool (11 degrees C). Each exercise bout consisted of treadmill running at 17 m/min and 0% grade. Tissue HSP70 levels for all groups were determined using analysis of variance in two factorial design (2 x 3). Baseline rectal temperature was similar for all three groups. In the control and hot temperature groups, final rectal temperatures differed from the baseline values (p<.05). The rectal temperature from the control/exercise group were 38.5+/-0.3 degrees C at rest and 39.8+/-0.3 degrees C at exhaustion, the hot/exercise group were 38.4+/-0.3 degrees C at rest and 41.2+/-0.9 degrees C at exhaustion and the cool/exercise group were 38.2+/-0.3 degrees C at rest and 38.5+/-0.2 degrees C at exhaustion. The running time was 102.0+/-39.5 min at the control/exercise group, 44.1+/-18.0 min at the hot/exercise group, and 55.4+/-11.9 min at the cool/exercise group. The level of soleus, cardiac and extensor digitorium longus (EDL) HSP70 in cool temperature does not change during a single bout of submaximal exercise. Whereas a single bout of submaximal exercise in hot and control ambient temperatures increases HSP70 accumulation in locomotor muscles, such as the soleus and cardiac, but not in the EDL tissue. This study shows that the changes of HSP70 level induced by a single bout of submaximal exercise at various ambient temperatures (control, hot and cool) depend on the rectal temperature.     

Effect of hydration status on thirst, drinking, and related hormonal responses during low-intensity exercise in the heat.

During exercise-heat stress, ad libitum drinking frequently fails to match sweat output, resulting in deleterious changes in hormonal, circulatory, thermoregulatory, and psychological status. This condition, known as voluntary dehydration, is largely based on perceived thirst. To examine the role of preexercise dehydration on thirst and drinking during exercise-heat stress, 10 healthy men (21 +/- 1 yr, 57 +/- 1 ml x kg(-1) x min(-1) maximal aerobic power) performed four randomized walking trials (90 min, 5.6 km/h, 5% grade) in the heat (33 degrees C, 56% relative humidity). Trials differed in preexercise hydration status [euhydrated (Eu) or hypohydrated to -3.8 +/- 0.2% baseline body weight (Hy)] and water intake during exercise [no water (NW) or water ad libitum (W)]. Blood samples taken preexercise and immediately postexercise were analyzed for hematocrit, hemoglobin, serum aldosterone, plasma osmolality (P(osm)), plasma vasopressin (P(AVP)), and plasma renin activity (PRA). Thirst was evaluated at similar times using a subjective nine-point scale. Subjects were thirstier before (6.65 +/- 0.65) and drank more during Hy+W (1.65 +/- 0.18 liters) than Eu+W (1.59 +/- 0.41 and 0.31 +/- 0.11 liters, respectively). Postexercise measures of P(osm) and P(AVP) were significantly greater during Hy+NW and plasma volume lower [Hy+NW = -5.5 +/- 1.4% vs. Hy+W = +1.0 +/- 2.5% (P = 0.059), Eu+NW = -0.7 +/- 0.6% (P < 0.05), Eu+W = +0.5 +/- 1.6% (P < 0.05)] than all other trials. Except for thirst and drinking, however, no Hy+W values differed from Eu+NW or Eu+W values. In conclusion, dehydration preceding low-intensity exercise in the heat magnifies thirst-driven drinking during exercise-heat stress. Such changes result in similar fluid regulatory hormonal responses and comparable modifications in plasma volume regardless of preexercise hydration state.     

Regional hemodynamics during postexercise hypotension. II. Cutaneous circulation.

After an acute bout of exercise, there is an unexplained elevation in systemic vascular conductance that is not completely offset by an increase in cardiac output, resulting in a postexercise hypotension. The contributions of the splanchnic and renal circulations are examined in a companion paper (Pricher MP, Holowatz LA, Williams JT, Lockwood JM, and Halliwill JR. J Appl Physiol 97: 2065-2070, 2004). The purpose of this study was to determine the contribution of the cutaneous circulation in postexercise hypotension under thermoneutral conditions (approximately 23 degrees C). Arterial blood pressure was measured via an automated sphygmomanometer, internal temperature was measured via an ingestible pill, and skin temperature was measured with eight thermocouples. Red blood cell flux (laser-Doppler flowmetry) was monitored at four skin sites (chest, forearm, thigh, and leg), and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure) and scaled as percent maximal CVC (local heating to 43 degrees C). Ten subjects [6 men and 4 women; age 23 +/- 1 yr; peak O(2) uptake (Vo(2 peak)) 45.8 +/- 2.0 ml.kg(-1).min(-1)] volunteered for this study. After supine rest (30 min), subjects exercised on a bicycle ergometer for 1 h at 60% of their Vo(2 peak) and were then positioned supine for 90 min. Exercise elicited a postexercise hypotension reaching a nadir at 46.0 +/- 4.5 min postexercise (77 +/- 1 vs. 82 +/- 2 mmHg preexercise; P < 0.05). Internal temperature increased (38.0 +/- 0.1 vs. 36.7 +/- 0.1 degrees C preexercise; P < 0.05), remaining elevated at 90 min postexercise (36.9 +/- 0.1 degrees C vs. preexercise; P < 0.05). CVC at all four skin sites was elevated by the exercise bout (P < 0.05), returning to preexercise values within 50 min postexercise (P > 0.05). Therefore, although transient changes in CVC occur postexercise, they do not appear to play an obligatory role in mediating postexercise hypotension under thermoneutral conditions.     

Thermal and metabolic responses to cold by men and by eumenorrheic and amenorrheic women

Previous work has suggested that men (M) are more sensitive to cold stress than women. There have also been observations that suggest that amenorrheic women (AW) are less thermally responsive than eumenorrheic women (EW). We investigated the hypothesis that M, EW, and AW would have different responses to cold stress. The subjects (6/group) were tested four times: twice at rest for 60 min (5 and 22 degrees C) and twice in a progressive exercise test (5 and 22 degrees C). At rest at 22 degrees C AW had a lower O2 uptake (VO2) than M and lower rectal (Tre) and finger temperatures than EW. At rest at 5 degrees C both AW and EW had lower skin temperature (Tsk) than M, but there were no group differences in peripheral Tsk sites. M increased VO2 after 10 min and EW after 20 min of cold stress; however, AW did not increase metabolism until 60 min. In the two exercise tests Tre increased in proportion to relative work load; in the 5 degrees C test there was little evidence that exercise increased Tsk sites above rest levels. Few of the metabolic or thermal differences could be accounted for by body fatness, body surface area (BSA), or BSA/kg. The data support the hypothesis that M, EW, and AW have different responses to cold stress.     

Conductive and convective heat flows of exercising humans in cold water

The apparent conductance (Kss, in W.m-2.degrees C-1) of a given region of superficial shell (on the thigh, fat + skin) was determined on four nonsweating and nonshivering subjects, resting and exercising (200 W) in water [water temperature (Tw) 22-23 degrees C] Kss = Hss/(Tsf-Tsk) where Hss is the skin-to-water heat flow directly measured by heat flow transducers and Tsf and Tsk are the temperatures of the subcutaneous fat at a known depth below the skin surface and of the skin surface, respectively. The convective heat flow (qc) through the superficial shell was then estimated as qc = (Tsf - Tsk).(Kss - Kss,min), assuming that at rest Kss was minimal (Kss,min) and resting qc = 0. The duration of immersion was set to allow rectal temperature (Tre) to reach approximately 37 degrees C at the end of rest and approximately 38 degrees C at the end of exercise. Except at the highest Tw used, Kss at the start of exercise was always Kss,min and averaged 51 W.m-2.degrees C-1 (range 33-57 W.m-2.degrees C-1) across subjects, and qc was zero. At the end of exercise at the highest Tw used for each subject, Kss averaged 97 W.m-2.degrees C-1 (range 77-108 W.m-2.degrees C-1) and qc averaged 53% (range 48-61%) of Hss (mean Hss = 233 W.m-2).(ABSTRACT TRUNCATED AT 250 WORDS)     

Hydration during exercise. Effects on thermal and cardiovascular adjustments

Five young unacclimatised subjects were exposed for 4 h at 34 degrees C (10 degrees C dew-point temperature and 0.6 m X s-1 air velocity), while exercising on a bicycle ergometer: 25 min work--5 min rest cycles for 2 hours followed by 20 min work--10 min rest cycles for two further hours. 5 experimental sessions were carried out: one without rehydration (NO FLUID) resulting in 3.1% mean loss of body weight (delta Mb), and four sessions with 20 degrees C fluid ingestion of spring water (WATER), hypotonic (HYPO), isotonic (ISO) and hypertonic (HYPER) solutions to study the effects of fluid osmolarity on rehydration. Mean final rehydration (+/- SE) after fluid intake was 82.2% (+/- 1.2). Heart rate was higher in NO FLUID while no difference among conditions was found in either delta Mb or hourly sweat rates. Sweating sensitivity was lowest in the dehydration condition, and highest in the WATER one. Modifications in plasma volume and osmolarity demonstrated that NO FLUID induced hyperosmotic hypovolemia, ISO rehydration rapidly led to plasma isoosmotic hypervolemia, while WATER led to slightly hypoosmotic normovolemia. It is concluded that adequate rehydration through ingestion of isotonic electrolyte-sucrose solution, although in quantities much smaller than evaporative heat loss, rapidly restored and expanded plasma volume. While osmolarity influenced sweating sensitivity, the plasma volume changes (delta PV) within the range -6% less than or equal to delta PV + 4% had little effect on temperature adjustments in our conditions.     

No effect of mild heat stress on the regulation of carbohydrate metabolism at the onset of exercise.

To investigate the influence of heat stress on the regulation of skeletal muscle carbohydrate metabolism, six active, but not specifically trained, men performed 5 min of cycling at a power output eliciting 70% maximal O2 uptake in either 20 degrees C (Con) or 40 degrees C (Heat) after 20 min of passive exposure to either environmental condition. Although muscle temperature (T(mu)) was similar at rest when comparing trials, 20 min of passive exposure and 5 min of exercise increased (P < 0.05) T(mu) in Heat compared with Con (37.5 +/- 0.1 vs. 36.9 +/- 0.1 degrees C at 5 min for Heat and Con, respectively). Rectal temperature and plasma epinephrine were not different at rest, preexercise, or 5 min of exercise between trials. Although intramuscular glycogen phosphorylase and pyruvate dehydrogenase activity increased (P < 0.05) at the onset of exercise, there were no differences in the activities of these regulatory enzymes when comparing Heat with Con. Accordingly, glycogen use in the first 5 min of exercise was not different when comparing Heat with Con. Similarly, no differences in intramuscular concentrations of glucose 6-phosphate, lactate, pyruvate, acetyl-CoA, creatine, phosphocreatine, or ATP were observed at any time point when comparing Heat with Con. These results demonstrate that, whereas mild heat stress results in a small difference in contracting T(mu), it does not alter the activities of the key regulatory enzymes for carbohydrate metabolism or glycogen use at the onset of exercise, when plasma epinephrine levels are unaltered.     

Characteristics of body heat balance of paraplegics during exercise in a hot environment

The purpose of this investigation was to clarify the characteristics of body temperature regulation in paraplegics due to spinal cord injury (SCI) during an arm cranking exercise in a hot environment. Twelve paraplegics with lesions located between Th3 and L1,2 and seven able-bodied subjects (AB) participated in this study. The subjects were exposed to a hot (33 degrees C) or a moderate temperature (25 degrees C) environment for one hour and during the last 10 min of the exposure, the subjects performed arm cranking exercises at an exercise intensity of 40 W. The skin temperatures at the chest, the upper arm, the thigh and the calf, the tympanic membrane temperature (Tty), and the skin blood flow of the thigh (SBFT) were continuously monitored during the experiment. Although no systematical variation was found in the Tty at 25 degrees C, the Tty at 33 degrees C in paraplegics during exercise was significantly greater than that at rest (P < 0.01), which indicated a pronounced heat stress for paraplegics at 33 degrees C. SBFT of paraplegics with high lesions of the SCI remained unchanged during the experiment at 25 degrees C and 33 degrees C, while paraplegics with low lesions in this study showed consecutive increases in SBFT during exercise in both environmental conditions similar to AB. The increased core temperature in paraplegics with high lesions was considered to be due to a lack of sweat response and vasomotor activity in the paralyzed area. On the basis of the findings in this study, it can be suggested that high core temperature without any increment of SBFT may be characterized as body heat balance of paraplegics with high lesions during exercise in a hot environment.     

Cooling different body surfaces during upper and lower body exercise

The effect of varying the body surface area being cooled by a liquid microclimate system was evaluated during exercise heat-stress conditions. Six male subjects performed a total of six exercise (O2 uptake = 1.2 l/min) tests in a hot environment (ambient temperature = 38 degrees C, relative humidity = 30%) while dressed in clothing having low moisture permeability and high insulation. Each subject completed two upper body exercise (U; arm crank) tests: 1) with only the torso surface (T) cooled; and 2) with the surfaces of both the torso and upper arms (TA) cooled [coolant temperature at the inlet (Ti) was 20 degrees C for all upper body tests]. Each subject also completed four lower body exercise (L; walking) tests: 1) with only the T cooled (Ti = 20 degrees C); 2) with only the T cooled (Ti = 26 degrees C); 3) with torso, upper arm, and thigh surface (TAT) cooled (Ti = 20 degrees C); and 4) with TAT cooled (Ti = 26 degrees C). During U exercise, TA cooling had no effects compared with cooling only T. During L exercise, sweat rates, heart rates, and rectal temperature (Tre) changes were less with TAT cooling compared with cooling only the T. Altering Ti had no effect on Tre changes, but higher heart rates were observed with 26 than with 20 degrees C. These data indicate that cooling arms during upper body exercise provides no thermoregulatory advantage, although cooling the thigh surfaces during lower body exercise does provide an advantage.     

Downhill running: a model of exercise hyperemia in the rat spinotrapezius muscle.

To utilize the rat spinotrapezius muscle as a model to investigate the microcirculatory consequences of exercise training, it is necessary to design an exercise protocol that recruits this muscle. There is evidence that the spinotrapezius is derecruited during standard treadmill exercise protocols performed on the uphill treadmill (i.e., 6 degrees incline). This investigation tested the hypothesis that downhill running would effectively recruit the spinotrapezius muscle as assessed by the presence of an exercise hyperemia response. We used radioactive 15-microm microspheres to determine blood flows in the spinotrapezius and selected hindlimb muscles of female Sprague-Dawley rats at rest and during downhill (i.e., -14 degrees incline; 331 +/- 5 g body wt, n = 7) and level (i.e., 0 degrees incline; 320 +/- 11 g body wt, n = 5) running at 30 m/min. Both level and downhill exercise increased blood flow to all hindlimb muscles (P < 0.01). However, in marked contrast to the absence of a hyperemic response to level running, blood flow to the spinotrapezius muscle increased from 26 +/- 6 ml.min(-1).100 g(-1) at rest to 69 +/- 8 ml.min(-1).100 g(-1) during downhill running (P < 0.01). These findings indicate that downhill running represents an exercise paradigm that recruits the spinotrapezius muscle and thereby constitutes a tenable physiological model for investigating the adaptations induced by exercise training (i.e., the mechanisms of altered microcirculatory control by transmission light microscopy).     

Thermoregulatory adjustments during continuous heat exposure

Body temperature regulation was studied in 6 male subjects during an acclimation procedure involving uninterrupted heat exposure for 5 successive days and nights in a hot dry environment (ambient temperature = 35 degrees C, dew-point temperature = 7 degrees C; air velocity = 0.2 m.s-1). Data were obtained at rest and during exercise (relative mechanical workload = 35% VO2max). At rest, hourly measurements were made of oesophageal and 4 local skin temperatures, to allow the calculation of mean skin temperature, and of body motility and heart rate. During the working periods these measurements were made at 5 min intervals. Hourly whole-body weight loss was measured at rest on a sensitive platform scale while in the working condition just before starting and immediately after completing the bicycle exercise. The results show that, in both exercise and at rest, the successive heat exposures increased the sweat gland output during the first 3 days. Afterwards, sweat rate decreased without any corresponding change in body temperature. For the fixed workload, the sweat rate decline was associated with a decrease in circulatory strain. Adjustments in both sweating and circulatory mechanisms occur in the first 3 days of continuous heat exposure. The overall sweat rate decline could involve a redistribution of the regional sweating rates which enhances the sweat gland activities of skin areas with maximal evaporative efficiencies.     

Preexercise sodium loading aids fluid balance and endurance for women exercising in the heat.

This study was conducted during the high-hormone phase of both natural and oral contraceptive pill (OCP)-mediated menstrual cycles to determine whether preexercise ingestion of a concentrated sodium beverage would increase plasma volume (PV), reduce physiological strain, and aid endurance of moderately trained women cycling in warm conditions. Thirteen trained cyclists [peak O(2) uptake 52 ml x kg(-1) x min(-1) (SD 2), age 26 yr (SD 6), weight 60.8 kg (SD 5)] who were oral contraceptive users (n = 6) or not (n = 7) completed this double-blind, crossover experiment. Cyclists ingested a concentrated-sodium (High Na(+): 164 mmol Na(+)/l) or low-sodium (Low Na(+): 10 mmol Na(+)/l) beverage (10 ml/kg) before cycling to exhaustion at 70% Peak O(2) uptake in warm conditions (32 degrees C, 50% relative humidity, air velocity 4.5 m/s). Beverage (approximately 628 ml) was ingested in seven portions across 60 min beginning 105 min before exercise, with no additional fluid given until the end of the trial. Trials were separated by one to two menstrual cycles. High Na(+) increased PV (calculated from hematocrit and hemoglobin concentration) before exercise, whereas Low Na(+) did not [-4.4 (SD 1.1) vs. -1.9% (SD 1.3); 95% confidence interval: for the difference 5.20, 6.92; P < 0.0001], and it involved greater time to exhaustion [98.8 (SD 25.6) vs. 78.7 (SD 24.6) min; 95% confidence interval: 13.3, 26.8; P < 0.0001]. Core temperature rose more quickly with Low Na(+) [1.6 degrees C/h (SD 0.2)] than High Na(+) [1.2 degrees C/h (SD 0.2); P = 0.04]. Plasma [AVP], [Na(+)] concentration, and osmolality, and urine volume, [Na(+)], and osmolality decreased with sodium loading (P < 0.05) independent of pill usage. Thus preexercise ingestion of a concentrated sodium beverage increased PV, reduced thermoregulatory strain, and increased exercise capacity for women in the high-hormone phase of natural and oral contraceptive pill-mediated menstrual cycles, in warm conditions.     

Effect of exercise and thermal stress on plasma volume.

Six male subjects exercised for 50 min at 25% (light exercise) and 55% (moderate exercise) of their estimated aerobic capacities in environments of 42 degrees C db, 35 degrees C wb and 30 degrees C db, 24 degrees C wb, respectively. Alterations in the hematocrit, hemoglobin, and plasma protein concentrations, and in the activity of an injected aliquot of isotopically labeled albumin were each used to calculate the percentage change in plasma volume occurring during exercise and recovery. Changes in each measure were consistent with a reduction in plasma volume during exercise and a return to preexercise levels during recovery. There was no significant difference between the measures when exercising in the heat, but during the more severe exercise in the cooler environment disproportional changes in protein, hematocrit, and hemoglobin were observed. Disproportional changes were also seen during the recovery phase, when the hematocrit and hemoglobin concentration indicated a more rapid return of the plasma volume to preexercise levels than did either the plasma protein concentration or albumin activity. During moderate exercise and recovery there was a 1% decrease in red cell volume. It is concluded that exercise accelerates the rate of protein movement from extravascular compartments to the intravascular compartment, leading to elevated plasma protein levels during recovery which favor the return of water to the intravascular space. Hemoglobin concentration is considered to be the most reliable measure of plasma volume change during exercise.