Recent evidence highlights the presence of a low-grade chronic systemic inflammatory state with the development and progression of cardiovascular disease (CVD) (12,32) and type II diabetes (T2D) (30,37). The importance of conventional risk factors such as hyperlipidemia, hypertension, and smoking for the development of these disease states is well established (17,31). However, it has been reported that more than 50% of myocardial infarctions and strokes occur in patients lacking hyperlipidemia and 15%-20% occur in those who do not smoke or present with hypertension (17,31). Hence, in conjunction with conventional risk factors, novel immunological risk factors are emerging as important screening adjuncts regarding prognostic insight into chronic disease risk (28,31). Two markers of immune system function that have been linked to the development of CVD and T2D include the inflammatory marker C-reactive protein (CRP) and its systemic precursor interleukin-6 (IL-6).
Prospective and cross-sectional epidemiological investigations have reported that elevated resting CRP concentrations (high risk, >3.0 mg·L−1) are associated with increased risk for first-ever CVD event (18,21), ischemic stroke and transient ischemic attack (33), development of hypertension (36), and carotid (34) and peripheral (39) artery diseases. Further, elevated baseline concentrations are associated with elevated fasting glucose (24) and fasting insulin (29) concentrations in non-T2D individuals and development of T2D in initially T2D-free subjects (30). Recently, guidelines have been endorsed for the use of CRP as a prognostic clinical marker of global cardiovascular and metabolic risk (28). Accordingly, the measurement of CRP has been suggested to offer prospective insight regarding the monitoring of chronic systemic inflammation and chronic disease risk (28).
Associated with the development of these diseased sates, abdominal obesity has been recently endorsed as an important risk factor for the development of metabolic syndrome and associated chronic diseases (1); which is not surprising given that visceral abdominal adipose tissue secretes two to three times the quantity of IL-6 compared with subcutaneous adipose stores (8,22). Moreover, dual-energy x-ray absorptiometry (DXA) and within-pair differences in monozygotic twins have demonstrated that intra-abdominal fat mass (IA-FM) is strongly correlated with CRP concentration, independent of genetic influence (9). In addition, a systematic review of 33 weight loss interventions has revealed a CRP reduction of 0.13 mg·L−1 for each 1.0 kg of body mass loss (35); however, regional analysis was not a feature of this study, and thus associations cannot be drawn as to the likely compartmental reductions that may have mediated the reductions in CRP concentration (35).
Cross-sectional investigations have demonstrated inverse associations between aerobic fitness and chronic systemic inflammation (2,27). As evidence of this, comparison of the Bruce protocol treadmill test performance and CRP concentration demonstrated a 0.061-mg·L−1 decrease in CRP concentration with each metabolic equivalent gained during the protocol (2). Moreover, another investigation demonstrated inverse associations between weekly exercise patterns and inflammatory markers (27). In comparison with sedentary subjects and after adjustment for gender, age, smoking habits, body mass index (BMI), total cholesterol, glucose, and blood pressure, subjects devoted to high physical activity reported 29% and 32% lower concentrations of CRP and IL-6, respectively (27). Hence, reduced aerobic exercise capacity and sedentariness seem to be associated with increased presence of chronic systemic inflammation and may provide a rationale for the use of exercise as a therapeutic modality (13).
Hepatic stimulation by IL-6 induces the synthesis and the systemic release of CRP as part of the acute-phase inflammatory response (9,30). The existing literature presents conflicting and inconsistent findings regarding the effects of exercise training on this response (7). For example, investigations have reported both attenuation (5,19,20,25,38) and no effect (7,11,15,23) of exercise training on CRP. Further, some investigations have reported a reduction in IL-6 with no subsequent effect on CRP (7,23), whereas others have reported the reverse (26,38). Moreover, studies reporting reductions in CRP, IA-FM, and total body fat mass (TB-FM) have reported no correlation between these reductions (20,25), which is in opposition to the previously demonstrated physiological association between adipose tissue and systemic inflammation (8,9,22). In addition to the large variance in reported subject samples (5,7,19,23,38), much of the published research has included clinically diagnosed subjects, thus reducing the transference of findings to nondiagnosed subject samples (20).
Therefore, due to the inconsistent findings on the effects of exercise training on systemic inflammatory markers, the purpose of the present study was to determine the respective effects of 10 wk of resistance or aerobic exercise training on CRP and IL-6 concentrations in a sedentary adult population matched for baseline CRP and IL-6 concentrations. A further purpose was to investigate whether potential reductions in CRP and IL-6 were associated with the modality of exercise performed or alterations in body composition, specifically reductions in IA-FM and TB-FM. On the basis of previous research, it was hypothesized that both interventions would reduce IL-6 and CRP concentration, and further that the aerobic intervention would result in a more pronounced reduction in CRP and IL-6 concentration, particularly in response to a hypothesized larger reduction in IA-FM and TB-FM.
One hundred and two sedentary subjects, including both male (n = 45) and female (n = 57) subjects, volunteered from the local community and were semirandomly assigned to a resistance group (male n = 16, female n = 19, total n = 35), an aerobic group (male n = 16, female n = 25, total n = 41, or a control group (male n = 13, female n = 13, total n = 26). Baseline characteristics of the study population are presented in Tables 1-3. At baseline, approximately 80% of subjects were randomly assigned to the respective groups; however, approximately 20% of subjects were assigned to a group according to a combination of either specific group preference or matching of pretraining IL-6 and CRP concentrations. At baseline, subjects were required to be sedentary, which was defined as no regular pattern of planned or incidental activity longer than 20 min in duration. Further study exclusion criteria included tobacco smoking (<1 yr cessation), hormone replacement therapy patients, those suffering from current or recent influenza illness (including flu shot recipients), recent surgical patients, rheumatoid arthritis patients, subjects with known immunological irregularities (such as low white blood cell count), and any other condition associated with a systemic inflammatory response. Subjects with orthopedic limitations were also advised against becoming involved in the study due to the musculoskeletal demands of both training programs. Subjects attended an information and a familiarization session in which all details of testing and training procedures were explained. All subjects gave verbal and written informed consent before engaging in testing procedures, and human ethics clearance was granted by the Institutional Ethics Committee.
Before and after the 10-wk training intervention, a health screening was performed on all subjects, which involved a consultation with a medical physician. During this session, documentation of past and current health information was provided to ensure the aforementioned exclusion criteria. After this consultation and after an overnight 10-12 h fast, subjects reported to a pathology clinic between 0700 and 0900 h and were seated for 20 min before providing a venous blood sample. At baseline and after exercise training, venous blood samples were obtained after a 4-d abstinence from exercise or physical activity to ensure that acute fluctuations in IL-6 and CRP concentration would have subsided before collection. In addition, subjects were screened for T2D, which was indicated by a fasting glucose measure of ≥7.0 mmol·L−1 or a glycosylated hemoglobin (HbA1c) measure of ≥6.5%; if T2D was suspected, the subject was excluded from study involvement. On the basis of previously recommended clinical guidelines, a measure of 10.0 mg·L−1 was the cutoff for CRP measures, which may have potentially reflected inflammation due to sepsis and thus may have obscured the identification of resting baseline CRP concentration (28).
Before and after intervention, subjects attended a testing session at the Institutional Exercise Science Laboratories for assessment of body composition, aerobic fitness, and muscular strength. After preintervention testing, the resistance and the aerobic subjects completed a 10-wk periodized and progressive exercise training program (Table 4), whereas subjects in the control group continued their normal sedentary life. Subjects from the three conditions were informed about the importance of maintaining their previous nutritional patterns, including food and beverage choice; dietary contribution from carbohydrate, fat, and protein; and serving quantity and feeding time. Although required to remain sedentary, subjects in the control group were provided with an exercise and physical activity diary and were required to log the type, the duration, and the intensity of any physical activity or exercise undertaken during the period. After the intervention period, the authors examined the exercise and physical activity diary of the control subjects to ensure conformity to the study requirements.
Table 4 presents the 10-wk periodized resistance and aerobic exercise training programs and includes information pertaining to the progression of exercises performed and the respective intensity, volume, and duration of training. Each training session for both the resistance and the aerobic groups commenced with a 5-min dynamic stretching warm-up routine, followed by the main respective group session, and concluded with 5 min of stretching exercises. The main session for the resistance group incorporated pulley-weight machine exercises (Panatta Sport, Apiro, Italy), which were performed at preintervention 10-repetition maximum (10RM) that is reported to approximate with 75% of a 1RM (3). Recovery between sets and exercises was standardized at 120 s, and an increase in resistance was warranted if two extra repetitions could be performed in the last set on two consecutive occasions, which promoted subjects to train proximally to "momentary muscle failure" by exercise completion (3). The main session for the aerobic group incorporated cycling exercise on Monark stationary cycle ergometers (Monark 828E; Monark Exercise AB, Varburg, Sweden), which incorporated the monitoring (Vantage NV, Polar, Finland) and the adjustment of HR through manual adjustment of pedaling resistance. Resistance and aerobic exercise training was performed within the Institutional Exercise Science Laboratories under full supervision by exercise physiologist research assistants who monitored all workout sessions. In addition, each session was monitored for HR, pedaling resistance, rating of perceived exertion (RPE), and cycling duration in the aerobic group and session exercises, resistance levels, and completion rates (exercises, sets, and repetitions) in the resistance group.
All preintervention and postintervention measures were conducted in a climate-controlled exercise physiology laboratory by the same research team and with time of day standardized. Anthropometric measures included height (stadiometer; Custom CSU, Bathurst, NSW, Australia), body mass (HW 150 K; A&D, Bradford, MA, USA), waist and hip girths (steel tape; EC P3 metric graduation, Sydney, NSW, Australia), and supine whole-body DXA scan for body composition (XR800, Norland, Cooper Surgical Company, Turnbull, CT, USA). Scanning resolution was set at 6.5 × 13.0 mm, and scanning speed was set at 260 mm·s−1. Subject scanning position was standardized for pretesting and posttesting analysis. The whole-body scan was analyzed (Illuminatus DXA, version 4.2.0, Turnbull, CT, USA), and total body lean mass (TB-LM), TB-FM, and IA-FM quantities were quantified in kilograms. The analysis of IA-FM was performed with the creation of a region of interest according to previously reported procedures (14). Muscular strength was measured with a 10RM test procedure, which incorporated chest press and leg press for identification of upper-body and lower-body strength, respectively. Multiple RM testing was used, first, to assist the identification of an initial training load (10RM) and, second, to minimize muscular soreness of the subjects due to their sedentary condition. Subjects were instructed in the appropriate operation of the pulley-weight machines and were familiarized with the strength test procedures. During strength assessment, subjects were required to attempt 10 repetitions of ascending resistances in which each attempt was separated by 3-5 min of recovery. The determination of 10RM for each upper- and lower-body exercise usually required two to three attempts (two to three sets). Aerobic fitness measures were obtained with the use of the aerobic power index (API) component of the trilevel fitness profile, which has been demonstrated as a highly reliable submaximal exercise protocol in sedentary subjects (40). The API protocol was performed on an electronically braked cycle ergometer (LODE Excalibur Sport; LODE BV, Groningen, The Netherlands). The API protocol is an incremental step protocol that commences at 25 W and increases in increments of 25 W each minute. HR was recorded each minute throughout the protocol (Vantage NV) and was combined with the subjects' mass and interpolated power output to calculate an API (fitness) (40).
Blood samples were collected into evacuated lithium heparin tubes for the analysis of CRP, IL-6, insulin, cholesterol, and triglycerides; in addition, fluoride oxalate tubes and ethylenediaminetetraacetic acid tubes were used for the analysis of glucose and glycosylated hemoglobin (HbA1c), respectively. All biochemistry variables were analyzed according to the manufacturer's instructions provided in the respective assay kits (Dade Behring Dimension Xpand; Siemens Healthcare Diagnostics, Sydney, Australia). Total cholesterol was assayed using an enzymatic method and a polychromatic end point technique measurement. HDL cholesterol (HDL-C) was measured using accelerator-selective detergent methodology. Triglycerides were assayed using an enzymatic method and a bichromatic end point technique measurement. LDL cholesterol was calculated using the Friedwald equation, which incorporates total cholesterol, HDL-C, and triglyceride measures. Glucose was assayed using an enzymatic method and a bichromatic end point technique measurement. Insulin was measured using a solid-phase, two-site chemiluminescent immunometric assay. CRP was manually diluted according to the manufacturer's instructions and analyzed with the particle-enhanced turbidimetric immunoassay technique. IL-6 was analyzed with a solid-phase, enzyme-labeled, chemiluminescent sequential immunometric assay. HbA1c was measured using automated high-performance liquid chromatography methodology (Bio-Rad Variant, Sydney, Australia). Intra- and interassay coefficients of variation were less than 5.0% for all biochemistry variables.
All data are reported as mean ± SD. A repeated-measures (condition × time) ANOVA was used to determine significant differences between the respective groups (resistance, aerobic, and control). Where a significant main effect and/or interaction was observed, one-way ANOVA of preintervention to postintervention differences (absolute values) with Tukey's HSD post hoc tests was applied to determine the source of significance, which was set at P ≤ 0.05. Paired sample t-tests with Bonferroni adjustment were conducted on all measured variables to determine within-group significance. Finally, Pearson product moment correlations were calculated to identify any significant associations between CRP baseline, CRP change, and baselines and change in other measured variables. All statistical procedures were performed using the Statistical Package for the Social Sciences for Windows (version 16.0; SPSS Inc., Chicago, IL).
Muscular Strength and Aerobic Fitness
Table 1 presents preintervention and postintervention within- and between-group results for muscular strength and aerobic fitness variables. Preintervention comparisons between conditions revealed significant differences (P < 0.05) in baseline strength, with a higher 10RM lower-body strength in the control compared with aerobic and resistance groups, whereas 10RM upper-body strength was also higher compared with the aerobic group. However, after the intervention period, there was no improvement in strength or aerobic fitness measures for the control group. The training session completion rate of both the resistance and the aerobic groups was 27 of the 30 organized sessions (91%). The resistance group increased 10RM upper-body strength by 46.5% ± 21.9% and 10RM lower-body strength by 56.6% ± 23.3% (Table 1; P < 0.05), which was a significantly larger improvement than the aerobic and the control groups, respectively (P < 0.05). The resistance training group also improved time to target HR (THR) in the aerobic fitness test by 7.4% ± 12.6% (P < 0.05); however, no improvements were reported for final stage of test and calculated API (P > 0.05). After training, the aerobic group significantly improved time to THR by 20.9% ± 8.6%, final stage of test by 16.8% ± 12.3%, and calculated API by 22.5% ± 11.1% (Table 1; P < 0.05). The improvements in time to THR, final stage of test, and calculated API were significantly greater than the improvements of the resistance and control groups, respectively (P < 0.05). In addition, the aerobic group also demonstrated a significant 25.8% ± 24.6% increase in 10RM lower-body strength (P < 0.05).
Anthropometry and DXA
Table 2 presents preintervention and postintervention within- and between-group data for the measured anthropometric and DXA variables. Preintervention comparisons revealed no significant differences between groups (P > 0.05) for any body composition variable. The control group experienced an increase in hip girth and TB-LM (kg) after the 10-wk period (P < 0.05). The resistance training group experienced a 1.0% ± 1.9% increase in body mass, which comprised a 3.7% ± 5.0% increase in TB-LM (kg) and a 3.4% ± 6.6% decrease in TB-FM (%) (Table 2; P < 0.05). The increase in TB-LM was significantly larger than the increase in the aerobic group (P < 0.05). The resistance group also experienced a 3.5% ± 7.2% decrease in IA-FM and a 1.5% ± 2.7% decrease in waist girth (P < 0.05). In addition, the decrease in waist girth, hip girth, and IA-FM was significantly larger than the changes in the control group (P < 0.05). Moreover, the aerobic group also demonstrated reductions (Table 2; P < 0.05) in variables relating to body composition, including a 1.0% ± 2.3% decrease in body mass, a 0.9% ± 2.2% decrease in BMI, a 2.4% ± 3.0% decrease in waist girth, a 2.0% ± 2.2% decrease in hip girth, a 7.7% ± 7.8% decrease in IA-FM, and a 3.7% ± 4.9% and 3.4% ± 4.2% decrease in TB-FM (kg) and TB-FM (%), respectively. The aerobic training group also exhibited a 1.5% ± 3.5% increase in TB-LM (P < 0.05). The decreases in body mass, BMI, and IA-FM were significantly larger than the resistance and the control groups (Table 2; P < 0.05). Further, the decrease in waist and hip girth was also significantly larger than those demonstrated by the control group (P < 0.05).
Preintervention and postintervention within- and between-group biochemistry variables are presented in Table 3. Before the intervention, there were no significant differences (P > 0.05) between conditions for any variable. For the control condition, the only biochemistry variable that was significantly changed after the intervention was an increase in fasting glucose (P < 0.05). Both the 10-wk resistance and the aerobic exercise programs had no effect on baseline IL-6 concentration (P > 0.05); however, the resistance group experienced a significant 32.7% ± 27.2% decrease in CRP concentration (Table 3; P < 0.05). Post hoc analyses demonstrated a trend for a difference in CRP to the postintervention control group (P = 0.08) and the aerobic group (P = 0.11). The aerobic exercise group did not significantly reduce CRP concentration in response to the exercise program; however, a trend for a reduction was evident (16.1 ± 39.7%; P = 0.06). The resistance group also experienced a 1.1% ± 8.7% increase in total cholesterol, which was significantly different (P < 0.05) to the reduction exhibited by the aerobic group (P < 0.05). The resistance group also experienced a 4.9% ± 11.3% and a 5.4% ± 5.1% increase in fasting glucose concentration and HbA1c concentration, respectively (P < 0.05). Similar to the resistance group, the aerobic group also featured a 5.1% ± 4.7% increase in HbA1c concentration (P < 0.05). The increase reported for HbA1c for the resistance and the aerobic groups was different compared with the small decrease experienced by the control (P < 0.05); however, these increases were minor and did not alter T2D risk classification.
Correlations between CRP and other variables at baseline.
Table 5 presents Pearson correlation coefficients and associated significance levels between baseline CRP and other preintervention variable values. At baseline, BMI, hip girth, IA-FM, TB-FM (kg), and TB-FM (%) were all moderately positively correlated with baseline CRP concentration (all r values ≥0.25; P < 0.05). Baseline TB-LM (kg) and TB-LM (%) were weakly (r = -0.23; P < 0.05) and moderately (r = -0.36; P < 0.05) inversely correlated with baseline CRP concentration, respectively. At baseline, IL-6 was moderately positively correlated with CRP (r = 0.35; P < 0.05); however, no other biochemistry variables demonstrated significant correlations with baseline CRP (all r values ≤0.16; P > 0.05). Preintervention to postintervention change in CRP concentration demonstrated a correlation with baseline CRP concentration (r = 0.23; P < 0.05). At baseline, final stage of test and API demonstrated moderate inverse correlation with preintervention CRP concentration (all r values ≥0.26; P < 0.05), and time to THR featured a weak inverse correlation (r = -0.24; P < 0.05).
Correlations between CRP change and other variable change
Table 6 presents Pearson correlation coefficients and associated significance levels between preintervention and postintervention change in CRP concentration and changes in other variables. Changes in body mass and waist-to-hip ratio were weakly positively correlated with the change in CRP concentration (all r values ≥ 0.21; P < 0.05). The change in total/HDL-C ratio and HbA1c demonstrated weak inverse correlations with the change in CRP concentration (all r values ≤ -0.22; P < 0.05). Change in 10RM lower-body strength produced a moderate inverse correlation with change in CRP concentration (r = -0.25; P < 0.05), whereas change in 10RM upper-body strength demonstrated a moderate inverse correlation with change in CRP concentration (r = -0.22; P < 0.05). No correlations were evident between change in CRP concentration and change in the measures of aerobic fitness (all r values ≤ 0.04; P > 0.05).
The purpose of the present study was to evaluate the effects of resistance or aerobic exercise training, respectively, to attenuate elevated IL-6 and CRP concentrations in a sedentary and disease-free population. The baseline CRP concentrations reported in this study were classified as "high risk" according to recently published guidelines (28) and similar (30) or elevated (18,21) compared with previous investigations that demonstrated prospective disease association. Moreover, baseline IL-6 concentration was similar (18,30) or elevated (21) in comparison with that reported in these same investigations. At study baseline and according to the prospective association between elevated chronic systemic inflammation and chronic disease risk, the finding that blood lipid and glycemic control measures were in the normal range while IL-6 and CRP were elevated provides prospective context to the findings that approximately half of all myocardial infarction and stroke patients present with "normal" lipid levels (17,31). Similar to other investigations, subjects in the present study were sedentary at baseline and demonstrated an inverse association between aerobic fitness and inflammatory marker concentration (2,27). Hence, it is likely that the subject population in the current study presented with increased atherosclerotic and metabolic risk, despite conventional risk screening markers not necessarily resulting in a classification of "at risk."
After the 10-wk exercise training period, the IL-6 concentration of both the exercise groups and the control group remained unchanged; however, a significant reduction in CRP concentration was experienced by the resistance training group. At baseline, CRP was moderately correlated with IL-6, highlighting the proposed relationship between systemic IL-6 release and systemic CRP concentration (9). After exercise training, IL-6 remained unaltered, which, given the reduction in CRP by the resistance group, is similar to findings reported by previous studies (26,38). Recent evidence after 1 yr of moderate resistance training (26) also reported a reduction in CRP with no change in IL-6. Moreover, this recent study also reported no change in blood lipids, fasting glucose, fasting insulin, and body mass or fat mass and a significant increase in TB-LM, which corroborate findings for the resistance group in the present study.
The improvement in 10RM upper- and lower-body strength in the resistance group was accompanied by an improvement in TB-LM that was significantly greater than the aerobic group. This increase in TB-LM implies that the resistance group exhibited more protein synthesis and/or protein degradation and subsequently experienced greater skeletal muscle hypertrophy (6). At baseline, TB-LM (kg) was weakly correlated to CRP concentration (r = 0.23); however, when TB-LM was correlated as a percentage of body mass, the strength of the association increased markedly (r = 0.36). Despite the baseline correlation between TB-LM and CRP concentration, 10RM upper- and lower-body strength was not correlated to baseline CRP concentration. However, after exercise training, reductions in CRP concentration were correlated to 10RM lower- and upper-body strength improvements. Similar to previous investigations (5,26), the present study supports resistance exercise training in the reduction of elevated CRP concentrations.
After exercise training, significant aerobic fitness improvements in time to THR, final stage of test, and calculated API measures were reported for the aerobic group compared with the resistance and control groups. The improvement in these measures suggests that aerobic adaptations accompanied the 10-wk training program, including an improved subject HR response to the API test protocol, indicative of stroke volume and blood volume adaptations to aerobic exercise training (4). At baseline, all aerobic fitness measures were moderately and inversely correlated with CRP concentration (r > -0.24); however, despite correlations between baseline CRP concentration and aerobic fitness measures, posttraining aerobic fitness improvements were not correlated to reductions in CRP concentration (r > -0.04). Similar to the present study, two other investigations also reported moderate inverse correlations between CRP and aerobic fitness at baseline (20,25). In addition, these investigations also demonstrated no association between improvement in aerobic fitness measures and reduction in CRP concentration (20,25).
Regarding body composition, all pretraining adipose tissue measures were moderately correlated to CRP concentration (r > 0.31), which is in support of findings from previous investigations (20,25). After training, the aerobic group demonstrated a reduction in measures of adiposity to a larger extent than the resistance training group. Further, the aerobic group also demonstrated significant improvements in all but one of the measured anthropometric variables, with the decreases in body mass, BMI, and IA-FM all significantly larger than the resistance group. Moreover, of the posttraining body composition measures, only body mass correlated to the reduction in CRP concentration, which was likely due to the comparatively larger increase in body mass exhibited by the resistance group, while concomitantly reporting the most notable CRP reduction. Moreover, reduction in CRP concentration was not correlated with improvement in TB-LM measures. Together, the posttraining IA-FM, TB-FM, and TB-LM DXA results from the present 10-wk study reinforce a lack of association between reduction in CRP and alteration of body composition. Regarding resistance exercise training, these results suggest that attenuation of low-grade systemic inflammation need not necessarily occur in the presence of clinically meaningful alterations of body composition.
In elucidating the mechanisms potentially responsible for the attenuation of CRP, a study of the effects of blood mononuclear cell and associated cytokine activity reported a 35% decrease in CRP concentration after 6 months of aerobic exercise (16). In comparison with a preexercise training blood sample, a postexercise training blood sample demonstrated suppressive effects over the pro-atherogenic cytokines IL-1α and tumor necrosis factor α (TNF-α) and an augmented effect toward the anti-inflammatory cytokines IL-4, IL-10, and transforming growth factor β-1 (16). In another investigation, 12 wk of resistance exercise performed three times per week, similar to the protocol in the present study, reported a significant reduction in TNF-α messenger RNA activity and TNF-α protein expression (10). Moreover, at study baseline, a strong inverse relationship between muscle protein synthesis rate and muscle TNF-α protein content was also reported (10). Accordingly, in the present study, the resistance group experienced a significant increase in TB-LM, which is indicative of an enhanced protein synthesis rate due to the resistance exercise stimulus. As such, it may be the suppression of proinflammatory responses related to the enhanced protein synthesis rate that results in a more pronounced reduction in CRP concentration (10,16). A limitation of the present study is that TNF-α was not measured; however, although speculative, it is possible that the resistance group may have suppressed TNF-α and other cytokine activity associated with blood mononuclear cells as has been previously reported after exercise (10,16). Hence, future exercise studies should further investigate myofibrillar protein signaling pathways, which may involve mechanisms that repress proinflammatory signaling pathways and thus the potential for increases in proinflammatory markers associated with chronic systemic inflammation.
In conclusion, 10 wk of resistance or aerobic exercise training in sedentary disease-free subjects did not affect elevated baseline IL-6 concentration; however, resistance training attenuated elevated baseline CRP concentration from "high-risk" (3.57 mg·L−1) to "moderate-risk" (2.40 mg·L−1) status, and aerobic exercise training demonstrated a trend for reduction. In addition, the reduction in CRP concentration in the resistance group presented despite markedly less reduction in intra-abdominal and total body adipose tissue measures than the aerobic group. The findings of the present study have implications for sedentary populations and suggest that resistance exercise training may attenuate elevated chronic systemic inflammation before clinically meaningful reductions in adipose tissue. It is recommended that future studies should investigate muscle protein signalling pathways and muscle protein synthesis related to resistance exercise training and its effect on pro- and anti-inflammatory cytokines.
The authors would like to acknowledge the Institute of Clinical Pathology and Medical Research, Westmead Hospital, NSW, Australia, and the institutional laboratory technical staff for their technical research assistance. They would also like to acknowledge the subjects for their involvement in the three respective groups and contribution to the study findings and Mrs. Jane Thompson for her organization of collaborative screening procedures. Finally, the authors would like to state that the results of this study do not constitute endorsement by the American College of Sports Medicine.
Disclosure statement of funding received: This research undertaking was solely funded by Charles Sturt University and not any of the following organizations: the National Institutes of Health, the Wellcome Trust, or the Howard Hughes Medical Institute.
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