Heat shock protein concentration and clarity of porcine lenses incubated at elevated temperatures.

PURPOSE: To quantify the concentration of heat shock proteins in lenses in lens organ culture at elevated temperatures, and to examine the relation between elevated temperature and lens clarity. METHODS: Pig lenses obtained from a local abattoir were dissected aseptically and incubated in medium M199 without serum for 4 days to stabilize, and lenses with protein leakage of less than 10 mg/l were obtained for heat shock exposure. Heat shock was performed by incubation for 1 h in M199 without serum at various temperatures ranging from 37 °C to 55 °C. After incubation for 24 h, cataract blurring of the images was assessed using Scantox™ and Scion Image analysis of the lens photographs. Lens homogenates were subsequently analyzed for Hsp70 and Hsp27 with western blotting. RESULTS: The degree of cataract blurring of the images increased with increasing temperature, but the two functional measures provided different results. Focal length inconsistency, as assessed with the back vertex distance standard error of the mean (BVD SEM; the variability in focal lengths measured at 20 equally spaced locations across the lens, Scantox™), increased nearly linearly with the heat treatment temperature. In contrast, decreased clarity, evident by a fuzzy image with lower contrast, was not markedly altered as the temperature rose until a threshold of approximately 47.5 °C. The inducible isoform of the Hsp70 family (Hsp70) of heat shock proteins was increased at all temperatures above the control except those above 50 °C. Changes in Hsp27 were less clear as the protein content increased only at the incubation temperatures of 39 °C and 48.5 °C. CONCLUSIONS: The porcine lens demonstrates subtle changes in the variability of the focal length, and the variability increases as the incubation temperature rises. In contrast, lens clarity is relatively stable at temperatures up to 47.5 °C, above which dramatic changes, indicative of the formation of cataracts, occur. The lens content of Hsp70 was elevated in lenses exposed to heat shock only up to 50 °C. These data suggest that in a stressful environment, Hsp70 may be associated with protection against loss of clarity. In addition, the functional measures BVD SEM and clarity assess different qualities of the lens, with the former likely more sensitive to subtle changes in the protein structure.

Changes in skeletal muscle morphology and biochemistry after cardiac transplantation.

Skeletal muscle biopsies (vastus lateralis) were performed in 12 patients (mean age 47 +/- 11 years) before and at 3 and 12 months after cardiac transplantation. Fiber type analysis revealed a predominance of type II fibers before cardiac transplantation (66 +/- 10%); the ratio did not change after transplantation. Fiber cross-sectional area increased by 35% to 39% in all fiber types by 12 months after cardiac transplantation. Fiber cross-sectional area, however, remained below the reported normal values. The number of capillaries surrounding each fiber did not change after cardiac transplantation. Skeletal muscle enzyme activity of phosphofructokinase, citrate synthase, and beta-hydroxyacyl coenzyme A dehydrogenase increased by 26%, 47%, and 63%, respectively, after cardiac transplantation (p < 0.05). Peak oxygen uptake also increased significantly after cardiac transplantation (19.5 +/- 8.1 ml/kg/min at 12 months vs 9.8 +/- 1.4 ml/kg/min before transplant, p < 0.01); however, uptake remained 40% below that of predicted. Thus, significant improvement in skeletal muscle morphology and biochemistry occurs in the first year after cardiac transplantation in association with improved exercise capacity. Recovery, however, may be incomplete, which could explain residual impairment of exercise capacity in these patients.

Sleep deprivation: effects on work capacity, self-paced walking, contractile properties and perceived exertion.

The primary purpose of this study was to examine the effect of a 48-hour period of sleep deprivation on the performance of selected physical work tasks [30-45% of maximum oxygen consumption (VO2max)]. In addition, this study assessed the effect of continual performance of physical work during sleep deprivation on standardized physiological and psychological test scores. Nineteen male subjects performed six different physical tasks, designed to involve all major muscle groups, during a 48-hour period of sleep deprivation. Fourteen subjects served as sleep-deprivation controls. Performance on all physical work tasks decreased significantly. Neither sleep deprivation (SD) or sleep deprivation in conjunction with continuous physical work (SDW) had any effect on muscle contractile properties, anaerobic power measures or resting blood glucose and lactate concentrations. Only SD subjects demonstrated a decline in cardiorespiratory function. Self-selected walking pace decreased and perceived exertion increased significantly in the SDW group. Positive and negative mood scores were adversely affected in both groups, the total change being greatest in SD subjects. The results indicate that performance of physical work tasks requiring 30-45% VO2max declines significantly over a 48-hour period of sleep deprivation. However, maximal physiological function is not unduly compromised by either the work tasks in conjunction with sleep deprivation or by sleep deprivation alone.

Isoproterenol potentiates exercise-induction of Hsp70 in cardiac and skeletal muscle.

The response to exercise stress is characterized by an increase in circulating catecholamines and rapid synthesis of the inducible member of the 70 kDa family of heat shock proteins (Hsp70). Cell culture studies indicate that Hsp70 expression is influenced by beta-adrenergic receptor intermediates including cyclic AMP (cAMP) and cAMP dependent protein kinase (PKA). Thus, in the present investigation, the effect of a beta-adrenergic agonist, isoproterenol (ISO; 10 mg/kg) and a beta-adrenergic antagonist, nadolol (NAD; 25 mg/kg), on the in vivo expression of Hsp70 in rodent cardiac and skeletal muscle following moderate (MOD; 17 m/min) and exhaustive (EXH; 30 m/min) exercise was examined. While ISO alone did not induce Hsp70 synthesis, ISO treatment potentiated Hsp70 expression following MOD in the white vastus and heart (395+/-29 and 483+/-29% greater than control respectively, P < 0.05). Furthermore, this effect was reversed with combined beta-adrenergic agonist and antagonist treatment (ISO+NAD) indicating that the isoproterenol induced increase in post-exercise Hsp70 expression was mediated via beta-adrenergic receptor activity. However, there were no differences in Hsp70 levels among treatment groups following EXH. The failure of NAD to attenuate Hsp70 accumulation following EXH suggests that beta-adrenergic receptor activity is not the main signal in the induction of Hsp70 following exercise. Hsp70 induction was dependent on exercise intensity and ISO administration prior to MOD resulted in Hsp70 levels similar to those observed following EXH. The results from the present investigation indicate that beta-adrenergic receptor stimulation does not induce Hsp70 synthesis per se, but may be one factor involved in the complex regulation of the stress response to exercise in vivo.

Shifts in rat plantaris motor unit characteristics with aging and compensatory overload.

Contractile characteristics of single motor units from plantaris muscles of young (6 mo), middle-aged (14 mo), and older (20 mo) rats were examined. Some of the muscles were subjected to a short-term (30 days) compensatory overload. After overload, the absolute increase in muscle weight was less for the 20-mo-old rats (38%) than the other groups (62%). However, when muscle weight per unit body weight was examined, the ratio was increased to a similar extent for all age groups. Aging was associated with an increase in slow (6 mo, 12.5%; 14 mo, 17.7%; 20 mo, 30.2%) and transitional (6 mo, 2.5%; 14 mo, 15.2%; 20 mo, 12.7%) motor unit proportions. This increase initially occurred at the expense of fast-fatigable motor units (6 mo, 36.3%; 14 mo, 13.9%; 20 mo, 20.7%) and then fast-intermediate units (6 mo, 40%; 14 mo, 39.2%; 20 mo, 26.7%). In addition, the maximal tension of individual motor units tended to increase with age. In younger rats compensatory overload produced changes in the motor unit profile similar to those that occurred with aging. In contrast, overload of the plantaris from 20-mo-old rats resulted in an increase in the force contribution from fast motor units. These results demonstrate that aging is accompanied by a gradual reorganization of the skeletal muscle motor unit pool, such that there is a loss of fast motor units and an increase in the proportion of slow motor units. While compensatory overload initially appears to mimic the aging effect, in older animals it may delay or reverse some of the age-related changes.

Appearance of "transitional" motor units in overloaded rat skeletal muscle.

The contractile characteristics of single motor units, isolated from rat plantaris muscles subjected to short-term (30 days) compensatory overload, were assessed to determine whether motor units in transition could be detected. In the control plantaris 88% of the motor units were classified as fast. After overload, a large decline (26.5%) in the proportion of typical fast motor units was noted. The estimated contribution of fast fatigable units to whole muscle tetanic tension (Po 200) also declined (from 55 to 25%), whereas that of fast intermediate motor units increased (from 33 to 55%). In the overloaded plantaris, motor units that exhibited unusual "sag" and contraction time characteristics were detected. These motor units, which could be further subdivided into two distinct types by a variety of indexes, exhibited characteristics intermediate to fast and slow units and therefore were termed "transitional." Transitional units accounted for 12% of the estimated whole muscle Po200 after overload. These experiments characterize novel classifications of motor units undergoing transformation and further detail the motor unit shift that accompanies compensatory overload.

Differential microvascular response to disuse in rat hindlimb skeletal muscles.

The aim of the study was to address discrepant findings in the literature regarding coupling between decreased functional demand during disuse and reduced capillarity. We previously reported [K. Tyml, O. Mathieu-Costello, and E. Noble. Microvasc. Res. 49: 17-32, 1995] that severe disuse of rat extensor digitorum longus (EDL) muscle caused by a 2-wk application of tetrodotoxin (TTX) on the sciatic nerve is not accompanied by capillary loss. Using the same animal model, the present study examined whether this absence of coupling could be explained in terms of 1) too short a duration of disuse and 2) muscle-specific response to disuse. Fischer 344 rats were exposed to either no treatment (control) or to 2- or 8-wk TTX applications. Fiber size, capillary density per fiber cross-sectional area, and capillary-to-fiber (C/F) ratio were determined by morphometry in the EDL muscle (control, 2- and 8-wk groups) and in the superficial portion of medial gastrocnemius (Gas) muscle (control, 2 wk). In both muscles, microvascular blood flow was evaluated by intravital microscopy [red blood cell velocity in capillaries (V(RBC))] and by laser Doppler flowmetry (LDF). Regardless of duration of TTX application or muscle type, TTX-induced disuse resulted in a significant reduction of fiber area (44-71%). However, capillary density increased in EDL muscle (both at 2 and 8 wk) but not in Gas muscle. C/F ratio decreased in EDL muscle at 8 wk (18%) and in Gas muscle (39%). This indicates that the effect on capillarity depended on duration of disuse and on muscle type. V(RBC) and LDF signal were significantly larger in EDL than in Gas muscle. Analysis of change in capillarity vs. V(RBC) suggested that the outcome of disuse may be modulated by blood flow. We conclude that the duration of skeletal muscle disuse per se does not dictate capillary loss, and we hypothesize that discrepant findings of coupling between functional demand and capillarity could be due to the presence/absence of flow-related angiogenesis superimposed on the capillary removal process during disuse.

Time course of changes in capillarization in hypertrophied rat plantaris muscle.

The time course of angiogenesis during hypertrophy of the rat plantaris muscle was studied by using a unilateral, synergistic ablation model. Animals (n = 6/group) were euthanized 2, 5, 7, 15, 21, and 30 days postmyectomy. Sections from both the hypertrophied and contralateral muscles were simultaneously stained for capillaries and muscle fiber type. Mean fiber cross-sectional area (FA) and various indexes of capillarity were determined by using a video analysis system. The capillary supply to individual fibers, assessed as the FA supplied per capillary contact, remained unchanged until day 21 (compared with day 2) and exhibited a significant increase at day 30. Analysis of the time course of capillary development on the basis of the number of capillary contacts per fiber, and of hypertrophy on the basis of FA, yielded half-lives of 10.1 and 11.2 days, respectively. It was concluded that angiogenesis during muscle overload is tightly coupled to the changes in FA, which could suggest that the two processes are initiated and/or driven by some common factor(s).

Effect of vitamin E deprivation and exercise training on induction of HSP70.

To investigate the effect of dietary vitamin E deprivation and chronic exercise on the relative content of selected isoforms of the heat-shock protein 70 (HSP70) family in rat hindlimb muscle, vitamin E was withheld for 16 wk from female rats that underwent treadmill run training during the final 8 wk. As indicated by increased (P < 0.05) content of the stress-inducible isoform (HSP72), training did stress the exercising muscles. However, vitamin E deficiency did not alter HSP72 content in nontrained rats and was associated with a lesser induction (P < 0.01) in some muscles of trained animals. The constitutive isoform, which exhibited similar levels in muscles of varying fiber types, was demonstrated to be largely refractory to exercise, with an equivocal response to vitamin E deprivation. HSP72 content was correlated to type I myosin heavy chain (MHC-I) content but only in muscles of sedentary normal-diet rats. After training, HSP72 content in a muscle essentially devoid of MHC-I (superficial vastus lateralis) reached levels comparable to those in a muscle high in MHC-I (soleus).

Muscle capillarization O2 diffusion distance, and VO2 kinetics in old and young individuals.

The relationships between muscle capillarization, estimated O2 diffusion distance from capillary to mitochondria, and O2 uptake (VO2) kinetics were studied in 11 young (mean age, 25.9 yr) and 9 old (mean age, 66.0 yr) adults. VO2 kinetics were determined by calculating the time constants (tau) for the phase 2 VO2 adjustment to and recovery from the average of 12 repeats of a 6-min, moderate-intensity plantar flexion exercise. Muscle capillarization was determined from cross sections of biopsy material taken from lateral gastrocnemius. Young and old groups had similar VO2 kinetics (tau VO2-on = 44 vs. 48 s; tau VO2-off = 33 vs. 44 s, for young and old, respectively), muscle capillarization, and estimated O2 diffusion distances. Muscle capillarization, expressed as capillary density or average number of capillary contacts per fiber/average fiber area, and the estimates of diffusion distance were significantly correlated to VO2-off kinetics in the young (r = -0.68 to -0.83; P < 0.05). We conclude that 1) capillarization and VO2 kinetics during exercise of a muscle group accustomed to everyday activity (e.g., walking) are well maintained in old individuals, and 2) in the young, recovery of VO2 after exercise is faster, with a greater capillary supply over a given muscle fiber area or shorter O2 diffusion distances.

Differential expression of stress proteins in rat myocardium after free wheel or treadmill run training.

High-intensity treadmill exercise increases the expression of a cardioprotective, inducible 72-kDa stress protein (SP72) in cardiac muscle. This investigation examined whether voluntary free wheel exercise training would be sufficient to confer a similar response. Male Sprague-Dawley rats were randomly assigned to either treadmill (TM-Tr) or free wheel (FW-Tr) training groups. By the end of the 8-wk training period, TM-Tr animals ran 1 h/day, 5 days/wk up a 10% grade, covering a distance of 8,282 m/wk. FW-Tr rats ran, on average, 5,300 m/wk, with one-third of the animals covering distances similar to those for the TM-Tr group. At the time of death, hearts of trained and caged sedentary control (Sed) animals were divided into left (LV) and right (RV) ventricles. Citrate synthase activity and the relative immunoblot contents of SP72, SP73 (the constitutive isoform of the SP70 family), and a 75-kDa mitochondrial chaperone (SP75) were subsequently determined. LV and RV did not differ on any measure, and SP73, SP75, and citrate synthase were not affected by training. Cardiac SP72 levels were elevated over fourfold in both ventricles of TM-Tr compared with RV of FW-Sed rats. Despite the animals having run a similar total distance, cardiac SP72 content in FW-Tr rats was not different from that in Sed animals. These data indicate that voluntary exercise training is insufficient to elicit an elevation of SP72 in rat heart and suggest that exercise intensity may be a critical factor in evoking the cardioprotective SP72 response.

Exercise-induced glycogenolysis in sympathectomized rats.

The role of the adrenergic system in regulating glycogenolysis during exercise was studied in rats. Alterations in the adrenergic system were produced by injections of 6-hydroxydopamine (6-OHD), surgical removal of the adrenal medulla (ADMX), or the combination of ADMX and 6-OHD injection. Exercise was treadmill running at 22 m/min for 60 min. Colonic temperature averaged 2.8 degrees C higher in the exercised than control rats. Exercise reduced the glycogen of the liver and skeletal muscles of all groups. The glycogen concentrations of the soleus and red portion of the gastrocnemius muscles of the ADMX and ADMX-6-OHD groups were about 3.8 and 2.5 times higher after exercise than those of the normal-exercised rats. Glycogen depletion of the white portion of the gastrocnemius muscle was similar for all exercised groups. 6-OHD treatment depleted the catecholamines of the myocardium. These results demonstrate that glycogen depletion during exercise occurs in rats devoid of adrenergic control. However, differences between types of skeletal muscle suggest that factors other than the adrenergic system may be involved in controlling glycogen metabolism during exercise.

A decade of aerobic endurance training: histological evidence for fibre type transformation.

BACKGROUND: Researchers employing a variety of training methods have demonstrated a fast-to-slow fibre transformation in animal skeletal muscle. The observation as to whether this occurs in exercise trained humans is limited and equivocal. EXPERIMENTAL DESIGN: to examine this issue, skeletal muscle from seven subjects who had participated in a decade or more of high intensity aerobic training (DT) and six nontrained (NT) subjects was obtained by muscle biopsy from the vastus lateralis muscle (VL) and subjected to a modified myofibrillar ATPase technique to identify muscle fibre types. Muscle tissue was histochemically treated by exposure to an alkaline preincubation (pH 9.9), an acid preincubation (pH 4.3 or 4.6) and the formate-KCI preincubation buffer (pH 4.54), previously employed in animal studies. RESULTS: The formate-KCl preincubation medium identified all major fibre types at a single pH in human subjects. The percentage of type I fibres in DT was 70.9% vs 37.7% in NT (p<0.01), while the type IIa fibres in DT (25.3%) was much lower (p<0.01) than NT (51.8%). Surprisingly, type IIa fibres in the DT group displayed lesser oxidative staining intensity (p<0.01) than type IIa fibres from the NT group. Mean cross-sectional area of type I fibres for DT (6233.9+/-1421.7 microm2) was greater (p<0.05) than either type I (5746.8+/-1135.2 microm2) or II (5693.5+/-1214.6 microm2) from NT. CONCLUSIONS: The results revealed that endurance training may promote a transition from type II to type I muscle fibre types and occurs at the expense of the type II fibre population.

Effect of dietary manipulation on a high intensity performance test.

The effects of dietary manipulation (low- or high-carbohydrate) on performance of a short-duration exercise were studied with endurance- and intermittent-trained athletes. Eight subjects performed a depletion drill of 10 one minute workbouts at 7 W/kg and 85 rpm on a cycle ergometer. The subjects followed a dietary regimen of three days on a low-carbohydrate diet followed by three days on a high-carbohydrate diet. Muscle biopsy samples were taken immediately prior to and immediately after the testing sessions. Dietary manipulation did not affect resting muscle glycogen levels. However, subjects accustomed to continuous training regimens used less glycogen, produced less muscle lactate and exercised longer than subjects accustomed to intermittent training programs. These biochemical changes appeared to be related to the fibre type distribution and the training background of the athletes.

A model of poorly controlled type 1 Diabetes Mellitus and its treatment with aerobic exercise training.

BACKGROUND: Modern exogenous insulin therapy can improve the quality of life of Type 1 Diabetic Mellitus (T1DM) patients, although maintenance of normal glycaemic levels is often a challenge given the variety of factors that alter it. A number of studies have examined the effect of exercise in T1DM; however, the majority of experimental studies have utilized diabetic rodents with severe hyperglycaemia. Given that T1DM patients are likely to refrain from hyperglycaemia, studies examining the effects of regular exercise in which blood glucose is poorly controlled would better represent the T1DM population. METHODS: The current study examined the ability of a ten-week aerobic exercise training program to modify markers of cardiovascular function and bone health in STZ-induced diabetic rodents maintained in the 9-15 mM glycaemic range through insulin therapy. RESULTS: Moderate hyperglycaemia, when prolonged, leads to significant changes in cardiac structure, bone health, and glucose handling capacity. Ten weeks of exercise was able to alleviate many of these deleterious events as no significant cardiovascular functional alterations were evident except a reduction in resting heart rate and an increase in stroke volume index. Further, despite changes in cardiac dimensions, exercise was able to elevate cardiac output index and increase the E/A ratio of exercising diabetic animals which would be indicative of improvements of cardiac function. CONCLUSIONS: Together, this study demonstrates that despite moderate hyperglycaemia, the combined role of a ten-week exercise training program coupled with insulin therapy is able to alleviate many of the well-known complications associated with diabetes progression.

Myocardial accumulation and localization of the inducible 70-kDa heat shock protein, Hsp70, following exercise.

Exercise increases the 70-kDa heat shock protein (Hsp70) in the myocardium, and this exercise-induced increase is associated with significantly improved cardiac recovery following insult. However, while heat shock has been shown to elevate Hsp70 primarily in the cardiac vasculature of the myocardium, the localization following exercise is unknown. Male Sprague-Dawley rats performed continuous treadmill running at 30 m/min for 60 min (2% incline) on either 1 or 5 consecutive days. At 30 min and 24 h following exercise, hearts were extirpated, and the left ventricle was isolated, OCT-cork mounted, and sectioned for immunofluorescent analysis. Whereas immunofluorescent analysis revealed little to no Hsp70 in control hearts and 30 min postexercise, the accumulation of Hsp70 24 h after a single exercise bout or 5 days of training was predominantly located in large blood vessels and, in particular, colocalized with a marker of smooth muscle. Furthermore, higher core temperatures attained during exercise led to more abundant accumulation in smaller vessels and the endothelium. It is concluded that the accumulation of myocardial Hsp70 following acute exercise predominantly occurs in a cell type-specific manner, such that changes in the cardiac vasculature account for much of the increase. This accumulation appears first in the smooth muscle of larger vessels and then increases in smaller vessels and the endothelium, as core temperature attained during exercise increases. This finding supports the observations after heat shock and further suggests that the vasculature is a primary target in exercise-induced cardioprotection.

Exercise is the primary factor associated with Hsp70 induction in muscle of treadmill running rats.

AIM: The cytoprotective, inducible stress protein, Hsp70, increases in muscles of rodents subjected to strenuous treadmill running. Most treadmill running protocols employ negative reinforcement to encourage animals to exercise. As these stimuli may themselves activate stress responses, the present investigation was conducted to determine their contribution to the exercise-induced expression of Hsp70. METHODS: Twenty-one male Sprague-Dawley rats were randomly divided into three equal groups including an exercise group (EX), which ran on a treadmill at 30 m min(-1) for 60 min; a stimulation group (STIM), which was not allowed to run, but was stimulated with compressed air and mild electric shock concurrently with their exercising cohort; and a control group (CON), which was housed in the treadmill room during the exercise period. Animals were killed 24 h post-experiment and hearts (H), soleii (SOL) and white gastrocnemii (WG) were harvested and analysed for Hsp70 content (mean% +/- SEM of standard). RESULTS: Significant increases in Hsp70 (as a % of standard) were noted in H and WG (H = 77.4 +/- 8.5; WG = 93.9 +/- 18.4) of EX but not in STIM (H = 32.5 +/- 4.6; WG = 32.0 +/- 3.4) or CON (H = 20.5 +/- 3.7; WG = 32.4 +/- 7.4). In SOL, Hsp70 expression in EX (126.7 +/- 6.2) was different from STIM (98.3 +/- 10.9) only. This occurred, despite the fact that all groups were exposed to a stressful environment and exhibited elevated (P < 0.001) temperatures (EX -41.2 +/- 0.1 degrees C > STIM -40.5 +/- 0.2 degrees C > CON -39.0 +/- 0.1 degrees C) indicative of a general stress response. CONCLUSIONS: These data suggest that exercise per se, rather than environmental conditions or noxious stimuli, are responsible for the induction of Hsp70 in rat muscle during treadmill running.

Castration inhibits exercise-induced accumulation of Hsp70 in male rodent hearts.

Intense exercise leads to accumulation of the inducible member of the 70-kDa family of heat shock proteins, Hsp70, in male, but not female, hearts. Estrogen is at least partially responsible for this difference. Because androgen receptors are expressed in the heart and castration leads to decreases in calcium regulatory proteins and altered cardiac function, testosterone (T) or its metabolites could also be involved. We hypothesized that removal of endogenous T production through castration would reduce cardiac Hsp70 accumulation after an acute exercise bout, whereas castrated animals supplemented with 5alpha-dihydrotestosterone (DHT) would show the intact male response. Fifty-four 8-wk-old male Sprague-Dawley rats were divided into intact, castrated, or castrated + DHT groups (n = 18/group). At 11 wk of age, 12 animals in each group undertook a 60-min bout of treadmill running at 30 m/min (2% incline) while the remaining 6 in each group remained sedentary. At 30 min or 24 h after exercise (n = 6/time point), blood and hearts were harvested for analysis. Serum T was undetectable in castrated and DHT-treated castrated rats, whereas serum DHT was significantly reduced in castrated animals only (approximately 60% reduction) (P < 0.05). Although there were no differences in constitutive levels of Hsp70 protein, exercise significantly increased cardiac hsp70 mRNA and protein in intact and DHT-supplemented rats, but not in castrated animals (P < 0.05). To examine whether castration eliminated the ability to respond to stress, another six intact and six castrated animals were subjected to a 15-min period of hyperthermia (core temperature raised to 42 degrees C) and killed 24 h later. As opposed to exercise, castrated animals subjected to heat shock exhibited increases in Hsp70 above nonshocked (i.e., sedentary) animals, similarly to intact males (P < 0.05). These data suggest that androgens, in addition to estrogen, play a role in the sexual dimorphism observed in the stress response to exercise but not heat shock.

Stress proteins: the exercise response.

A class of proteins that undergoes preferential synthesis following a variety of stressors has been demonstrated to carry out important cellular functions under both stressed and nonstressed conditions. These so-called heat shock (HSP) or stress (SP) proteins have been termed "molecular chaperones" and play important roles in cellular transportation, assembly/degradation, and cell survival. This review provides a basic introduction to the function and regulation of these proteins. Emphasis is placed on members of the HSP 70 family of proteins (especially HSP 72) and their role in cellular protection, their pattern of distribution in skeletal muscle, and changes in their expression following exercise and exercise training.