Abstract: This study examined whether the exercise-increased extracellular heat shock protein 72 (eHsp72) levels in rats was associated with body temperature elevation during exercise. In all, 26 female Sprague-Dawley rats (3 mo old) were assigned randomly to control (CON; n = 8), exercise under warm temperature (WEx; n = 9), or exercise under cold temperature (CEx; n = 9). The WEx and CEx were trained at 25 degrees C or 4 degrees C, respectively, for nine days using a treadmill. Before and immediately after the final exercise bout, the colonic temperatures were measured as an index of body temperature. The animals were subsequently anesthetized, and blood samples were collected and centrifuged. Plasma samples were obtained to assess their eHsp72 levels. Only the colonic temperature in WEx was increased significantly (P < 0.05) by exercise. The eHsp72 level in WEx was significantly higher (P < 0.05) than that of either the CON or CEx. However, no significant difference was found between CON and CEx. Regression analyses revealed that the eHsp72 level increased as a function of the body temperature. In another experiment, the eHsp72 level of animals with body temperature that was passively elevated through similar kinetics to those of the exercise was studied. Results of this experiment showed that mere body temperature elevation was insufficient to induce eHsp72 responses. Collectively, our results suggest that body temperature elevation during exercise is important for induction of exercise-increased eHsp72. In addition, the possible role of body temperature elevation is displayed when the exercise stressor is combined with it.
Abstract: Alpha (alpha)-actinin-3 is located in the skeletal muscle Z-line and forms actin-actin crosslinks. An interesting property of alpha-actinin-3 is its expression pattern, which is restricted to fast type II skeletal muscle fibers. However, little is known about the response of alpha-actinin-3 levels to changes in skeletal muscle such as fiber type transformation. This study examined alpha-actinin-3 levels in the soleus muscles of rats subjected to hindlimb unloading, which causes a slow-to-fast fiber transformation in the soleus muscle. After unloading, type II myosin heavy chain (MyHC) and fast myosin levels increased significantly (P<0.0001 for type II MyHC, P<0.005 for fast myosin). Along with these increases in fast fibers, alpha-actinin-3 expression levels increased significantly (P<0.0007) and dramatically. These results indicate that alpha-actinin-3 levels increase concomitantly with increases in skeletal muscle fast fibers.
Abstract: OBJECTIVE: To test the hypothesis that microwave hyperthermia treatment (MHT) increases heat shock proteins (HSPs) in the human vastus lateralis muscle. METHODS: Four untrained healthy male volunteers participated in this study. The lateral side of the thigh of one leg (heated leg) was heated with a microwave generator (2.5 GHz, 150 W) for 20 min. At 1 day after the MHT, a muscle sample was taken from the heated leg. A control sample was taken from the unheated leg on another day of the MHT. For both legs, HSP90, HSP72 and HSP27 levels were compared. RESULTS: The HSP90, HSP72 and HSP27 levels in heated legs were significantly higher than those in control legs (p<0.05). CONCLUSIONS: Application of MHT can increase the levels of several HSPs in human skeletal muscle.
Abstract: OBJECTIVE: To investigate the changes in temperature of human muscle during microwave hyperthermia. METHODS: Skin surface and muscle temperatures were measured in 11 healthy adult men (mean (SD) age 24.3 (2.2) years; height 174.2 (6.1) cm; weight 70.0 (5.3) kg) during a 30 min exposure of the thigh to 434 MHz microwave hyperthermia. Skin temperature was maintained at the pilot temperature of 40 degrees C, and the temperature of the water in the bolus was 38 degrees C. The peak power output was set at 60 W and controlled automatically to maintain the pilot temperature. The temperature was measured in the vastus lateralis muscle at an average muscle depth of 2.0 (0.2) cm, using a 23 G Teflon-shielded thermocouple. Biopsy specimens were obtained for light microscopy from three subjects. A muscle-equivalent phantom was used to evaluate the vertical heating pattern. RESULTS: Both skin and muscle temperatures increased from baseline, and muscle temperature was higher than skin temperature (skin temperature 39.2 (0.5) degrees C, temperature rise 5.0 (1.5) degrees C; muscle temperature 43.7 (0.8) degrees C, temperature rise 8.9 (1.4) degrees C). At the end of the hyperthermia treatment, muscle temperature decreased to 39.8 (0.9) degrees C, but was still 4.8 (1.5) degrees C higher than the baseline. No signs of muscle damage were observed on the basis of the blood creatine kinase activity and histological sections. CONCLUSIONS: The results show that the 434 MHz microwave hyperthermia treatment increased and maintained muscle temperature locally by 6.3-11.4 degrees C without muscle damage. These findings suggest that the microwave hyperthermia system provides effective and safe treatment.
Abstract: The purpose of the present study was to investigate whether duration of static stretching could affect the maximal voluntary contraction (MVC).Volunteer male subjects (n = 10) underwent 2 different durations of static stretching of their hamstring muscles in the dominant leg: 30 and 60 seconds. No static stretching condition was used as a control condition. Before and after each stretching trial, hamstring flexibility was measured by a sit and reach test. MVC was then measured using the maximal effort of knee flexion. The hamstring flexibility was significantly increased by 30 and 60 seconds of static stretching (control: 0.5 +/- 1.1 cm; 30 seconds: 2.1 +/- 1.8 cm; 60 seconds: 3.0 +/- 1.6 cm); however, there was no significant difference between 30 and 60 seconds of static stretching conditions. The MVC was significantly lowered with 60 seconds of static stretching compared to the control and 30 seconds of the stretching conditions (control: 287.6 +/- 24.0 N; 30 seconds: 281.8 +/- 24.2 N; 60 seconds: 262.4 +/- 36.2 N). However, there was no significant difference between control and 30 seconds of static stretching conditions. Therefore, it was concluded that the short duration (30 seconds) of static stretching did not have a negative effect on the muscle force production.
Abstract: The purpose of this study was to investigate whether hypoxia can alter anaerobic energy release during supramaximal exercise. Seven male subjects performed 12 submaximal cycling tests to establish the relationship between workload and O2 demand. The subjects also performed 40 s Wingate tests (WT) under normoxia (room air), two levels of moderate hypoxia of 16.4% O2 and 12.7% O2. We measured the power output and oxygen uptake (VO2) during each test and estimated the O2 demand, O2 deficit and percentage of anaerobic energy release (%AnAER). These data were analyzed for each 20 s interval. At all intervals, there were no differences in Pmean per body mass (BM)(-1), O2 demand per BM(-1) or O2 deficit per BM(-1) among the three O2 conditions. However, under hypoxia of 12.7%, VO2 per BM(-1) was significantly decreased and %AnAER was significantly increased in the late phase (20-40 s) of the WT, compared to normoxia (P<0.05). There were no such significant differences between normoxia and hypoxia of 16.4%. Thus, the present results show that the degree of hypoxia affects the magnitude of the hypoxia-induced increase in anaerobic energy release in the late phase of the WT and suggest that certain degrees of hypoxia induce significant increases in the amount of anaerobic energy released, compared to normoxia.
Abstract: The purpose of this study was twofold: (i) to investigate if sprint-interval training (SIT) alters myosin heavy chain (MyHC) isoform composition and bioenergetic properties within the rat diaphragm, and (ii) to determine if mild normobaric hypoxia would enhance the effects of SIT-induced diaphragmatic adaptation. Male Wistar rats (8 weeks old) were randomly assigned to one of four groups (n = 7/group): (i) normoxic control (NC); (ii) normoxic training (NT); (iii) hypoxic control (HC); or (iv) hypoxic training (HT). The NT and HT groups were engaged in SIT (1 min sprint and 2-5 min rest, 6-10 sets/day, 5-6 days/week) on a treadmill for 9 weeks. Animals in the HC and HT groups were exposed to normobaric hypoxia (14.5% O(2)) during an SIT program from the 4th week of the training period. After completion of the training program, MyHC composition, citrate synthase (CS) activity, and lactate dehydrogenase (LDH) activity in the diaphragm and plantaris muscle were analyzed. An analysis of diaphragmatic MyHC composition demonstrated increased type IIa and decreased type IId/x for both training groups (P < 0.05), with the HT group producing greater changes than the NT group (P < 0.05). The plantaris muscle, however, showed increased Type IIa and IId/x and decreased Type IIb for both the NT and HT groups (P < 0.05). CS activity increased only for the training groups (P < 0.05), and this change was greater for the HT group in the diaphragm and for the NT group in the plantaris muscle (P < 0.05). Further, diaphragmatic LDH activity in HT was significantly lower (P < 0.05) than in HC and NT. These findings demonstrated that SIT could induce alterations in MyHC composition from fast to slow within type II isoforms and also improve the oxidative capacity in the diaphragm and plantaris muscles. It is of importance that our data revealed that SIT-induced diaphragmatic adaptations were enhanced when SIT was performed in normobaric hypoxia.
