Exercise-induced improvements in myocardial antioxidant capacity: the antioxidant players and cardioprotection.

Endurance exercise training is known to promote beneficial adaptations to numerous tissues including the heart. Indeed, endurance exercise training results in a cardioprotective phenotype that resists injury during an ischemia-reperfusion (IR) insult. Because IR-induced cardiac injury is due, in part, to increased production of radicals and other reactive oxygen species, many studies have explored the impact of exercise training on myocardial antioxidant capacity. Unfortunately, the literature describing the effects of exercise on the cardiac antioxidant capacity is widely inconsistent. Nonetheless, a growing body of evidence indicates that regular bouts of endurance exercise promote an increase in the expression of both superoxide dismutase 1 and 2 in cardiac mitochondria. Moreover, emerging evidence suggests that exercise also increases accessory antioxidant enzymes in the heart. Importantly, robust evidence indicates that as few as five consecutive days of endurance exercise training results in a cardiac phenotype that resists IR-induced arrhythmias, myocardial stunning, and infarction. Further, mechanistic studies indicate that exercise-induced increases in mitochondrial superoxide dismutase 2 play a key role in this adaptation. Future studies are required to provide a complete picture regarding the cellular adaptations that are responsible for exercise-induced cardioprotection.

Relation between foot arch index and ankle strength in elite gymnasts: a preliminary study.

BACKGROUND: Gymnasts usually start intensive training from early childhood. The impact of such strenuous training on the musculoskeletal system is not clear. OBJECTIVES: To evaluate the relation between muscle strength of the ankle joint and foot structure in gymnasts. METHODS: The study population comprised 20 high level male gymnasts and 17 non-athletic healthy male controls. Arch indices were measured using a podoscope. Ankle plantar/dorsiflexion and eversion/inversion strengths were measured using a Biodex 3 dynamometer within the protocol of concentric/concentric five repetitions at 30 degrees /s velocity. RESULTS: The mean arch index of the right and left foot of the gymnasts and the controls were respectively: 31.4 (29.1), 34.01 (34.65); 60.01 (30.3), 63.75 (32.27). Both the arch indices and the ankle dorsiflexion strengths were lower in the gymnasts. Although no correlation was found between strength and arch index in the control group, a significant correlation was observed between eversion strengths and arch indices of the gymnasts (r = 0.41, p = 0.02). CONCLUSIONS: Whether or not the findings indicate sport specific adaptation or less training of the ankle dorsiflexors, prospective data are required to elucidate the tendency for pes cavus in gymnasts, for whom stabilisation of the foot is a priority.

Multiple osteochondroses and avulsion fracture of anterior superior iliac spine in a soccer player.

Apophysitis describes a chronic traction injury at the insertion site of a tendon. There is a gradual onset of pain with no clear history of injury. Without adequate preventive methods, an avulsion fracture may result. The case is here reported of an apophyseal avulsion fracture of the anterior superior iliac spine in an adolescent caused by playing football before the end of treatment for apophysitis. An open reduction and internal fixation was performed followed by a rehabilitation programme. No complications occurred, and the patient had returned to his previous level of sporting activity after six weeks.

Differences in sole arch indices in various sports.

BACKGROUND: There are controversial data about the relation between foot morphology and athletic injuries of the lower extremity. Studies in soldiers have shown some relationship, whereas those involving athletes have not shown any significant relationship. The reason for these differences is not clear. OBJECTIVE: To determine the effect of various sports on sole arch indices (AIs). METHOD: A total of 116 elite male athletes (24 soccer players, 23 wrestlers, 19 weightlifters, 30 handball players, and 20 gymnasts) and 30 non-athletic men were included in this cross sectional study. Images of both soles were taken in a podoscope and transferred to a computer using a digital still camera. AIs were calculated from the stored images. RESULTS: The AI of the right sole of the gymnasts was significantly lower than that of the soccer players, wrestlers, and non-athletic controls (p<0.01). The AI of the right sole of the wrestlers was significantly higher than that of the soccer players, handball players, weightlifters, gymnasts, and non-athletic controls (p<0.03). The AI of the left sole of the gymnasts was significantly lower than that of the wrestlers and non-athletic controls (p<0.001). The AI of the left sole of the wrestlers was significantly higher than that of the soccer players, handball players, and gymnasts (p<0.007). The AI of both soles in handball players was significantly lower than those of the non-athletic subjects (p = 0.049). The correlation between the AI of the left and right foot was poor in the soccer players, handball players, and wrestlers (r = 0.31, 0.69, and 0.56 respectively), but was high in the gymnasts, weightlifters, and non-athletic controls (r = 0.96, 0.88, and 0.80 respectively). CONCLUSION: The AIs of the gymnasts and wrestlers were significantly different from those of other sportsmen studied, and those of the gymnasts and handball players were significantly different from those of non-athletic controls.

Short-term exercise improves myocardial tolerance to in vivo ischemia-reperfusion in the rat.

These experiments examined the independent effects of short-term exercise and heat stress on myocardial responses during in vivo ischemia-reperfusion (I/R). Female Sprague-Dawley rats (4 mo old) were randomly assigned to one of four experimental groups: 1) control, 2) 3 consecutive days of treadmill exercise [60 min/day at 60-70% maximal O2 uptake (VO2 max)], 3) 5 consecutive days of treadmill exercise (60 min/day at 60-70% VO2 max), and 4) whole body heat stress (15 min at 42 degrees C). Twenty-four hours after heat stress or exercise, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was maintained for 30-min followed by a 30-min period of reperfusion. Compared with control, both heat-stressed animals and exercised animals (3 and 5 days) maintained higher (P < 0.05) left ventricular developed pressure (LVDP), maximum rate of left ventricular pressure development (+dP/dt), and maximum rate of left ventricular pressure decline (-dP/dt) at all measurement periods during both ischemia and reperfusion. No differences existed between heat-stressed and exercise groups in LVDP, +dP/dt, and -dP/dt at any time during ischemia or reperfusion. Both heat stress and exercise resulted in an increase (P < 0.05) in the relative levels of left ventricular heat shock protein 72 (HSP72). Furthermore, exercise (3 and 5 days) increased (P < 0.05) myocardial glutathione levels and manganese superoxide dismutase activity. These data indicate that 3-5 consecutive days of exercise improves myocardial contractile performance during in vivo I/R and that this exercise-induced myocardial protection is associated with an increase in both myocardial HSP72 and cardiac antioxidant defenses.

Exercise training increases heat shock protein in skeletal muscles of old rats.

PURPOSE: The effects of chronic exercise training on the expression of heat shock protein (HSP) in skeletal muscle of senescent animals are unknown. Therefore, the purpose of this study was to investigate the effects of chronic exercise training on skeletal muscle HSP expression in both young and old rats. METHODS: Young adult (3 months) and old (23 months) female Fisher 344 rats were assigned to either a sedentary control or an endurance exercise trained group (N = 6 per group). Exercised animals ran (60 min.d-1, 5 d.wk-1) on a treadmill at approximately 77% VO2peak for 10 wk. After completion of the training program, the soleus (SOL), plantaris (PL), and the red (RG) and white portions (WG) of the gastrocnemius muscles were excised, and citrate synthase (CS) activity and the relative levels of HSP72 were determined. RESULTS: Training resulted in increases (P < 0.05) in VO2peak in both young (67.6 +/- 3.1 vs 86.9 +/- 1.6 mL.kg-1.min-1) and old animals (54.5 +/- 1.8 vs 68.2 +/- 2.2 mL.kg-1.min-1). Training increased CS activity and the relative levels of HSP72 (P < 0.05) in all four skeletal muscles in both young and old animals. Specifically, compared with age-matched sedentary controls, exercise training resulted in increased (P < 0.05) levels of HSP72 in skeletal muscles of both young (SOL + 22%, PL +94%, RG + 44%, WG + 243%) and old animals (SOL +15%, PL +73%, RG +38%, WG +150%). CONCLUSIONS: These findings reveal that the exercise-induced accumulation of HSP72 in skeletal muscle differs between fast and slow muscles. Further, these data indicate that the exercise-induced accumulation of HSP72 in highly oxidative skeletal muscles (SOL and RG) is similar between young and old animals. In contrast, aging is associated with a blunted expression of HSP72 in fast skeletal muscles (PL and WG) in response to chronic exercise.

Exercise, heat shock proteins, and myocardial protection from I-R injury.

Heat shock proteins (HSPs) play a critical role in maintaining cellular homeostasis and protecting cells during episodes of acute stress. Specifically, HSPs of the 70 kDa family (i.e., HSP72) are important in preventing ischemia-reperfusion induced apoptosis, necrosis, and oxidative injury in a variety of cell types including the cardiac myocyte. Evidence indicates that HSP72 may contribute to cellular protection against a variety of stresses by preventing protein aggregation, assisting in the refolding of damaged proteins, and chaperoning nascent polypeptides along ribosomes. Endurance exercise is a physiological stress that can be used to elevate myocardial levels of HSP72. It is now clear that endurance exercise training can elevate myocardial HSP72 by 400-500% in young adult animals. Importantly, an exercise-induced elevation in myocardial HSPs is associated with a reduction in ischemia-reperfusion (I-R) injury in the heart. Although it seems likely that exercise-induced elevations in myocardial levels of HSPs play an important role in this protection against an I-R insult, new evidence suggests that other factors may also be involved. This is an important area for future research.

Gene expression of catecholamine biosynthetic enzymes following exercise: modulation by age.

Both age and exercise training are associated with tissue specific alterations in the catecholaminergic system. We examined the effect of short-term exercise training on tyrosine hydroxylase and dopamine beta-hydroxylase gene expression in adrenals and specific brain regions with aging. In addition, we examined activator protein-1 and cyclic AMP response element transcription factor binding activity in the adrenal medulla. Male, six- and 24-month-old F-344 rats were exercised by treadmill running for five consecutive days. One group was killed immediately and a second group was killed 2h after the last training session. Exercise significantly elevated tyrosine hydroxylase messenger RNA equally in adrenals of both young and old rats. Training had no effect on dopamine beta-hydroxylase messenger RNA in adrenals of young, but levels were elevated in old rats. Binding activities of both activator protein-1 and cyclic AMP response element binding protein were diminished with age in the adrenal medulla. Exercise training had no significant effect on the binding activity of cyclic AMP response element binding protein in either young or old animals, whereas activator protein-1 binding activity increased equally in young and old animals. Exercise training revealed divergent changes in tyrosine hydroxylase messenger RNA in brain catecholaminergic neurons. In the locus coeruleus and the ventral tegmental areas, training elevated tyrosine hydroxylase messenger RNA levels only in young rats. In the substantia nigra, there was no change in young, but a 45% increase in tyrosine hydroxylase messenger RNA in old rats. In the ventral tegmental area, training increased tyrosine hydroxylase gene expression 80% in young but not in old rats. These results indicate that short-term exercise training increases tyrosine hydroxylase messenger RNA levels in young animals in the adrenals, the locus coeruleus and the ventral tegmental area. The responses for exercise training of aged animals differed from the young in brain noradrenergic and dopaminergic nuclei, especially in the substantia nigra, and to some extent in the locus coeruleus and the ventral tegmental area.

Improved cardiac performance after ischemia in aged rats supplemented with vitamin E and alpha-lipoic acid.

The purpose of these experiments was to examine the effects of dietary antioxidant supplementation with vitamin E (VE) and alpha-lipoic acid (alpha-LA) on biochemical and physiological responses to in vivo myocardial ischemia-reperfusion (I-R) in aged rats. Male Fischer-334 rats (18 mo old) were assigned to either 1) a control diet (CON) or 2) a VE and alpha-LA supplemented diet (ANTIOX). After a 14-wk feeding period, animals in each group underwent an in vivo I-R protocol (25 min of myocardial ischemia and 15 min of reperfusion). During reperfusion, peak arterial pressure was significantly higher (P < 0.05) in ANTIOX animals compared with CON diet animals. I-R resulted in a significant increase (P < 0.05) in myocardial lipid peroxidation in CON diet animals but not in ANTIOX animals. Compared with ANTIOX animals, heart homogenates from CON animals experienced significantly less (P < 0.05) oxidative damage when exposed to five different in vitro radical producing systems. These data indicate that dietary supplementation with VE and alpha-LA protects the aged rat heart from I-R-induced lipid peroxidation by scavenging numerous reactive oxygen species. Importantly, this protection is associated with improved cardiac performance during reperfusion.

Effect of combined supplementation with vitamin E and alpha-lipoic acid on myocardial performance during in vivo ischaemia-reperfusion.

Reactive oxygen species (ROS) contribute significantly to myocardial ischaemia-reperfusion (I-R) injury. Recently the combination of the antioxidants vitamin E (VE) and alpha-lipoic acid (alpha-LA) has been reported to improve cardiac performance and reduce myocardial lipid peroxidation during in vitro I-R. The purpose of these experiments was to investigate the effects of VE and alpha-LA supplementation on cardiac performance, incidence of dysrhythmias and biochemical alterations during an in vivo myocardial I-R insult. Female Sprague-Dawley rats (4-months old) were assigned to one of the two dietary treatments: (1) control diet (CON) or (2) VE and alpha-LA supplementation (ANTIOXID). The CON diet was prepared to meet AIN-93M standards, which contains 75 IU VE kg-1 diet. The ANTIOXID diet contained 10 000 IU VE kg(-1) diet and 1.65 g alpha-LA kg(-1) diet. After the 14-week feeding period, significant differences (P<0.05) existed in mean myocardial VE levels between dietary groups. Animals in each experimental group were subjected to an in vivo I-R protocol which included 25 min of left anterior coronary artery occlusion followed by 10 min of reperfusion. No group differences (P>0.05) existed in cardiac performance (e.g. peak arterial pressure or ventricular work) or the incidence of ventricular dysrhythmias during the I-R protocol. Following I-R, two markers of lipid peroxidation were lower (P<0.05) in the ANTIOXID animals compared with CON. These data indicate that dietary supplementation of the antioxidants, VE and alpha-LA do not influence cardiac performance or the incidence of dysrhythmias but do decrease lipid peroxidation during in vivo I-R in young adult rats.

Heat stress attenuates skeletal muscle atrophy in hindlimb-unweighted rats.

This study tested the hypothesis that elevation of heat stress proteins by whole body hyperthermia is associated with a decrease in skeletal muscle atrophy induced by reduced contractile activity (i.e. , hindlimb unweighting). Female adult rats (6 mo old) were assigned to one of four experimental groups (n = 10/group): 1) sedentary control (Con), 2) heat stress (Heat), 3) hindlimb unweighting (HLU), or 4) heat stress before hindlimb unweighting (Heat+HLU). Animals in the Heat and Heat+HLU groups were exposed to 60 min of hyperthermia (colonic temperature approximately 41.6 degrees C). Six hours after heat stress, both the HLU and Heat+HLU groups were subjected to hindlimb unweighting for 8 days. After hindlimb unweighting, the animals were anesthetized, and the soleus muscles were removed, weighed, and analyzed for protein content and the relative levels of heat shock protein 72 (HSP72). Compared with control and HLU animals, the relative content of HSP72 in the soleus muscle was significantly elevated (P < 0.05) in both the Heat and Heat+HLU animals. Although hindlimb unweighting resulted in muscle atrophy in both the HLU and Heat+HLU animals, the loss of muscle weight and protein content was significantly less (P < 0.05) in the Heat+HLU animals. These data demonstrate that heat stress before hindlimb unweighting can reduce the rate of disuse muscle atrophy. We postulate that HSP70 and/or other stress proteins play a role in the control of muscle atrophy induced by reduced contractile activity.

Vitamin E deficiency fails to affect myocardial performance during in vivo ischemia-reperfusion.

Vitamin E content of cardiac tissue has been proposed to play a major role in the damage caused by myocardial ischemia-reperfusion (I-R). Previous studies using in vitro models have examined vitamin E deficiency and I-R-induced myocardial damage with equivocal results. The purpose of this study was to use an in vivo model of myocardial I-R to determine the effects of vitamin E deficiency on myocardial I-R-induced damage. Female Sprague-Dawley rats (4-mo old) were assigned to either: 1) control diet (CON), or 2) vitamin E deficient diet (VE-DEF). The CON diet was prepared to meet AIN-93M standards, which contains 75 IU vitamin E/kg diet. The VE-DEF diet was the AIN-93M diet prepared with tocopherol stripped corn oil and no vitamin E. Following a 14-week feeding period, significant differences (p < 0.05) existed in mean myocardial VE levels between groups (mean values +/- SEM: CON = 48.2 +/- 3.5; VE-DEF = 12.4 +/- 1.4 micrograms VE/g wet weight). Animals from both experimental groups were subjected to an in vivo I-R protocol consisting of 25 minutes of left coronary artery occlusion followed by 10 minutes of reperfusion. No group differences (p > 0.05) existed in cardiac performance (peak arterial pressure or ventricular work) or the incidence of ventricular arrhythmias during the I-R protocol. VE-DEF animals had significantly higher (p < 0.05) levels of myocardial lipid peroxidation and lower (p < 0.05) protein thiols following I-R compared to the CON animals. These data suggest that although vitamin E deficiency increases oxidative damage resulting from myocardial I-R, it does not affect cardiac performance during the insult.

Short-term exercise training improves diaphragm antioxidant capacity and endurance.

These experiments tested the hypothesis that short-term endurance exercise training would rapidly improve (within 5 days) the diaphragm oxidative/antioxidant capacity and protect the diaphragm against contraction-induced oxidative stress. To test this postulate, male Sprague-Dawley rats (6 weeks old) ran on a motorized treadmill for 5 consecutive days (40-60 min x day(-1)) at approximately 65% maximal oxygen uptake. Costal diaphragm strips were excised from both sedentary control (CON, n=14) and trained (TR, n=13) animals 24 h after the last exercise session, for measurement of in vitro contraction properties and selected biochemical parameters of oxidative/antioxidant capacity. Training did not alter diaphragm force-frequency characteristics over a full range of submaximal and maximal stimulation frequencies (P > 0.05). In contrast, training improved diaphragm resistance to fatigue as contraction forces were better-maintained by the diaphragms of the TR animals during a submaximal 60-min fatigue protocol (P < 0.05). Following the fatigue protocol, diaphragm strips from the TR animals contained 30% lower concentrations of lipid hydroperoxides compared to CON (P < 0.05). Biochemical analysis revealed that exercise training increased diaphragm oxidative and antioxidant capacity (citrate synthase activity +18%, catalase activity +24%, total superoxide dismutase activity +20%, glutathione concentration +10%) (P < 0.05). These data indicate that short-term exercise training can rapidly elevate oxidative capacity as well as enzymatic and non-enzymatic antioxidant defenses in the diaphragm. Furthermore, this up-regulation in antioxidant defenses would be accompanied by a reduction in contraction-induced lipid peroxidation and an increased fatigue resistance.

The effects of exercise duration on adrenal HSP72/73 induction in rats.

This study investigated the effects of varying durations of exercise training on heat shock proteins 72 and 73 (HSP72/73) induction in the rat adrenal gland. Female Sprague-Dawley rats (120 days old) were assigned to either a sedentary control group (C) or one of the three endurance exercise training groups. Trained animals ran on a treadmill at approximately 75% VO2max for 10 weeks (4-5 days week-1) at one of the three different exercise durations (30 min day-1=T30, 60 min day-1=T60, or 90 min day-1=T90). All durations of exercise training resulted in an increase in the HSP72 levels (P < 0.0001). The magnitude of the training-induced elevation in the HSP72 levels in the adrenal gland increased as a function of the training duration ( approximately 60-fold increase in T90; approximately 40-fold increase in T60; and approximately 15-fold increase in T30). Longer exercise durations (>60 min day-1), also resulted in small but significant increase in HSP73 level ( approximately 1.2-fold increase in both T60 and T90; P < 0.05). These results demonstrate that the physiological stress created by chronic treadmill running can induce both HSP72 and HSP73 in rat adrenal gland. Increased levels of adrenal HSP72/73 expression during rigorous exercise, may be one of the adaptive mechanisms of the adrenals to cope with an increased dose of stress.

Exercise-induced alterations in skeletal muscle myosin heavy chain phenotype: dose-response relationship.

This study investigated the effects of exercise training duration on the myosin heavy chain (MHC) isoform distribution in rat locomotor muscles. Female Sprague-Dawley rats (120 days old) were assigned to either a sedentary control group or to one of three endurance exercise training groups. Trained animals ran on a treadmill at approximately 75% maximal O2 uptake for 10 wk (4-5 days/wk) at one of three different exercise durations (30, 60, or 90 min/day). Training resulted in increases (P < 0.05) in citrate synthase activity in the soleus and extensor digitorum longus in both the 60 and 90 min/day duration groups and in the plantaris (Pla) in all three exercise groups. All durations of training resulted in a reduction (P < 0.05) in the percentage of MHCIIb and an increase (P < 0.05) in the percentage of MHCIIa in the Pla. The magnitude of change in the percentage of MHCIIb in the Pla increased as a function of the training duration. In the extensor digitorum longus, 90 min of daily exercise promoted a decrease (P < 0.05) in percentage of MHCIIb and increases (P < 0.05) in the percentages of MHCI, MHCIIa, and MHCIId/x. Finally, training durations >/=60 min resulted in an increase (P < 0.05) in the percentage of MHCI and a concomitant decrease (P < 0.05) in the percentage of MHCIIa in the soleus. These results demonstrate that increasing the training duration elevates the magnitude of the fast-to-slow shift in MHC phenotype in rat hindlimb muscles.

Exercise training protects against contraction-induced lipid peroxidation in the diaphragm.

Endurance exercise training promotes a small but significant increase in antioxidant enzyme activity in the costal diaphragm (DIA) of rodents. It is unclear if these training-induced improvements in muscle antioxidant capacity are large enough to reduce oxidative stress during prolonged contractile activity. To test the hypothesis that training-related increases in DIA antioxidant capacity reduces contraction-induced lipid peroxidation, we exercise trained adult female Sprague-Dawley (n = 7) rats on a motor-driven treadmill for 12 weeks at approximately 75% maximal O2 consumption (90 min/day). Control animals (n = 8) remained sedentary during the same 12-week period. After training, DIA strips from animals in both experimental groups were excised and subjected to an in vitro fatigue contractile protocol in which the muscle was stimulated for 60 min at a frequency of 30 Hz, every 2 s, with a train duration of 330 m. Compared to the controls, endurance training resulted in an increase (P < 0.05) in diaphragmatic non-protein thiols and in the activity of the antioxidant enzyme superoxide dismutase. Following the contractile protocol, lipid peroxidation was significantly lower (P < 0.05) in the trained DIA compared to the controls. These data support the hypothesis that endurance exercise training-induced increases in DIA antioxidant capacity protect the muscle against contractile-related oxidative stress.

Exercise training improves myocardial tolerance to in vivo ischemia-reperfusion in the rat.

Experimental studies examining the effects of regular exercise on cardiac responses to ischemia and reperfusion (I/R) are limited. Therefore, these experiments examined the effects of endurance exercise training on myocardial biochemical and physiological responses during in vivo I/R. Female Sprague-Dawley rats (4 mo old) were randomly assigned to either a sedentary control group or to an exercise training group. After a 10-wk endurance exercise training program, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was achieved by a ligature around the left coronary artery; occlusion was maintained for 20 min, followed by a 10-min period of reperfusion. Compared with untrained, exercise-trained animals maintained higher (P < 0.05) peak systolic blood pressure throughout I/R. Training resulted in a significant (P < 0.05) increase in ventricular nonprotein thiols, heat shock protein (HSP) 72, and the activities of superoxide dismutase (SOD), phosphofructokinase (PFK), and lactate dehydrogenase. Furthermore, compared with untrained controls, left ventricles from trained animals exhibited lower levels (P < 0. 05) of lipid peroxidation after I/R. These data demonstrate that endurance exercise training improves myocardial contractile performance and reduces lipid peroxidation during I/R in the rat in vivo. It appears likely that the improvement in the myocardial responses to I/R was related to training-induced increases in nonprotein thiols, HSP72, and the activities of SOD and PFK in the myocardium.

Exercise training reduces myocardial lipid peroxidation following short-term ischemia-reperfusion.

PURPOSE: The purpose of these experiments was to test the hypothesis that endurance exercise training will reduce myocardial lipid peroxidation following short-term ischemia and reperfusion (I-R). METHODS: Female Sprague-Dawley rats (4 months old) were randomly assigned to either a sedentary control group (N = 13) or to an exercise training group (N = 13). The exercise trained animals ran 4 d.wk-1 (90 min.d-1) at approximately 75% V02max. Following a 10-wk training program, animals were anesthetized, mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was achieved by a ligature around the left coronary artery; occlusion was maintained for 5 min followed by a 10-min period of reperfusion. RESULTS: Although training did not alter (P > 0.05) myocardial activities of antioxidant enzymes (superoxide dismutase and glutathione peroxidase), training was associated with significant increase (P > 0.05) in heat shock protein (HSP72) in the left ventricle. Compared with controls, trained animals exhibited significantly lower levels (P < 0.05) of myocardial lipid peroxidation following I-R. CONCLUSION: These data support the hypothesis that exercise training provides protection against myocardial lipid peroxidation induced by short-term I-R in vivo.

Bioenergetic characteristics of the costal and crural diaphragm in mammals.

These experiments compared oxidative and glycolytic enzyme activity in the costal and crural diaphragm in seven adult mammals (mouse, rat, rabbit, ferret, sheep, pig, cow) ranging in body mass from approximately 0.03 to 422 kg. Segments of the costal and crural diaphragm from the aforementioned species were homogenized to determine the activities of the glycolytic enzyme, lactate dehydrogenase (LDH), and the Krebs cycle enzyme, citrate synthase (CS). The results indicated that metabolic differences between the costal and crural diaphragm do not exist in all mammalian species. Specifically, CS activity differed (P < 0.05) between the costal and crural diaphragm (costal approximately 36% greater than crural) in only two species (rat and rabbit). Further, the oxidative capacity of the costal and crural diaphragm was significantly correlated with both breathing frequency and resting metabolic rate (r = 0.92 - 0.57; P < 0.05) across the species investigated. In contrast, glycolytic capacity was not significantly correlated (P > 0.05) with either breathing frequency or resting metabolic rate.

Myosin phenotype and bioenergetic characteristics of rat respiratory muscles.

These experiments examined the myosin phenotype and bioenergetic enzyme activities in rat respiratory muscles. Muscle samples were removed from adult female Sprague-Dawley rats (N = 8) and analyzed to determine the myosin heavy chain (MHC) and light chain (MLC) isoform content as well as the activities of myofibrillar ATPase (mATPase), citrate synthase (CS; Krebs cycle enzyme), and lactate dehydrogenase (LDH; glycolytic enzyme). Analysis revealed that CS activity and the % type I MHC and %IId MHC isoforms were greater in the costal diaphragm (CO-D) compared with those in the crural diaphragm (CR-D). In contrast, the % type IIb MHC was higher in the CR-D compared with that in the CO-D. LDH and mATPase activity were lower in both the CO-D and CR-D compared with that in the parasternal intercostals (PI), external intercostals (EI), internal intercostals (II), rectus abdominis (RA), and sternomastoid (SM) muscles. CS activity, % type I MHC, %IIa MHC, and the ratio of slow to total alkali MLC (1s/1s + 1f + 3f) were greater in the CO-D and CR-D compared with those in all other respiratory muscles. The RA contained the highest (P < 0.05) % type IIb MHC and lowest CS activity compared with that in all other muscles. Finally, CS activity, mATPase activity, and MHC phenotype did not differ among the PI, EI, II, and SM muscles. These differences in biochemical properties provide the muscles of the respiratory pump with great versatility in functional properties.