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)     

Effects of hypohydration on thermoregulation during exercise before and after 5-day aerobic training in a warm environment in young men

We examined whether enhanced cardiovascular and thermoregulatory responses during exercise after short-term aerobic training in a warm environment were reversed when plasma volume (PV) expansion was reversed by acute isotonic hypohydration. Seven young men performed aerobic training at the 70% peak oxygen consumption rate (Vo(?peak)) at 30°C atmospheric temperature and 50% relative humidity, 30 min/day for 5 days. Before and after training, we performed the thermoregulatory response test while measuring esophageal temperature (T(es)), forearm skin vascular conductance, sweat rate (SR), and PV during 30 min exercise at the metabolic rate equivalent to pretraining 65% Vo(?peak) in euhydration under the same environment as during training in four trials (euhydration and hypohydration, respectively). Hypohydration targeting 3% body mass was attained by combined treatment with low-salt meals to subjects from ~48 h before the test and administration of a diuretic ~4 h before the test. After training, the T(es) thresholds for cutaneous vasodilation and sweating decreased by 0.3 and 0.2°C (P = 0.008 and 0.012, respectively) when PV increased by ~10%. When PV before and after training was reduced to a similar level, ~10% reduction from that in euhydration before training, the training-induced reduction in the threshold for cutaneous vasodilation increased to a level similar to hypohydration before training (P = 0.093) while that for sweating remained significantly lower than that before training (P = 0.004). Thus the enhanced cutaneous vasodilation response after aerobic training in a warm environment was reversed when PV expansion was reversed while the enhanced SR response remained partially.     

Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress

Physical exercise exacerbates the cytotoxic effects of statins in skeletal muscle. Mitochondrial impairments may play an important role in the development of muscular symptoms following statin treatment. Our objective was to characterize mitochondrial function and reactive oxygen species (ROS) production in skeletal muscle after exhaustive exercise in atorvastatin-treated rats. The animals were divided into four groups: resting control (CONT; n = 8) and exercise rats (CONT+EXE; n = 8) as well as resting (ATO; n = 10) and exercise (ATO+EXE; n = 8) rats that were treated with atorvastatin (10 mg·kg(-1)·day(-1) for 2 wk). Exhaustive exercise showed that the distance that was covered by treated animals was reduced (P < 0.05). Using dihydroethidium staining, we showed that the ROS level was increased by 60% in the plantaris muscle of ATO compared with CONT rats and was highly increased in ATO+EXE (226%) compared with that in CONT+EXE rats. The maximal mitochondrial respiration (V(max)) was decreased in ATO rats compared with that in CONT rats (P < 0.01). In CONT+EXE rats, V(max) significantly increased compared with those in CONT rats (P < 0.05). V(max) was significantly lower in ATO+EXE rats (-39%) compared with that in CONT+EXE rats (P < 0.001). The distance that was covered by rats significantly correlated with V(max) (r = 0.62, P < 0.01). The glycogen content was decreased in ATO, CONT+EXE, and ATO+EXE rats compared with that in CONT rats (P < 0.05). GLUT-4 mRNA expression was higher after exhaustive exercise in CONT+EXE rats compared with the other groups (P < 0.05). Our results show that exhaustive exercise exacerbated metabolic perturbations and ROS production in skeletal muscle, which may reduce the exercise capacity and promote the muscular symptoms in sedentary atorvastatin-treated animals.     

Thermoregulatory, cardiovascular, and muscular factors related to exercise after precooling

The effect of slightly lowered body temperature on endurance time and possibly related physiological factors was studied in seven male volunteers exercising on a cycle ergometer at an ambient temperature (Ta) of 18 degrees C. Work load was increased to 40% in a stepwise manner (phase I, min 0-16) followed by a period at 80% of peak oxygen consumption (VO2) sustained to exhaustion. On one day, exercise was preceded by a double cold exposure (precooling test, PRET), resulting in a 204-kJ/m2 negative heat storage and a 4 and 0.2 degrees C lower mean skin and core temperature at the start of exercise compared with the control test (CONT). Core temperature dropped further during exercise in PRET. Endurance time at 80% of peak VO2 was increased by 12% (P less than 0.05) in PRET. Heart rate (HR) was decreased throughout PRET (P less than 0.05); oxygen pulse and arteriovenous O2 difference were significantly increased in phase I of PRET, whereas the PRET-CONT differences in stroke volume and cardiac output were not significant. In phase II of PRET (min 16-28, heavy exercise) sweat rate (SR) and heat conductivity, indicating forearm blood flow, were lower (-39%, P less than 0.001; -37%). Pedal rate (PR) was 9% lower (P less than 0.01) in phase II of PRET. At the termination of exercise, PRET-CONT differences in HR, SR, and PR had disappeared.     

Enhancement of arm exercise endurance capacity with dihydroxyacetone and pyruvate

The effects of dietary supplementation of dihydroxyacetone and pyruvate (DHAP) on endurance capacity and metabolic responses during arm exercise were determined in 10 untrained males (20-26 yr). Subjects performed arm ergometer exercise (60% peak O2 consumption) to exhaustion after consumption of standard diets (55% carbohydrate, 15% protein, 30% fat; 35 kcal/kg) containing either 100 g of Polycose (placebo, P) or DHAP (3:1, treatment) substituted for a portion of carbohydrate. The two diets were administered in a random order, and each was consumed for a 7-day period. Biopsy of the triceps muscle was obtained immediately before and after exercise. Blood samples were drawn through radial artery and axillary vein catheters at rest, after 60 min of exercise, and at exercise termination. Arm endurance was 133 +/- 20 min after P and 160 +/- 22 min after DHAP (P less than 0.01). Triceps glycogen at rest was 88 +/- 8 (P) and 130 +/- 19 mmol/kg (DHAP) (P less than 0.05). Whole arm arteriovenous glucose difference (mmol/l) was greater (P less than 0.05) for DHAP than P at rest (0.60 +/- 0.12 vs. 0.05 +/- 0.09) and after 60 min of exercise (1.00 +/- 0.12 vs. 0.36 +/- 0.11), but it did not differ at exhaustion. Neither respiratory exchange ratio nor respiratory quotient differed between trials at rest, after 60 min of exercise, or at exhaustion. Plasma free fatty acid, glycerol, beta-hydroxybutyrate, catecholamines, and insulin were similar during rest and exercise for both diets. Feeding DHAP for 7 days increased arm muscle glucose extraction before and during exercise, thereby enhancing submaximal arm endurance capacity.     

Thermoregulatory and aerobic changes after endurance training in a hypobaric hypoxic and warm environment.

Plasma volume (PV) expansion by endurance training and/or heat acclimatization is known to increase aerobic and thermoregulatory capacities in humans. Also, higher erythrocyte volume (EV) fractions in blood are known to improve these capacities. We tested the hypothesis that training in a hypobaric hypoxic and warm environment would increase peak aerobic power (VO(2)(peak)) and forearm skin vascular conductance (FVC) response to increased esophageal temperature (T(es)) more than training in either environment alone, by increasing both PV and EV. Twenty men were divided into four training regimens (n = 5 each): low-altitude cool (610-m altitude, 20 degrees C ambient temperature, 50% relative humidity), high-altitude cool (2,000 m, 20 degrees C), low-altitude warm (610 m, 30 degrees C), and high-altitude warm (HW; 2,000 m, 30 degrees C). They exercised on a cycle ergometer at 60% VO(2)(peak) for 1 h/day for 10 days in a climate chamber. After training, PV increased in all trials, but EV increased in only high-altitude trials (both P < 0.05). VO(2)(peak) increased in all trials (P < 0.05) but without any significant differences among trials. FVC response to increased T(es) was measured during exercise at 60% of the pretraining VO(2)(peak) at 610 m and 30 degrees C. After the training, T(es) threshold for increasing FVC decreased in warm trials (P < 0.05) but not in cool trials and was significantly lower in HW than in cool trials (P < 0.05). The slope of FVC increase/T(es) increase increased in all trials (P < 0.05) except for high-altitude cool (P > 0.4) and was significantly higher in HW than in cool trials (P < 0.05). Thus, against our hypothesis, the VO(2)(peak) for HW did not increase more than in other trials. Moreover, slope of FVC increase/T(es) increase in HW increased most, despite the similar increase in blood volume, suggesting that factors other than blood volume were involved in the highest FVC response in HW.     

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.     

Enhanced leg exercise endurance with a high-carbohydrate diet and dihydroxyacetone and pyruvate

The effects of dietary supplementation of dihydroxyacetone and pyruvate (DHAP) on metabolic responses and endurance capacity during leg exercise were determined in eight untrained males (20-30 yr). During the 7 days before exercise, a high-carbohydrate diet was consumed (70% carbohydrate, 18% protein, 12% fat; 35 kcal/kg body weight). One hundred grams of either Polycose (placebo) or dihydroxyacetone and pyruvate (treatment, 3:1) were substituted for a portion of carbohydrate. Dietary conditions were randomized, and subjects consumed each diet separated by 7-14 days. After each diet, cycle ergometer exercise (70% of peak oxygen consumption) was performed to exhaustion. Biopsy of the vastus lateralis muscle was obtained before and after exercise. Blood samples were drawn through radial artery and femoral vein catheters at rest, after 30 min of exercise, and at exercise termination. Leg endurance was 66 +/- 4 and 79 +/- 2 min after placebo and DHAP, respectively (P less than 0.01). Muscle glycogen at rest and exhaustion did not differ between diets. Whole leg arteriovenous glucose difference was greater (P less than 0.05) for DHAP than for placebo at rest (0.36 +/- 0.05 vs. 0.19 +/- 0.07 mM) and after 30 min of exercise (1.06 +/- 0.14 vs. 0.65 +/- 0.10 mM) but did not differ at exhaustion. Plasma free fatty acids, glycerol, and beta-hydroxybutyrate were similar during rest and exercise for both diets. Estimated total glucose oxidation during exercise was 165 +/- 17 and 203 +/- 15 g after placebo and DHAP, respectively (P less than 0.05). It is concluded that feeding of DHAP for 7 days in conjunction with a high carbohydrate diet enhances leg exercise endurance capacity by increasing glucose extraction by muscle.     

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.     

Menstrual cycle phase affects temperature regulation during endurance exercise.

We investigated whether menstrual cycle phase would affect temperature regulation during an endurance exercise bout performed at room temperature (Ta) of 22 degrees C and 60% relative humidity. Nine eumenorrheic women [age 27.2 +/- 3.7 yr, peak O2 uptake (VO2) 2.52 +/- 0.35 l/min] performed 60 min of cycle exercise at 65% of peak VO2. Subjects were tested in both midfollicular (F) and midluteal (L) phases, although one woman did not show a rise in serum progesterone (P4) that is typically evident 1 wk after ovulation. VO2, rectal (Tre) and skin (Tsk) temperatures, heart rates (HR), and ratings of perceived exertion (RPE) were measured throughout exercise. Sweat loss (SL) was estimated from pre- and postexercise body weight differences. VO2, SL, and Tsk were not affected by menstrual cycle phase. Preexercise Tre was 0.3 degrees C higher during L than during F conditions, and this difference increased to 0.6 degrees C by the end of exercise (P less than 0.01). Compared with F, HRs during L were approximately 10 beats/min greater (P less than 0.001) at all times, whereas RPE responses were significantly greater (P less than 0.01) by 50 min of cycling. No differences in any measured values were found in the subject whose P4 was low in both test conditions. Results indicate that thermoregulation (specifically, regulation of Tre), as well as cardiovascular strain and perception of exercise, was adversely affected during the L phase.     

Effect of exercise hemoconcentration and hyperosmolality on exercise responses

We investigated the effects of a decrease in plasma volume (PV) and an increase in plasma osmolality during exercise on circulatory and thermoregulatory responses. Six subjects cycled at approximately 65% of their maximum O2 uptake in a warm environment (30 degrees C, 40% relative humidity). After 30 min of control (C) exercise (no infusion), PV decreased 13.0%, or 419 +/- 106 (SD) ml, heart rate (HR) increased to 167 +/- 3 beats/min, and esophageal temperature (Tes) rose to 38.19 +/- 0.09 degrees C (SE). During infusion studies (INF), infusates were started after 10 min of exercise. The infusates contained 5% albumin suspended in 0.45, 0.9, or 3.0% saline. The volume of each infusate was adjusted so that during the last 10 min of exercise PV was maintained at the preexercise level and osmolality was allowed to differ. HR was significantly lower (10-16 beats/min) during INF than during C. Tes was reduced significantly during INF, with trends for increased skin blood flow and decreased sweating rates. No significant differences in HR, Tes, or sweating rate occurred between the three infusion conditions. We conclude that the decrease in PV, which normally accompanies moderate cycle exercise, compromises circulatory and thermal regulations. Increases in osmolality appear to have small if any effects during such short-term exercise.     

Endurance training decreases plasma glucose turnover and oxidation during moderate-intensity exercise in men

To assess the effects of endurance training on plasma glucose kinetics during moderate-intensity exercise in men, seven men were studied before and after 12 wk of strenuous exercise training (3 days/wk running, 3 days/wk cycling). After priming of the glucose and bicarbonate pools, [U-13C] glucose was infused continuously during 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake (VO2) to determine glucose turnover and oxidation. Training increased cycle ergometer peak VO2 by 23% and decreased the respiratory exchange ratio during the final 30 min of exercise from 0.89 +/- 0.01 to 0.85 +/- 0.01 (SE) (P less than 0.001). Plasma glucose turnover during exercise decreased from 44.6 +/- 3.5 mumol.kg fat-free mass (FFM)-1.min-1 before training to 31.5 +/- 4.3 after training (P less than 0.001), whereas plasma glucose clearance (i.e., rate of disappearance/plasma glucose concentration) fell from 9.5 +/- 0.6 to 6.4 +/- 0.8 ml.kg FFM-1.min-1 (P less than 0.001). Oxidation of plasma-derived glucose, which accounted for approximately 90% of plasma glucose disappearance in both the untrained and trained states, decreased from 41.1 +/- 3.4 mumol.kg FFM-1.min-1 before training to 27.7 +/- 4.8 after training (P less than 0.001). This decrease could account for roughly one-half of the total reduction in the amount of carbohydrate utilized during the final 30 min of exercise in the trained compared with the untrained state.     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

Intracranial self-stimulation motivates treadmill running in rats.

Most animal running models have traditionally used aversive motivators to induce exercise tasks. This study demonstrates treadmill running motivated by reinforcement of intracranial self-stimulation (ICSS), providing an alternative model with which to study physiological responses to exercise. Twenty-nine male Sprague-Dawley rats were stereotaxically implanted with bipolar electrodes aimed at the ventral tegmental area of the brain. After 7 days of operant lever-press training for ICSS, rats that pressed at least 50 presses/min were randomly divided into three conditions: exercise-reinforcing brain stimulation (Ex-St), exercise-aversive shock (Ex-Sh), and sedentary controls (C). Ex-St and Ex-Sh ran for 30 min at 25 m/min at 5% grade for 2 wk with ICSS and electric shock as the motivator, respectively, while C did not run. At the end of 2 wk, Ex-St and Ex-Sh performed an endurance run. Results show that Ex-St ran longer than Ex-Sh [63 +/- 10 vs. 42 +/- 10 (SD) min; P less than 0.05]. HR was higher in Ex-St than in C (P less than 0.05). Rectal temperature increased similarly in both exercise groups. This model provides a highly effective method to motivate treadmill running in rats and as such can be used to characterize physiological responses to exercise without the potentially confounding influence of stress associated with an aversive shock motivator.     

Ultrastructural morphometry of matrical changes induced by exercise and food restriction in the rat calcaneal tendon.

The ultrastructural morphometry of collagen fibril populations in 24 calcaneal tendons obtained from 12 Fischer 344 rats were studied to elucidate matrical changes induced by food restriction and/or endurance exercise. Rats were randomly assigned to four equal groups: ad libitum control (AC), ad libitum exercise (AE), restricted diet control (RC) and restricted diet exercise (RE) groups. Beginning from 6 weeks of age, animals in the two food restriction groups were fed 60% of the mean food consumption of ad libitum fed rats. Then, starting from 6-7 months of age, the rats in the two exercise groups performed 40-50 min of treadmill running at 1.2-1.6 miles h-1 every day for a total of 10 weeks. Endurance training did not significantly alter body weight, but food restriction with or without exercise resulted in a significant loss of body weight. In ad libitum fed controls, food restriction alone did not significantly alter the mean collagen fibril CSA, but predisposed a preponderance of small-sized collagen fibrils. Endurance training per se induced a significant (32%) increase in mean fibril CSA (P less than 0.05), but this adaptive response to exercise was prevented by food restriction, as indicated by a 33% decline in fibril CSA (P less than 0.05). These findings demonstrate that dietary restriction modifies the adaptation of tendon collagen morphometry in response to endurance training, and that weight loss is better achieved with food restriction than endurance exercise.     

Exercise-induced HSP-72 elevation and cardioprotection against infarct and apoptosis.

Successive bouts of endurance exercise are associated with both increased cardiac levels of heat shock protein-72 (HSP-72) and improved cardioprotection against ischemia-reperfusion (I/R)-induced cardiac cell death. Although overexpression of HSP-72 has been shown to be cardioprotective in transgenic animals, it is unclear whether increased levels of HSP-72 are essential for exercise-induced cardioprotection against I/R-mediated cell death. We tested the hypothesis that exercise-induced increases in myocardial levels of HSP-72 are required to achieve exercise-mediated protection against I/R-induced cardiac cell death. To test this postulate, we investigated the effect of preventing the exercise-induced increase in cardiac HSP-72 on myocardial infarction and apoptosis after 50 min of in vivo ischemia and 120 min of reperfusion. Adult male rats remained sedentary or performed successive bouts of endurance exercise in cold (8 degrees C) or warm (22 degrees C) environments. We found that, compared with sedentary control animals, exercise in a warm environment significantly increased myocardial HSP-72 content. In contrast, exercise in the cold environment prevented the exercise-induced increase in myocardial HSP-72 levels. After in vivo myocardial I/R, infarct size was reduced in both exercised groups compared with sedentary animals. Furthermore, compared with sedentary rats, I/R-induced myocardial apoptosis (as indicated by terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling-positive nuclei and caspase-3 activity) was attenuated in both groups of exercised animals. Therefore, although HSP-72 has cardioprotective properties, our results reveal that increased myocardial levels of HSP-72 (above control) are not essential for exercise-induced protection against I/R-induced myocardial infarction and apoptosis.     

Characterization of exercise-induced hyperketonemia in streptozotocin-diabetic rats and the effects on it of prolonged training

Exercise-induced hyperketonemia was investigated using streptozotocin (STZ)-diabetic rats subjected to running exercise on a treadmill. The degrees of hyperketonemia after 50, 55 and 60% VO2max of exercises were similar in mild diabetic rats (fasting plasma glucose; FPG less than 11 mM). The degree of hyperketonemia (especially an increase in acetoacetate; AcAc) after 60% VO2max of exercise was correlated with FPG (P less than 0.01) and basal plasma ketone bodies (P less than 0.01). Prolonged training with 60% VO2max of exercise for 30 min 3 times per week for 6 wks reduced the increase in plasma ketone bodies induced by the exercise in both mild (FPG less than 11 mM) and severe (FPG greater than 22 mM) diabetic rats. The exercise-induced increase in plasma glucagon in mild diabetic rats and free fatty acids (FFA) in severe diabetic rats are also reduced by the training. These results demonstrate that exercise-induced hyper-AcAc-emia correlated with the FPG level is reduced by prolonged training in diabetic rats, and might suggest that exercise-induced hyperketonemia is reduced by long-term exercise training also in diabetic patients.     

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.     

Is exhaustive training adequate preparation for endurance performance?

Our purpose was to test the significance of exhaustive training in aerobic or endurance capacity. The extent of adaptations to endurance training was evaluated by assessing the increase in physical performance capability and oxidative markers in the organs of rats trained by various exercise programs. Rats were trained by treadmill running 5 days.week-1 at 30 m.min-1 for 8 weeks by one of three protocols: T1-60 min.day-1; T2-120 min.day-1; and T3-120 min.day-1 (3 days.week-1) and to exhaustion (2 days.week-1). Groups T2 and T3 ran for longer than T1 in an endurance exercise test (P less than 0.05), in which the animals ran at 30 m.min-1 to exhaustion; no difference was observed between groups T2 and T3. All 3 trained groups showed a similar increase (20-27%) in the fast-twitch oxidative-glycolytic (FOG) fibers with a concomitant decrease in the fast-twitch glycolytic (FG) fiber population in gastrocnemius (p less than 0.05). The capillary supply in gastrocnemius increased with the duration of exercise (p less than 0.05): no difference was found between groups T2 and T3. Likewise, no distinction was seen between groups T2 and T3 in the increase in succinate dehydrogenase activity in gastrocnemius and the heart. These results suggest that the maximal adaptive response to endurance training does not require daily exhaustive exercise.     

Training does not protect against exhaustive exercise-induced lactate transport capacity alterations

The effects of endurance training on lactate transport capacity remain controversial. This study examined whether endurance training 1) alters lactate transport capacity, 2) can protect against exhaustive exercise-induced lactate transport alteration, and 3) can modify heart and oxidative muscle monocarboxylate transporter 1 (MCT1) content. Forty male Wistar rats were divided into control (C), trained (T), exhaustively exercised (E), and trained and exercised (TE) groups. Rats in the T and TE groups ran on a treadmill (1 h/day, 5 days/wk at 25 m/min, 10% incline) for 5 wk; C and E were familiarized with the exercise task for 5 min/day. Before being killed, E and TE rats underwent exhaustive exercise (25 m/min, 10% grade), which lasted 80 and 204 min, respectively (P < 0.05). Although lactate transport measurements (zero-trans) did not differ between groups C and T, both E and TE groups presented an apparent loss of protein saturation properties. In the trained groups, MCT1 content increased in soleus (+28% for T and +26% for TE; P < 0.05) and heart muscle (+36% for T and +33% for TE; P < 0.05). Moreover, despite the metabolic adaptations typically observed after endurance training, we also noted increased lipid peroxidation byproducts after exhaustive exercise. We concluded that 1) endurance training does not alter lactate transport capacity, 2) exhaustive exercise-induced lactate transport alteration is not prevented by training despite increased MCT1 content, and 3) exercise-induced oxidative stress may enhance the passive diffusion responsible for the apparent loss of saturation properties, possibly masking lactate transport regulation.