Studies using histological and ultrastructural techniques have documented damage to muscles that performed unaccustomed eccentric exercise(9,11,17,32). If tissue damage occurs, a series of acute inflammatory responses to heal the tissue should follow(2). In a review paper, Smith (36) addressed the question of whether acute inflammation was the underlying mechanism in delayed-onset muscle soreness. Several studies have contributed data supporting an inflammatory response after damage-inducing exercise(3,8,18), although results have been equivocal(25,30,36,43).
Pain, swelling, and the loss of muscle function that accompany muscle soreness are classic signs of inflammation (25,36). After eccentric exercise, enlargement of the muscle has been documented by an increase in circumference (4,14). Recent studies examined muscles after eccentric exercise using magnetic resonance imaging(MRI) (10,22,28,31,34). For example, Shellock et al. (34) evaluated elbow flexors that performed exhaustive eccentric exercise by means of MR T2-weighted images, and found increases in T2 relaxation times; these changes lasted as long as 75 d after exercise. An increase in the T2 relaxation time is considered indicative of edema (31,34,42). Ultrasonography shows that edema of muscle due to trauma, ischemia, infarction, or infection markedly increase echointensity of muscle bundles(21,41). Therefore, muscle damage after eccentric exercise would be also visualized by ultrasonography.
Part of the inflammatory reaction to muscle injury includes a systemic response in addition to the changes observed locally at the muscle. This response, known as the acute-phase reaction, is initiated by substances produced by several cell types, including monocytes or macrophage action at the site of injury (2,19,25,30). These substances are called cytokines, and they play central roles in control of immune response, acute-phase response, inflammatory reactions, and tissue repair process (30). In at least 60 designated cytokines(30), studies examining exercise have focused on changes in interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α)(3,6,8,18,37,38). Changes in interleukin-2 (IL-2) were also reported following exercise(7). IL-1, IL-6, and TNF-α have numerous local and systemic effect, and this is followed by increase in plasma concentrations of acute-phase proteins, such as hepatic-derived C-reactive protein (CRP)(2,25,39). Inflammation also causes a redistribution of trace minerals in the body, and a marked reduction in serum levels of zinc and iron is a hallmark of the acute-phase response(24,25,35). It is also known that inflammation is associated with an increase in cortisol(2,43).
Although several studies have examined the acute-phase reaction after strenuous endurance-type exercises, few studies have reported changes in cytokines and other inflammatory markers in the blood after a local eccentric exercise. Only Miles et al. (23) reported perturbations in circulating cortisol and IL-1 levels after an eccentric arm and leg exercise. Although there is evidence pointing to an inflammatory reaction with exercise-induced muscle damage, this evidence comes from an assortment of studies using different exercise regimens causing various degrees of muscle damage and evaluating only one or two aspects of inflammation(36). No study has attempted to comprehensively evaluate the inflammatory response using several markers of inflammation so that a time course can be assessed for the various markers.
Therefore, it was the purpose of this study to investigate muscle swelling with circumference measures, MRI, ultrasonography, changes in several inflammatory markers in the blood, and muscle function testing following a high-force eccentric exercise of the elbow flexors.
METHODS
Subjects
Male students (N = 14), who had not been involved in any resistance training program, participated as subjects. Medical checks confirmed that all subjects were free of musculoskeletal disorders and in good health. The risks and benefits of the study were explained in an informed-consent document. A written consent was obtained from the subjects in accordance with the “Policy statement regarding the use of human subjects and informed consent” of the Medicine and Science in Sports and Exercise. The experiment was reviewed and approved by the ethical committee of Yokohama City University. The mean (SD) age, height, and weight, were 21.9 ± 1.9 yr, 171.6 ± 3.1 cm, and 60.9 ± 7.5 kg, respectively. All of the subjects (N = 14) received all measurements except MRI. Six of 14 subjects were randomly chosen for MRI. The physical characteristics of this subsample were not significantly different from those of the 14 subjects.
Exercise
The subjects performed a bout of exercise with the elbow flexors of the nondominant arm. The exercise consisted of 24 maximal eccentric actions on a modified arm curl machine (4,27). Subjects were requested to maximally resist the actions in which the subject's arm was forcibly extended from an elbow flexed (the elbow joint angle was approximately 50°) to an elbow extended position (the elbow joint angle was approximately 170°). Each action lasted 3 s and was repeated every 15 s (27).
Measurements
The following indicators were used to evaluate the degree of muscle damage and inflammatory responses: maximal isometric force, range of motion, circumference, soreness, ultrasound images, MRI, and plasma levels of creatine kinase (CK), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), tumor necrosis factor-α(TNF-α), C-reactive protein (CRP), cortisol, and zinc. All of the measurements, except MRI, were taken immediately before and after the exercise as well as for 5 d post-exercise. These measurements were taken at the same time of the day (1 h) for each subject, but the measurement time varied among the subjects (9:00-14:00). MRI were taken at pre- and 1, 3, 6, and 10 d post-exercise; as well as 23, 31, and 58 d post-exercise.
Muscle Function Tests
Maximal isometric force of the elbow flexors (MIF) was measured with the elbow joint angle at 90° on an arm curl machine (27) by means of a transducer (9E01-L33, NEC San-Ei Co. Ltd., Japan) connected to a digital indicator (9E54-7D, NEC-San-Ei Co. Ltd., Japan). Range of motion (ROM) of the elbow joint angle was evaluated by measuring the flexed (FANG) and relaxed (RANG) elbow joint angle using a goniometer(4,27). FANG was measured when the subject tried to fully flex the elbow to touch the shoulder by the palm, keeping the elbow at the side. RANG was measured when the subject relaxed the arm, allowing it to hang down by the side. ROM was calculated by subtracting FANG from RANG. A semipermanent marker was used to identify the landmarks for the goniometer measure placement.
Muscle Soreness
Perception of muscle soreness (SOR) was assessed using an analog scale of a 50-mm continuous line that represents “no pain” at one side (0 mm) and “very painful” at the other side (50 mm). Subjects were asked to indicate the soreness level on the line when an investigator palpated over the biceps brachii and extended the elbow (27).
Circumference
Circumference was assessed by a tape measure at four sites (4, 6, 8, and 10 cm above the elbow joint) on the upper arm when the subject let the arm hang down by the side. All measurement sites were identified with a semi-permanent marker, and the same investigator took the measurements. The accuracy of this measurement was shown to be within 2 mm (27).
Ultrasonography
Ultrasonography (USG) was assessed for all subjects using SSD-120 (Aloka Co. Ltd., Japan). The subjects placed their arm relaxed in a palm-up position on a table (the elbow joint angle was consistent throughout the measurements) and a 7.5 MHz linear probe was placed on the same four sites as the CIR measurements for the transverse scans of the biceps brachii and brachialis.
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) was performed with a 0.5-T 21.3 MHz superconducting magnet with a transmit body coil and a receive knee coil(SMT-50X, Shimadzu Co. Ltd., Japan). For the assessment, subjects lay in a supine position with their arm placed over their head. T1-weighted (T1), T2-weighted (T2), and proton density (Proton) spin echo images were obtained with the following parameters: axial imaging plane: 500/26 (TR/TE) for T1; 2000/90 for T2; and 2,000/20 for Proton; 256 × 256 matrix, two excitations, 20-cm field of view, 10-mm (T1) or 8-mm (T2 and Proton) slice thickness, with a 2-mm intersection gap. Ten (T1) or 12 (T2 and Proton) slice images were taken from the upper arm, and the elbow joint was used as a landmark for a consistent scanning over days. T2 relaxation times of a region of interest (ROI) were determined with the software provided by the manufacture of the MR unit (27). Three circular ROI (each area = 200 mm2) were set in the transverse section of the brachialis or biceps brachii, which indicated an increase in signal intensity; care was taken not to include an area other than muscle, such as artery and fat. The mean value of the T2 relaxation times from three ROI was used as the value. A ROI was set at the center of the triceps brachii, and used as a reference.
Biochemical Markers
Approximately 5 ml of blood were collected from the antecubital fossa of the nonexercised arm in lithium heparin-coated tubes (Terumo Co. Ltd., Japan) and immediately centrifuged for 10 min to obtain plasma. Plasma samples were frozen and stored at -20° until analysis. CK, AST, and LDH activities were measured spectrophotometrically by means of ultraviolet test kits (Dinabot Co. Ltd., Japan). Since a previous study (27) showed that AST and LDH also increased significantly when muscle damage was severe, the present study measured AST and LDH to ascertain the degree of muscle damage predicted by CK activity. The upper limits of the reference range for CK, AST, and LDH were 200 IU·l-1, 50 IU·l-1, and 150 IU·l-1, respectively.
Plasma concentration of IL-1α, IL-1β, and TNF-α were determined by enzyme-linked immunosorbent assay (ELISA) using test kits(Ootsuka Pharmaceutical Co. Ltd., Japan). Plasma concentration of IL-2 and IL-6 were also analyzed by ELISA method using test kits (Genzyme Corporation, U.S.A.). The detection limits of the assays were IL-1α (0.5 pg·ml-1), IL-1β (2 pg·ml-1), TNF-α (1 pg·ml-1), IL-2 (100 pg·ml-1), and IL-6 (18 pg·ml-1). Reproducibility determined by coefficient of variation(CV) of the intra and interassays were less than 7.7% (IL-1α), 9.8%(IL-1β), 5.0% (TNF-α), 10% (IL-2), and 9.5% (IL-6). In each assay, standard samples were used to draw a standard curve, and control samples were run to ensure that kit reagents were functioning.
C-reactive protein (CRP) and cortisol were measured by fluorescence polarization immunoassay (FPIA) using TDX CRP and TDX cortisol kits, respectively (Dinabot Co. Ltd., Japan). The detection limit of the assay for CRP was 0.3 mg·100 ml-1, and for cortisol was 0.45-60 g·100 ml-1. Control samples were run to ensure the validity of the assays. Serum concentration of zinc was determined by an atomic absorption method (26).
Statistics
Means and standard errors were computed for all data. The data were analyzed with a repeated measures analysis of variance (ANOVA). If the ANOVA detected significance, Tukey's post-hoc test was performed. Statistical significance was set at P < 0.05.
RESULTS
Muscle Function
MIF dropped significantly, to approximately 55% of the pre-exercise level immediately after exercise. The force was still below 70% of the pre-exercise level at 5 d after exercise. ROM also decreased significantly immediately after exercise to about 30°, and did not show evidence of recovery for the next 3 d, then gradually recovered.
Muscle Soreness
SOR developed 1 d after exercise and was sustained until 3 d after exercise. SOR during palpation and extending the elbow joint increased significantly, and there was no significant difference between the two soreness measures. Peak soreness values for palpation and extension were 37.5± 3.3 mm and 37.0 ± 4.5 mm, respectively.
Circumference
The time course of the changes in upper arm circumference at all four portions were not significantly different. As shown in Figure 1, circumferences at the middle (8 cm above the elbow joint) and distal (4 cm above the elbow joint) portions increased significantly over the 5 d after exercise. One of the subjects showed a 4.3 cm increase (the largest increase among subjects) in the distal part of the upper arm circumference at 4 d after exercise. Swelling was conspicuous on the upper arm of all subjects at 3 d after exercise, and the swelling gradually moved down from the middle to the distal part at 4-5 d post-exercise, then to the forearm after that. The larger increase in the circumference at the distal portion seen after 3 d post-exercise seemed to indicate the shift of the swelling portion. When palpating the upper arm, “pitting” edema (when the skin is pressed firmly with the finger, the skin will maintain the depression produced by the finger) was not obvious for 5 d after exercise. Obvious pitting edema started to be observed in the forearm at 4-5 d after exercise. The pitting edema in the forearm became more conspicuous 6-10 d after exercise. Since the skin over the upper arm was stretched and stiff because of swelling, a “pit” was not maintained in the upper arm 6-10 d after exercise.
Ultrasonography
Figures 2 and 3 demonstrate transverse scans of the biceps brachii and brachialis pre- and post-exercise. Eight of 14 subjects showed an increase in echointensity predominantly in the brachialis 3-5 d after exercise (Fig. 2). Increased echointensity in both the brachialis and biceps brachii was revealed by six subjects(Fig. 3). Ultrasonography also showed an increase in muscle thickness detected by measuring the distance between the skin and the edge of the humerus. Maximal increase in the muscle thickness was observed 3-4 d after exercise, and the amount of increase ranged from 0.6 cm to 2.2 cm. The subcutaneous thickness of the upper arm remained unchanged for 5 d after exercise (Figs. 2 and 3). The larger and more conspicuous was the area of high echointensity, the larger was the increase in muscle thickness. In Figure 3, the subject who showed a profound increase in echointensity showed higher CK activity (17,552 IU·l-1) compared with the subject presented inFigure 2, who showed fewer changes in the echointensity and CK increase (4184 IU·l-1).
Magnetic Resonance Imaging
Enlargement of the cross-sectional area of the elbow flexor muscles was clearly observed by T1; and T2 images showed not only the enlargement, but also profound increases in signal intensity. Twelve serial sections of the upper arm at 3 d post-exercise by T2 images are shown inFigure 4. Increased signal intensity occurred predominantly in the brachialis (Fig. 4) for all subjects(N = 6); however, three subjects had increased signal intensity in the biceps brachii as well Fig. 5). Interestingly, the subjects whose biceps brachii also showed an increase in echointensity belonged to the subject group that demonstrated an increase in echointensity of the ultrasonography, both in the brachialis and biceps brachii(Fig. 3).
Figure 5 presents changes in T2 images taken at approximately 5 cm above the elbow joint for a subject where increased signal intensity developed in both the biceps brachii and brachialis. Most profound increased signal intensity was seen at 3 or 6 d after exercise, and it was still obvious 23 d post-exercise. Increases in the subcutaneous area over the biceps brachii were not observed for 3 d after exercise, then the thickness of the subcutaneous layer increased significantly 6 and 10 d after exercise.
Changes in T2 relaxation time of six subjects are shown inFigure 6. The changes vary among the subjects, but all subjects showed maximal increases in T2 relaxation time 3 or 6 d after exercise. T2 relaxation time did not return to the baseline at 10 d after exercise, but it returned to the baseline by 23 d after exercise except for one subject (shown in Fig. 5). The T2 relaxation time of this subject returned to the baseline at 31 d after exercise.
Biochemical Markers
There was a large intersubject variability in the enzyme responses among the subjects. CK, AST, and LDH showed significant increases following exercise, and the time course of changes in the enzymes was similar. The enzyme activities reached the peak at 4 d after exercise, and were still elevated at 5 d post-exercise (Table 1).
In the assays for the cytokines, the control samples were in expected ranges. IL-1α, IL-1β, IL-2, IL-6, and TNF-α were not detected immediately before and after exercise, nor any time after exercise. The subjects whose CK level was more than 20,000 IU l·-1 also did not show detectable concentrations of any cytokines. These cytokines are usually not detected in plasma of healthy, rested subjects in the methods of this study.
The baseline values for CRP and cortisol were 0.26 ± 0.09 mg·100 ml-1 and 9.7 ± 1.1 μg·100 ml-1, respectively. They did not show significant changes following exercise(Table 1). Zinc also did not change significantly after exercise (Table 1).
DISCUSSION
The eccentric exercise in this study produced prolonged loss in muscle function, severe muscle soreness, and large increases in plasma CK, AST, and LDH activities. These changes were similar to those reported in previous studies (4,26,27). This suggested that severe damage was produced in the exercised muscle. Following damage, a series of acute inflammatory responses should occur to heal the damaged tissue(2,19,36). Soreness and swelling, classic signs of acute inflammation (36), developed in the exercised muscle. Muscle soreness developed 1-3 d after exercise, and the largest increase in circumference was observed 4-5 d after exercise(Fig. 1). It should be noted that swelling continued to develop after the soreness level significantly reduced. One of the physical stimuli for the sensation of muscle soreness may be the pressure within the muscle compartment (5), but swelling itself does not necessarily cause soreness (14).
The increases in circumference (Fig. 1), muscle thickness (Figs. 2 and 3), and muscle area(Fig. 5), appear to be related to inflammatory swelling. Swelling is due to accumulation of fluid in the area, and when fluid accumulation exceeds capability of lymphatic drainage, edema is produced(12). Pitting edema indicates swelling in the subcutaneous area (12). The present study found that the swelling observed in the upper arm after exercise was not pitting edema, and a significant increase in subcutaneous thickness was not seen in the ultrasonography (Figs. 2 and 3). Using a similar exercise model, Howell et al. (15) estimated that about 65% of the swelling in the middle region of the elbow flexor muscles was in the muscle compartment, and the rest was in the subcutaneous compartment at 1-10 d after exercise. In the present study, the swelling in the subcutaneous area of the upper arm seemed to be less compared with the estimation by Howell et al. (15). The MR pictures of D6 and D10(Fig. 5) showed an increase in the subcutaneous thickness over the biceps brachii; however, pitting edema in the upper arm was not obvious at this time. This was considered to be due to pressure from the muscles, because the biceps brachii and brachialis were swelling and stiff, and the skin over the muscles was stretched. When pressing the skin to make pit, movement of fluid in the subcutaneous area did not appear to be induced. However, pitting edema was seen in the forearm at this time, because there was no pressure from the muscles in the forearm. This would suggest that most of the fluid accumulation in the upper arm took place in the endomysium of muscle fibers or in the intracellular space of the fibers, and stayed there at least 5 d after exercise. It is assumed that the accumulated fluid moved toward the outside of the perimysium gradually over the 10 d. The obvious pitting edema in the forearm may be caused by movement of the fluid from the damaged area by means of gravity.
In ultrasonography, the muscle bundles are depicted hypoechoically(41). Studies have suggested that ultrasonography might be useful for screening muscle diseases (20,29) and soft tissue injury (1), and increased echointensity is a common feature of degenerative muscle (29). Edema of muscle due to trauma, ischemia, infarction, or infection will markedly increase echointensity of muscle bundles (41). The increased echointensity (Figs. 2 and 3) seemed to reflect muscle damage and/or an inflammatory response, because the increase in echointensity appeared to be related to plasma enzyme levels after exercise. Increase in circumference or muscle thickness might be due to two different phenomena: inflammatory swelling and protein synthesis(36). The accumulation of fluid in the tissues is the main cause of swelling up to 2 d at most, and this may be followed by the production of connective tissue (33). Increased echointensity in the ultrasonography that became prominent 3 d post-exercise might be associated with the production of new connective tissue. It is possible to assume that the delayed large increase in muscle thickness and circumference is associated with connective tissue proliferation to some degree.
Swelling of the biceps brachii and brachialis was also evident in the MRI(Figs. 4 and 5). Changes in MR pictures in this study were similar to those shown by Shellock et al. (34) and Rodenberg et al. (31) that used a similar exercise protocol to the present study. As shown by Shellock et al.(34), subclinical abnormalities in MRI last for a long time after exercise (Fig. 5). An increase in signal intensity of MRI (T2 relaxation time) is considered to be due to edema(22,34,42). T2 relaxation time peaked 3 or 6 d after exercise and still elevated 10 d after exercise (Fig. 6). Although the MRI and ultrasonography were not performed at the same time, both techniques may have revealed the same phenomena. When the brachialis and biceps brachii showed high signal intensity in MR pictures(Fig. 5), increased echointensity was seen in both muscles in the ultrasonography (Fig. 3). When only the brachialis showed high signal intensity in MR pictures (Fig. 4), increased echointensity was found in only the brachialis(Fig. 2). Moreover, when comparing the responses among subjects, the larger the increase in T2 relaxation time, the more profound increase in echo of the ultrasonography. It seems likely that changes in the echointensity and T2 signal were caused by the same factors. Morphological studies using human subjects have shown that greater numbers of infiltrating cells were seen in the muscle 9-20 d after eccentric exercise of the elbow flexors (17,32). Therefore, infiltrating cells do not seem to be a factor. The amount and distribution of free water or interstitial edema from extracellular matrix disruption may contribute to the increased signal intensity (31).
The exercise in the present study produced some indications of inflammatory response, such as swelling and soreness, and large increases in plasma enzyme activities (Table 1). Since inflammatory reactions and tissue repair processes are regulated by cytokines(25,30), significant changes in cytokines and other inflammatory markers were expected. However, mediators of acute-phase response in the blood did not change significantly after exercise. Although increases in plasma levels of cytokines have been shown in previous studies(3,6-8,37,38,40), most of the studies used strenuous endurance exercise, and the significant increase was observed by 24 h after the exercise. Only two studies used eccentric exercise, but these also had an endurance component. Increases in plasma IL-1β and TNF-α were found 6 h after 45-min downhill running(3), and increases in IL-1 were found after 45-min eccentric cycle exercise (8). However, the local muscular eccentric exercise in the present study did not increase IL-1α, IL-1β, IL-2, IL-6, and TNF-α. These cytokines were not detectable, either before or after the exercise in this study.
One of the reasons for the different results between the present study and previous ones (3,8) might be the difference in assays. Evans et al. (8) measured plasma IL-1 activity by means of thymocyte proliferation (bioassay), which is very sensitive. Cannon et al. (3) used a radio-immunoassay that is considered to be a more direct method to detect IL-1β and TNF-α. They reported that IL-1β and TNF-α were distributed near the detection limits of the assays, although some subjects showed increased levels of IL-1β and TNF-α 6 h after exercise. The present study used ELISA to determine plasma concentration of cytokines. These immunoassays are reliable and highly specific, but cannot distinguish biologically active molecules from inactive molecules (30). The assays used in the present study would have been sensitive enough to detect the cytokine levels that had been found in previous studies, if the cytokines had increased significantly.
If the increase in cytokines is related to muscle damage, one might expect a large increase in plasma concentration of cytokines when CK levels are very high (3-5 d after exercise). However, no increase in cytokines was found at any time after exercise. It appears that cytokine levels do not correlate with parameters of muscle damage, such as release of CK (15). Miles et al. (23) reported that large fluctuations in IL-1 began at 18 h, with an upward trend peaking at 96 h, after eccentric exercise that used larger amounts of muscle, such as the elbow flexors and quadriceps, as well as hamstrings. The amount of muscle mass involved in exercise might be a factor. Previous studies found increases in plasma IL-1(8) or IL-1β and TNF-α (3) at 3 or 6 h after exercise. Therefore, the present study might have missed the increase, because blood samples were not taken between immediately post-exercise and 24 h after exercise. Espersen et al. (7) found a significant increase in IL-2 at 24 h after 5-km competition running. In acute myocardial infarction, IL-6 began to rise at 9 h, peaked at 28 h, and remained elevated 2 d after symptom recognition (16). Considering that the muscle damage and repair process seemed to last a long period of time after the exercise in the present study, it is reasonable to assume that some cytokines remain elevated for 24 h, or longer, after exercise. However, this was not the case. Therefore, it seems unlikely that cytokines changed significantly within 2-24 h after eccentric exercise in the present study. Sprenger et al. (38) suggested that muscle damage is not the underlying mechanism of exercise-induced cytokine increase.
Two previous studies (39,43) showed a increase in CRP 24-48 h following long-distance running, but no study has examined changes in CRP after a resistance exercise. Compared with the previous studies(39,43), CK levels after exercise were much higher in the present study. Since levels 100-fold or more above normal concentrations may be attained with severe tissue injury(19), a significant increase in CRP was expected. However, no subject showed an above-normal concentration of CRP after exercise(Table 1). Products of the acute-phase reaction, such as CRP, are induced by cytokines, mainly IL-6 (25). Since cytokines did not increase in the present study, no increase in CRP seemed likely.
Cortisol also did not change after exercise (Table 1). Increases in cortisol have been observed after resistance exercise(13), and perturbations in cortisol have been reported after eccentric exercise by Miles et al. (23). Since the time of blood sampling was not consistent among the subjects (09:00-14:00) in the present study, the results of cortisol should be discussed with care. The secretory rate of cortisol is high in the early morning but low in the late evening (23). The blood sampling time was consistent for each subject in the present study; it can be said that cortisol did not increase dramatically. It is known that alterations in concentration of trace minerals in the blood, such as copper, zinc, and iron, occur during the acute-phase response (19). Inflammation would cause a decrease in serum zinc (25), yet zinc remained unchanged(Table 1). This was in accordance with our previous study(26).
In conclusion, the local muscular eccentric exercise in this study produced significant changes in muscle damage indicators and swelling. Although profound swelling and soreness, which are signs of inflammatory response, occurred after exercise, none of the plasma levels of inflammatory markers measured in this study showed significant changes. Although there are some similarities in response between exercise-induced muscle damage and an inflammatory response accompanying infection or tissue injury, the responses in exercise-induced muscle damage appear to be different from a classical understanding of the tissue damage/repair process.
;)
Figure 1-Changes in upper arm circumference at the middle (CIRM; 8 cm above the elbow joint) and the distal (CIRD; 4 cm above the elbow joint) portion immediately before (PRE) and after (POST) as well as for 5 d after exercise. Mean (±SE) values of 14 subjects are presented.*: P < 0.05 compared with the pre-exercise values.
Figure 2-Transverse scan of the biceps brachii and brachialis muscle of a subject (Subj. OHT) who showed increased echointensity in the brachialis. The time course of changes in scan images is shown at before (pre) and for 5 d after exercise (D1-D5). In the “PRE” picture, “1” denotes the biceps brachii, “2” indicates the brachialis,“3” shows the humerus, and a : large arrow points to the subcutaneous compartment. Between the small arrows , the subcutaneous thickness is shown (2.7 mm). The thickness did not change after exercise (see D5; 2.7 mm). Peak plasma CK activity of the subject is shown.
Figure 3-Transverse scan of the biceps brachii and brachialis muscle of a subject (Subj. CHB) who showed increased echointensity in both the biceps brachii and brachialis. Denotations are same as : Figure 2 . The subcutaneous thickness did not change before (see PRE; 3.2 mm) and after (see D5; 3.2 mm) exercise. Peak plasma CK activity of the subject is shown. Figure 4-Twelve serial sections of T2-weighted MR imaging of a subject's upper arm at 3 d after exercise. Picture #1 shows the transverse slice of approximately 2 cm above the elbow joint. Each picture number represents a different section that was scanned every 1 cm interval toward the shoulder. As indicated in picture #8, “1” denotes the biceps brachii, “2” shows the brachialis, “3” indicates the humerus, “4” represents the triceps brachii, and the white layer surrounding the muscles shown by an : arrow is the subcutaneous compartment.
Figure 5-Changes in T2-weighted MRI taken at approximately 6 cm above the elbow joint of a subject (Subj. H) before (PRE), 1 (D1), 3 (D3), 6(D6), 10 (D10), 23 (D23), 31 (D31), and 58 (D58) d after exercise. As shown in the picture “PRE”, “1” indicates the biceps brachii,“2” shows the brachialis, “3” denotes the humerus,“4” represents the triceps brachii, and an: arrow points to a part of the subcutaneous compartment. Not only the brachialis, but also the triceps brachii, is affected.
Figure 6-Changes in T2 relaxation time of six subjects before (PRE) as well as 1, 3, 6, 10, 23, 31, and 58 d after exercise. Mean (±SE) values of the six subjects are shown in : open circles .* P < 0.05 compared with the pre-exercise value.
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