Oxidation produces free radicals, which cause peroxidation, enzyme inhibition and genetic damage in muscle cells. Genetic damage to cells and tissues caused by free radicals facilitates aging. Therefore, the functional capacity of the antioxidant system against free radicals is important to protect cells and tissues. The health benefits of regular exercise are well documented in a large number of reports. Moderate exercise can result in greater health benefits than vigorous exercise, because intense activity may generate free radicals. This is evidenced by an increase in effects such as lipid peroxidation, glutathione oxidation, and oxidative protein damage. These are regarded as an indirect sign of muscle cell damage. During exercise, increased aerobic metabolism is a potential source of free radicals (oxidative stress) in mitochondria. In muscle cells, mitochondria are one important source of reactive intermediates that include superoxides, hydrogen peroxide, and possibly hydroxyl radicals. Unfortunately, because research focusing on oxidative stress and antioxidants following exercise has up to now been narrow in scope, the mechanism linking oxidative stress and antioxidants in muscle tissue during exercise, is not fully understood. Knowledge of the mechanism of free radical formation during exercise will be useful and may lead to the prevention of oxidative stress and damage associated with physical activity. Although the capability of an antioxidant system can be estimated by measuring the content or activity of cellular superoxide dismutase isozymes, catalase and glutathione peroxidase, scavenger capacity against free radicals in muscle cells has not been investigated. Recent progress in electronics has made it possible, using electron spin resonance and a spin-trapping technique, to determine and quantify the reactive oxygen species involved in chemical reactions. Biological applications of electron spin resonance include detecting the production of free radicals and radical scavenging activity in living specimens. This review paper provides a brief account of how exercise leads to oxidative stress and the link with antioxidants, and suggests future paths of research.

In skeletal muscle, carnitine is essential for the translocation of long-chain fatty-acids into the mitochondrial matrix for subsequent β-oxidation, and in the regulation of the mitochondrial acetyl coenzyme A/ free coenzyme A ratio by buffering excess acetyl groups. Based on the concept that increased carnitine availability is beneficial to skeletal muscle metabolic process, a large amount of research was directed towards investigating the effects of carnitine supplementation on exercise performance. However, it has been debated about contribution of carnitine for energy metabolism in skeletal muscle and whether carnitine supplementation can improve physical performance in healthy subjects. Recently, in order to resolve the issues, attention has been focused on the carnitine transport mechanism across the skeletal muscle plasma membrane. Due to lack of endogenous synthesis of carnitine in myocytes, skeletal muscles need to import this molecule from blood, suggesting that muscle carnitine uptake is most likely the limiting factor to muscle carnitine availability. It has been established that the specific carnitine transporter, OCTN2, is expressed in skeletal muscles and is assumed to transport carnitine into myocytes. Carnitine uptake capacity via the OCTN2, therefore, has been assumed to be one of the important factors to the skeletal muscle energy metabolism. The purpose of the review is to summarize the role of carnitine in skeletal muscle metabolism, and the current knowledge regarding the effect of carnitine supplementation of exercise performance. Furthermore, we summarize recent observations related to the carnitine transport mechanism in skeletal muscles including contribution of OCTN2 during muscle contraction.

A training experiment was carried out to investigate the difference in training effects between power-up type and bulk-up type strength training exercises from the aspects of muscle histochemical properties and capillary supply. The subjects were eleven healthy males. The power-up type group (five males) performed knee extension exercise for 5 sets at 90% of 1 RM (one repetition maximum) with a 3-min rest between sets (repetition method) . The bulk-up type group (six males) performed the same exercise for 9 sets at 80-40% of 1RM with a 30-s or 3-min rest between sets (interval method, multi-poundage system) . Both programs were carried out twice a week for 8 weeks.
The main results were as follows ;
1. Percentages of fiber types showed no recognizable changes in either group.
2. Fiber area was significantly increased for all fiber types (Type I, Type IIA, Type JIB) in both groups. However, the rate of increase was greatest for type IIA fiber, followed by type JIB fiber and then type I fiber. Moreover, the rate of increase for all fiber types in the bulk-up group was higher than that in the power-up group.
3. Percentage of fiber area showed no recognizable changes for any fiber types in the powerup group. However, the percentage area of type II fibers, especially type IIB fiber, was significantly decreased in the bulk-up group.
4. CC (Type I), CC (Type IIA) and CC (Type IIB) (number of capillaries in contact with each fiber type) were significantly increased in both groups. However, in comparison with CC (Type I), CC (Type IIA · Type IIB) showed a higher rate of increase in the power-up group. On the other hand, in comparison with CC (Type IIA · Type JIB), CC (Type I) showed a higher rate of increase in the bulk-up group. Also, compared with the power-up group, the bulk-up group showed a signifi-cantly higher rate of increase of CC (Type I) .
5. C/Fiber area (Type I), C/Fiber area (Type IIA) and C/Fiber area (Type IIB) (number of capillaries supplying each fiber area) were decreased in both groups.
The above results show that power-up type exercise leads mainly to hypertrophy of type I, type IIA and type IIB fibers without any change in percentage fiber type or percentage fiber area, whereas bulk-up type exercise leads mainly to hypertrophy of each fiber type with decreases in percentage area of type II fibers, especially type JIB fiber. Also, power-up type exercise leads mainly to an increase in the number of capillaries around type II fibers, whereas bulk-up type exercise leads mainly to an increase in the number of capillaries around type I fiber. However, capillary development around all fiber types did not necessary coincide with muscle hypertrophy in either exercise.
The authors reported previously that power-up type exercise is effective mainly for improving muscular strength and anaerobic power, whereas bulk-up type exercise is effective mainly for induc. ing hypertrophy and anaerobic endurance. The results of this study may help to clarify these effects from the viewpoint of the adaptations of muscle fibers and the capillary supply.

A study was conducted to clarify the effects of running intensity and duration of endurance training on myoglobin concentration ( [Mb] ) in rat skeletal muscles, and to clarify its temporal changes during the training. One hundred five male Wistar rats were divided into a training group and an untrained group. The training was carried out at 5 times a week for 12 weeks when the animals were 4 to 16 weeks of age. The training intensities were set at 20, 30 and 40 m/min with a duration of 60 min. The training duration was varied to 30, 60, 90 and 120 min when the rats were trained at 30 m/min. The temporal changes in the [Mb] were examined after the first, third and ninth week of training, during which the rats were trained at 40 m/min for 60 min per session. Three muscles (soleus: Sol, plantaris: P1, gastrocnemius-surface/deep: Gas-S, Gas-D) were analyzed for the [Mb] and citrate synthase activity (CS activity) . With regard to the intensity of training, the [Mb] increased with exercise intensity in Sol, Gas-D and P1, but not in Gas-S. P1 showed a greater increase of the [Mb] than Sol or Gas-D. On the other hand, CS activity in red muscle (Sol and Gas-D) increased even at low intensity, whereas white muscle (fast-twitch muscle: Pl and Gas-S) showed a significant increase in CS activity at an intensity of 40m/min. As to the duration of training, the [Mb] increased with the duration of running at 30 m/min of intensity, and showed the maximal adaptation with 90-min duration in all muscles except for Gas-S. Changes in CS activity according to the duration of running were similar to those for the [Mb] in all muscles. Finally, the [Mb] increased significantly with prolongation of the training period (after the 1 st, 3 rd and 9 th weeks training) in all muscles except Gas-S. However, the adaptive response of Mb tended to be delayed as compared with CS activity. These results suggest that 1) the response of Mb to training stimuli can depend on the muscle specificity (fiber type composition or the initial [Mb] ), and level of motor unit recruitment in usual, 2) Mb synthesis can be enhanced by an increase of training intensity, 3) a training duration of 90 min can bring out the Mb adaptation maximally and 4) the adaptive response of Mb would need more time as compared with CS activity.

The effects of low- and high-intensity endurance training on the capillary network of rat left ventricle were studied morphometrically. Eighteen male albino rats of Wistar strain (4-wk-old) were assigned at random to a sedentary control group (Cont, n=8) and two trained groups which were both subjected to exercise on a motor-driven treadmill for 60 min a day, 5 days/wk for 9 weeks from 7 wks to 16 wks of age with different running speed; the low-intensity trained group (T-20, n=5) ran at 20 m/min and the high-intensity trained group (T-40, n=5) at 40 m/min. All morphometric parameters for the capillary and muscle fiber were determined in perfusion-fixed hearts. After the training period, the average muscle fiber cross-sectional area in the T-20 and the T-40 was not significantly different from the Cont. There were no significant differences in the capillary density and the capillary-to-fiber ratio between any groups, suggesting no significant change in capillary number. On the other hand, the number of capillary with large luminal diameter (8-10 μm) in the T-40 but not the T-20 was significantly greater than the Cont. These results indicate that the high-intensity endurance training causes enlargement of the capillary luminal area, while neither the low-nor the high-intesnity endurance training stimulate the proliferation of capillaries in the left ventriclular myocardium. In conclusion, a structure of the capillary network of rat left ventricle responds to the high-intensity endurance training by enlarging capillary luminal area rather than by increasing capillary number.

The purpose of this study was to investigate the hypothesis that the reduction in walking ability is due to muscle atrophy in the lower limb muscles with aging using equational structure modeling as well as investigate the influence of muscle on walking ability. The subjects consisted of 127 persons (57 males and 70 females) aged 20-84 year, who were grouped into 6 age brackets of 20-39, 40-49, 50-59, 60-69, 70-74, and 75 or older. Using MRI, muscle cross-sectional area was measured on psoas major and thigh muscle (divided into extensor and flexor) . For walking patterns, each subject walked along a 7-m walking passage at normal speed for VTR-recording of the motion. The resulting pictures were used to analyze stride length, trunk inclination and walking speeds. Walking speeds showed a statistically significant decrease in value from the 50's age group in males and the 60's age group in females when compared with the 20-39 age bracket (p<0.05) . In males, a significant co-relationship was observed only between the muscle cross-sectional area of thigh extensor and walking speed (p<0.01) while in females, a significant co-relationship was found between the muscle cross-sectional area of psoas major (p<0.001) /thigh muscle extensor (p<0.01) and walking speed. These results indicate that the muscle atrophy with aging in psoas major and thigh muscle extensor is a factor responsible for the decrease in walking speed. Meanwhile, a difference in sex was observed between the muscle cross-sectional area of psoas major and walking speed. It was considered that the muscle atrophy rate of the female's psoas major being higher than the male's influenced this. Furthermore, it was suggested possibility that the decline of walking ability is due to decreased muscle mass of the lower limbs with aging.

The effect of daily physical activity on oxidative stress is still an unknown issue, especially in middle-aged and elderly individuals. In this study, we examined the relationships of oxidative stress and antioxidant capacity with daily physical activity, taking into consideration the dietary antioxidant vitamin intake (vitamin B₂, C and E) of middle-aged and elderly people (66.0±7.0 years, n= 21; 10 males and 11 females, including 5 male trained runners) . Daily physical activity was measured using both a calorie counter and a questionnaire over a period of two weeks. The plasma concentration of thiobarbituric acid reactive substance ( [TBARS] ) and both oxidized and reduced glutathione concentrations ( [GSSG] and [GSH] ) in whole blood were determined in blood samples obtained at rest and immediately after two periods of acute exercise: maximal cycle ergometric exercise and steady state cycle exercise at 80% of ventilatory threshold (VT) for 30 minutes. At a given statistically controlled dietary antioxidant vitamin intake level (vitamin B₂, C and E), the amount of daily physical activity was associated with neither [TBARS], [GSH] and the ratio of [GSSG] / [GSH] at rest, nor changes in levels of these substances after both exercise tests. These data suggest that the amount of daily physical activity may have little influence on oxidative stress or antioxidant capacity at rest and after acute cycle ergometric exercise. Further investigation would be necessary to clarify how much volume or intensity of physical activity induces increased oxidative stress, from the aspect of habitual physical training and nutrition.