Correction: Redox correlation in muscle lengthening and immune response in eccentric exercise.

[This corrects the article DOI: 10.1371/journal.pone.0208799.].

Redox correlation in muscle lengthening and immune response in eccentric exercise.

This study was designed to examine the potential involvement of reactive oxygen species in skeletal muscle dysfunction linked with stretching in a mouse model and to explore the effects of combined antioxidant intake on peripheral leukocyte apoptosis following eccentrically-biased downhill runs in human subjects. In the mouse model, diaphragmatic muscle was stretched by 30% of its optimal length, followed by 5-min contraction. Muscle function and extracellular reactive oxygen species release was measured ex vivo. In human models, participants performed two trials of downhill running either with or without antioxidant supplementation, followed by apoptotic assay of inflammatory cells in the blood. The results showed that stretch led to decreased muscle function and prominent ROS increase during muscle contraction. In human models, we observed an elevation in circulating leukocyte apoptosis 24-48 hours following acute downhill runs. However, there is an attenuated leukocyte apoptosis following the second bout of downhill run. Interestingly, the combination of ascorbic acid (vitamin C) and α-tocopherol (vitamin E) supplementation attenuated the decrease in B-cell lymphoma 2 (Bcl-2) at 24 hours following acute downhill running. These data collectively suggest that significant ROS formation can be induced by muscle-lengthening associated with eccentric exercise, which is accompanied by compromised muscle function. The combination of antioxidants supplementation appears to have a protective role via the attenuation of decrease in anti-apoptotic protein.

Resistance exercise training-induced decrease in circulating inflammatory CD14+CD16+ monocyte percentage without weight loss in older adults.

PURPOSE: Exercise training reduces systemic inflammation in weight-stable people, but concurrent diet-induced body weight loss is not well studied. We hypothesized that resistance training would decrease inflammatory monocyte percentage and improve biomarkers associated with disease risk, independent of weight loss. METHODS: Forty physically inactive (PI) subjects (58.0 ± 5.7 years; BMI 30.1 ± 4.3 kg m(-2)) completed baseline testing, and 26 of these subjects completed 12-week of resistance training exercises while consuming either their usual, weight-maintenance diet (RE, n = 14) or an energy-restricted diet (RE-ER, n = 12). Nine physically active (PA) subjects served as a comparison group (60.1 ± 6.1 years; BMI 25.8 ± 3.1 kg m(-2)). RESULTS: At baseline, circulating CD14+CD16+ monocyte percentage, C-reactive protein, and cholesterol were higher in PI vs. PA. Post-intervention, RE subjects had a ~35 % decrease in circulating CD14+CD16+, and a lower LPS-stimulated TNFα and IL-6 production, while RE-ER subjects had lower cholesterol than RE. CONCLUSIONS: These findings indicate that resistance training is an effective means for older, overweight adults to reduce systemic inflammation. The unexpected lack of response with concurrent energy restriction underscores the need for further research on the use of resistance training and diet to reduce inflammation.

Leukocyte apoptosis and pro-/anti-apoptotic proteins following downhill running.

The purposes of this study were to determine the effect of eccentric exercise-induced muscle damage on the induction of apoptosis in peripheral blood leukocytes and to investigate if the elevation in apoptotic leukocytes was mediated by changes in the concentration of anti-/pro-apoptotic proteins in circulation. Twelve moderately trained subjects performed three 40 min treadmill runs at ~70% VO(2max): a level run (L) followed by two downhill runs (DH1 and DH2). Blood samples were taken at rest (PRE) and immediately (POST), 2, 24, and 48 h after each run. Data were analyzed using two-way repeated measures analysis of variance with post hoc Tukey tests. Creatine kinase (CK) activity was significantly elevated at 24 and 48 h following DH1 (P < 0.01). The proportion (%) of apoptotic leukocytes was significantly elevated at POST and 2 h following all three runs, and up to 48 h following DH1 (P < 0.01). Bax at 24-h post and Bax/Bcl-2 ratio at 24- (P < 0.01) and 48-h post (P < 0.05) following DH1 were greater than PRE (P < 0.05). An acute bout of moderate intensity downhill running altered CK activity, Bax concentration and the Bax/Bcl-2 ratio in circulating leukocytes resulting in a greater apoptotic response at 24- and 48-h post-exercise compared to level grade running or a second downhill run. Although the mechanism by which these proteins are altered by unaccustomed eccentric exercise is currently unknown, the differential response to DH1 versus L and DH2 indicates that it may be related to exercise-induced muscle damage.

Excess postexercise oxygen consumption after aerobic exercise training.

Literature examining the effects of aerobic exercise training on excess postexercise oxygen consumption (EPOC) is sparse. In this study, 9 male participants (19-32 yr) trained (EX) for 12 wk, and 10 in a control group (CON) maintained normal activity. VO(2max), rectal temperature (T(re)), epinephrine, norepinephrine, free fatty acids (FFA), insulin, glucose, blood lactate (BLA), and EPOC were measured before (PRE) and after (POST) the intervention. EPOC at PRE was measured for 120 min after 30 min of treadmill running at 70% VO(2max). EX completed 2 EPOC trials at POST, i.e., at the same absolute (ABS) and relative (REL) intensity; 1 EPOC test for CON served as both the ABS and REL trial because no significant change in VO(2max) was noted. During the ABS trial, total EPOC decreased significantly (p < .01) from PRE (39.4 ± 3.6 kcal) to POST (31.7 ± 2.2 kcal). T(re), epinephrine, insulin, glucose, and BLA at end-exercise or during recovery were significantly lower and FFA significantly higher after training. Training did not significantly affect EPOC during the REL trial; however, epinephrine was significantly lower, and norepinephrine and FFA, significantly higher, at endexercise after training. Results indicate that EPOC varies as a function of relative rather than absolute metabolic stress and that training improves the efficiency of metabolic regulation during recovery from exercise. Mechanisms for the decreased magnitude of EPOC in the ABS trial include decreases in BLA, T(re), and perhaps epinephrine-mediated hepatic glucose production and insulin-mediated glucose uptake.

Resting metabolic rate after endurance exercise training.

PURPOSE: 1) To examine the effect of a 12-wk endurance exercise training program on RMR and 2) to provide insight into the mechanisms responsible for alterations in RMR that may occur after exercise training. METHODS: Male participants (19-32 yr) in an exercise group (EX; n = 9) performed jogging and/or running 3-4 d x wk(-1), 25-40 min per session, at 60%-80% VO2max, whereas subjects in a control group (CON; n = 10) maintained their normal activity patterns. Body composition, VO2max, RMR, epinephrine, norepinephrine, total thyroxine, free thyroxine, insulin, free fatty acids, and glucose were measured before and after the intervention. RESULTS: Training resulted in a significant increase in VO2max in EX (46.2 +/- 1.2 to 51.0 +/- 1.3 mL x kg(-1) x min(-1), P < 0.001). Absolute and relative values for RMR did not significantly change in EX after training. Mean values for epinephrine, norepinephrine, total thyroxine, insulin, and glucose did not significantly change in either group; however, free thyroxine decreased significantly after training in EX (P = 0.04). Training also resulted in a significant increase in free fatty acid concentration in EX (0.37 +/- 0.03 to 0.48 +/- 0.04 mmol x L(-1), P < 0.001). RMR in CON decreased significantly when expressed as an absolute value (P < 0.01) and relative to body weight (P < 0.01), fat-free mass (P < 0.01), and fat mass (P = 0.04). CONCLUSIONS: The mechanism for the decrease in CON is unknown, but it may be related to seasonal variations in RMR. Training may have prevented a similar decline in RMR in EX and may be related to a training-induced increase in fat oxidation.

Predictors of calcium retention in adolescent boys.

CONTEXT: The relationship between calcium (Ca) intake and Ca retention in adolescent boys was recently reported. OBJECTIVE: This study evaluated the influence of Ca intake, serum hormone levels, biomarkers of bone metabolism, habitual physical activity, habitual Ca intake, and physical fitness on Ca retention in the same sample. DESIGN: This study was a randomized, cross-over design that consisted of two 3-wk metabolic balance periods. SETTING: The study took place on a university campus as a summer camp. PATIENTS OR OTHER PARTICIPANTS: A total of 31 American white boys (13-15 yr) participated in the study. INTERVENTIONS: Each subject consumed a controlled diet with one of five high-low Ca intake pairs that ranged from 670-2003 mg/d, which was manipulated utilizing a fortified beverage. MAIN OUTCOME MEASURES: Ca retention was determined by Ca intake minus urinary and fecal Ca excretion during each balance period. RESULTS: Ca intake explained 21.7% of the variability in Ca retention, and serum IGF-I concentration explained an additional 11.5%. Other serum hormone levels did not significantly add to the model. Biomarkers of bone metabolism, habitual physical activity, habitual Ca intake, and physical fitness were not significant predictors of Ca retention in adolescent boys. CONCLUSIONS: IGF-I, a regulator of growth during puberty, is an important predictor of Ca retention in adolescent boys. However, dietary Ca intake is an even greater predictor of Ca retention during this period of growth.

The latest on carbohydrate loading: a practical approach.

High dietary carbohydrate (CHO) intake for several days before competition (CHO loading) is known to increase muscle glycogen stores, with subsequent ergogenic performance benefits often seen in events longer than 90 min in duration. CHO-loading strategies vary in characteristics such as type and duration of dietary manipulation and the accompanying exercise/training activities. Additionally, glycogen concentration may remain elevated for up to 5 d. This versatility in CHO-loading strategies allows the athlete greater flexibility in tailoring pre-event preparation. Women who attempt to CHO load should be particularly attentive to both total energy intake and relative CHO intake; dietary CHO should exceed 8 g x kg body mass(-1) x d(-1) or 10 g x kg lean body mass(-1) x d(-1). As long as the amount ingested is adequate for loading, the type of CHO is less important, with the exception of 1-d loading protocols where the glycemic index may be an important consideration.

Neither gender nor menstrual cycle phase influences exercise-induced lymphocyte apoptosis in untrained subjects.

Lymphocyte apoptosis increases following maximal exercise. Estrogen hormones (E2) have been shown to protect lymphocytes from apoptosis in vitro, but it is unknown whether they can attenuate the apoptotic response to maximal exercise. The purpose of this study was to examine the effect of menstrual cycle variation on exercise-induced lymphocyte apoptosis in humans following exercise. Untrained healthy young men and regularly menstruating women not using hormonal contraceptives volunteered for the study. Women performed a maximal effort treadmill test for VO2 max once in the follicular phase (FOL) and once in the mid-luteal phase (ML) of their cycles. Men completed two VO2 max tests with periods of time between tests matched to those of the female subjects. Blood was collected before (PRE) and immediately after exercise (POST), and analyzed for apoptotic lymphocytes and estradiol. E2 concentrations in women were significantly greater during ML versus during FOL, both PRE and POST (p<0.0001). The percent of exercise-induced lymphocyte apoptosis was similar between women (23.2%+/-1.0%) and men (21.5%+/-0.4%). In women, the apoptotic response to maximal exercise was similar regardless of menstrual cycle phase (FOL=23.7%+/-0.9%, ML=22.7%+/-1.1%). Although elevated female sex hormones in vitro may exert anti-apoptotic effects, these data suggest that in vivo concentrations confer no protection to lymphocytes during exhaustive exercise.

Blood treatment influences the yield of apoptotic lymphocytes after maximal exercise.

PURPOSE: No systematic investigation has been reported assessing the effect of cell isolation processes on postexercise apoptosis. Therefore, the effect of cell isolation procedures on apoptosis was evaluated in this study. METHODS: Untrained healthy individuals participated (N=13). Blood samples obtained at rest and immediately after an incremental exercise test to exhaustion were partitioned into three treatments: 1) whole blood smears made immediately after the sample was obtained (WB), 2) cells subjected to density-gradient isolation before smears were made (ISO), and 3) samples allowed to sit at room temperature (i.e., time-treated) before centrifugation and smearing (TT). Blood smears were stained using the May-Grünwald Giemsa procedure and lymphocytes were evaluated under a light microscope for characteristic features of apoptosis. Data were analyzed using a 2x3 ANOVA. RESULTS: A significant interaction effect existed (P<0.0001) such that at rest, no difference was detected in the amount of lymphocyte apoptosis among WB, ISO, or TT samples. However, after exhaustive exercise, the amount of apoptotic lymphocytes was significantly greater in WB compared with ISO and TT samples (P<0.0001). CONCLUSION: Lymphocyte isolation results in a significant decrease in the percent of apoptotic lymphocytes after exhaustive exercise. This reduction is likely due to the time needed to isolate cells, rather than the isolation process itself. Because apoptosis is a time-sensitive process that occurs within minutes rather than hours, the length of time from initial sampling to the preparation of cells for assessment of apoptosis is critical and should be considered in future exercise studies.

Excess post-exercise oxygen consumption in spinal cord-injured men.

This study examined excess post-exercise oxygen consumption (EPOC) following arm cranking in men who had a traumatic spinal cord injury (SCI). Six physically active SCI men with a lesion level between T10 and T12 and six able-bodied (AB) men who were matched according to upper body peak VO(2) performed 30 min of arm-cranking at 65-70% peak VO(2). Baseline measurements were recorded during the last 10 min of a 40-min seated rest. Subjects remained seated during recovery for 40 min or until VO(2) returned to baseline, whichever was longer. Plasma lactate concentration was measured at rest, at the end of exercise, and at 10, 20 and 40 min of recovery. EPOC duration was not significantly different ( P>0.05) between SCI [23.2 (7.9) min; mean (SE)] and AB [35.0 (15.4) min] men, nor was there a significant group difference in EPOC magnitude [36.8 (7.8) kJ for SCI and 53.0 (22.8) kJ for AB]. There was no significant difference in recovery heart rate (HR) or respiratory exchange ratio (RER) between SCI and AB. However, HR measured at the end of the EPOC period was significantly elevated ( P<0.001) and RER significantly lower ( P<0.03) for both groups when compared to baseline. Lactate concentration was not significantly different between the groups at any sampling period. The findings suggest that physically active SCI men have a similar energy expenditure and time frame for recovery from arm crank exercise as their AB counterparts. Similar to what has been reported following lower body exercise, arm crank exercise elicits a higher HR and lower RER at end-EPOC when compared to pre-exercise values.

Carbohydrate loading and supplementation in endurance-trained women runners.

The purpose of this study was to examine the effect of carbohydrate (CHO) augmentation on endurance performance and substrate utilization in aerobically trained women. Eight endurance-trained women completed a 24.2-km (15 mile) self-paced treadmill performance run under three conditions: CHO supplementation (S), CHO loading and supplementation (L+S), and placebo (P). Dietary CHO was approximately 75% of energy intake for L+S and approximately 50% for both S and P. A 6% CHO-electrolyte solution (S and L+S) or placebo (P) was ingested preexercise (6 ml/kg) and every 20 min during exercise (3 ml/kg). Blood glucose was significantly higher at 40, 60, and 100 min during L+S, and at 60, 80, and 100 min during S compared with P (P < 0.05). Blood lactate was significantly higher (P < 0.05) during L+S than S and P. Blood glycerol was significantly lower (P < 0.05) at 20, 80, and 100 min during L+S, and at 80 and 100 min during S than P. The proportion of CHO (%) utilized during exercise was significantly higher (P < 0.05) during L+S (71.3 +/- 3.8%) and S (67.3 +/- 4.3%) than P (59.2 +/- 4.6%). Performance times (P > 0.05) were 132.5 +/- 6.3 min (S), 134.4 +/- 6.3 min (L+S), and 136.6 +/- 7.9 min (P). In conclusion, it appears that when CHO availability in women is increased through CHO loading and/or CHO supplementation, there is a concomitant increase in CHO utilization. However, this may not necessarily result in significantly improved performance.