Velocity Drives Greater Power Observed During Back Squat Using Cluster Sets.

This investigation compared the kinetics and kinematics of cluster sets (CLU) and traditional sets (TRD) during back squat in trained (RT) and untrained (UT) men. Twenty-four participants (RT = 12, 25 ± 1 year, 179.1 ± 2.2 cm, 84.6 ± 2.1 kg; UT = 12, 25 ± 1 year, 180.1 ± 1.8 cm, 85.4 ± 3.8 kg) performed TRD (4 × 10, 120-second rest) and CLU (4 × (2 × 5) 30 seconds between clusters; 90 seconds between sets) with 70% one repetition maximum, randomly. Kinematics and kinetics were sampled through force plate and linear position transducers. Resistance-trained produced greater overall force, velocity, and power; however, similar patterns were observed in all variables when comparing conditions. Cluster sets produced significantly greater force in isolated repetitions in sets 1-3, while consistently producing greater force due to a required reduction in load during set 4 resulting in greater total volume load (CLU, 3302.4 ± 102.7 kg; TRD, 3274.8 ± 102.8 kg). Velocity loss was lessened in CLU resulting in significantly higher velocities in sets 2 through 4. Furthermore, higher velocities were produced by CLU during later repetitions of each set. Cluster sets produced greater power output for an increasing number of repetitions in each set (set 1, 5 repetitions; sets 2 and 3, 6 repetitions; set 4, 8 repetitions), and the difference between conditions increased over subsequent sets. Time under tension increased over each set and was greater in TRD. This study demonstrates greater power output is driven by greater velocity when back squatting during CLU; therefore, velocity may be a useful measure by which to assess power.

Acute response to cluster sets in trained and untrained men.

PURPOSE: In traditional sets (TRD) repetitions are performed continuously, whereas cluster sets (CLU) allow a brief rest between groups of repetitions. We investigated the acute mechanical, metabolic, and hormonal response to CLU in men. METHODS: Twelve resistance-trained (RT) and 11 untrained (UT) men performed TRD (4 × 10 repetitions with 2 min rest) and CLU [4 × (2 × 5) with 1.5 min rest between sets 30 s rest between clusters] at 70 % 1RM back squat in random order. Seven days separated trials. Average power and time under tension (TUT) were calculated. Blood was sampled pre, sets 1, 2, and 3; immediate post-exercise, 5, 15, 30, 60 min post-exercise for blood lactate, total testosterone (TT), free testosterone (FT), growth hormone (GH), and cortisol. RESULTS: CLU produced greater average power at an increasing number of repetitions over each set with greater total volume load. TUT was shorter for RT and lower for CLU in repetitions 1, 6, 7, 8. Blood lactate was higher Set 2 through 30 min in TRD. RT had higher TT; however, the time course was similar between RT and UT. TT and FT increased immediate post-exercise and remained elevated 30 min in both conditions. GH was significantly greater during TRD with a similar pattern observed in both conditions. Cortisol was significantly lower at 30 min in CLU. CONCLUSION: CLU allowed greater total volume load, shorter TUT, greater average power, similar anabolic hormonal response, and less metabolic stress. The acute response was similar despite training status.

Temperature Measurement Inside Protective Headgear: Comparison With Core Temperatures and Indicators of Physiological Strain During Exercise in a Hot Environment.

Non-invasive temperature monitoring with a sensor inside protective headgear may be effective in detecting temperatures that are associated with heat illness. The purpose was to establish the relationship between in-hardhat temperatures (Tih) and core temperature (Tc) as measured by rectal (Tre) and esophageal (Tes) probes. Thirty males (age 24.57 ± 4.32 yrs.) completed two trials: continuous submaximal exercise (CSE) and a series of high intensity 30-s sprints (HIE) with a one-minute rest between each. Exercise in both conditions was in a 36(°)C environment (40% RH) while wearing a standard hardhat with sensors mounted on the forehead that were monitored remotely. Exercise continued until voluntary termination or until Tc reached 39.5(°)C. Temperatures, heart rate, cardiorespiratory, and perceptual responses were monitored throughout. A physiological strain index (PSI) was calculated from Tc and HR. The final temperatures in the CSE condition were 38.77 ± 0.41, 38.90 ± 0.49 and 39.29 ± 0.58(°)C and in the HIE condition, final temperatures were 38.76 ± 0.37, 38.91 ± 0.47, and 39.19 ± 0.57 f (o)C for Tih, Tre, and Tes, respectively. The PSI in CSE was 9.62 ± 062, 9.18 ± 1.11, and 10.04 ± 1.05, and in the HIE condition 9.67 ± 068, 9.29 ± 0.99. and 9.86 ± 1.02 based on Tih, Tre and Tes, respectively. The general agreement between the Tih and other temperature measures along with the consistency as indicated by a low coefficient of variation (approx. 1%) in the recordings of the Tih sensors at the point of termination suggest that this device, or similar devices, may have application as a warning system for impending heat-related problems.

Preexercise energy drink consumption does not improve endurance cycling performance but increases lactate, monocyte, and interleukin-6 response.

The purpose of this study was to investigate the influence of an energy drink (ED) on cycling performance and immune-related variables. Eleven trained male cyclists (33.4 ± 8.9 years; 81 ± 7.6 kg; maximal VO2, 52 ± 3.4 ml·kg(-1)·min(-1)) consumed 500 ml of (a) ED (2.0 g taurine, 1.2 g glucuronolactone, 160 mg caffeine, 56 g carbohydrate [CHO], and B vitamins), (b) cola matched for caffeine and CHO (CC), or (c) flavored placebo (PL: sparking water and flavoring) 50 minutes before racing in a randomized, crossover design. Performance was measured as time to complete (TTC) a 25-mile simulated road race. Blood was collected at baseline, 30 minutes after drink consumption, during exercise at miles 5 (M5), 15 (M15), and immediately (POEX) and 30 minutes (30minPO) after exercise. TTC was not different (p > 0.05) among trials (ED, 68.6 ± 2.7; CC, 68.9 ± 3.8; PL, 69.6 ± 3.8 minutes). Consumption of CC and ED elicited a mild hypoglycemia elicited a mild hypoglycemia during cycling. POEX interleukin-6 (IL-6) was greatest after ED, whereas CC IL-6 was greater than PL (10.2 ± 1.6, 6.7 ± 0.6, and 4.8 ± 0.7 pg·ml(-1), respectively; p < 0.001). Cycling increased leukocyte number in all conditions with ED leukocyte number greater than that of PL at M15 (9.8 ± 0.6, 8.5 ± 0.3 × 10(6) cells·mL(-1)). Energy drink induced an earlier recruitment of monocytes to the blood stream than CC. Mean fat oxidation was greater in PL compared with CC (0.43 ± 0.06 and 0.28 ± 0.04 g·min(-1); p = 0.033) but did not differ between ED (0.32 ± 0.06) and PL. Lactate was higher in ED compared with CC and PL at M5 and M15 (p = 0.003), but there was no significant influence of either ED or CC on performance. Carbohydrate and caffeine consumption before endurance cycling significantly increased the IL-6 release and leukocytosis, and the additional ingredients in ED seem to have further augmented these responses.

Exercise-associated hyponatremia: the influence of pre-exercise carbohydrate status combined with high volume fluid intake on sodium concentrations and fluid balance.

To evaluate the effect of hydration and carbohydrate (CHO) status on plasma sodium, fluid balance, and regulatory factors (IL-6 & ADH) during and after exercise; 10 males completed the following conditions: low CHO, euhydrated (fluid intake = sweat loss) (LCEH); low CHO, dehydrated (no fluid) (LCDH); high CHO, euhydrated (HCEH); and high CHO, dehydrated (HCDH). Each trial consisted of 90-min cycling at 60% VO(2) max in a 35°C environment followed by 3-h rehydration (RH). During RH, subjects received either 150% of sweat loss (LCDH & HCDH) or an additional 50% of sweat loss (LCEH and HCEH). Blood was analyzed for glucose, IL-6, ADH, and Na(+). Post-exercise Na(+) was greater (p < 0.001) for LCDH and HCDH (141.7 + 0.72 and 141.6 + 0.4 mM) versus LCEH and HCEH (136.4 + 0.6 and 135.9 + 0.3 mM). Post-exercise IL-6 was similar in all conditions, and post-exercise ADH was greater (p = 0.01) in dehydrated versus euhydrated conditions. The rate of urine production was greater in HCEH (7.59 + 3.0 mL/min) compared to all other conditions (3.86 + 2.2, 5.29 + 3.1, and 2.96 + 1.1 mL/min for LCDH, LCEH, and HCDH, respectively). Despite CHO and hydration manipulations, no regulatory effects of IL-6 and ADH on plasma [Na(+)] were observed. With euhydration during exercise and additional fluid consumed during recovery, a high-CHO status increased urinary output during recovery, and it decreased the frequency of hyponatremia (Na(+) < 135 mM). Therefore, a high-CHO status may provide some protection against exercise-associated hyponatremia.

Resistance and aerobic exercise: the influence of mode on the relationship between IL-6 and glucose tolerance in young men who are obese.

Regular exercise lowers indicators of disease risk including some inflammatory cytokines; however, the relationship between different modes of acute exercise, cytokine levels, and subsequent glucose tolerance is unclear. The purpose was to determine the effects of resistance (RES) and aerobic (AER) exercises on interleukin-6 (IL-6) and its association with glucose tolerance 24 hours after exercise. After testing for 1 repetition maximum (1RM) and VO2peak, 10 obese (body mass index > 30 kg · m(-2)), untrained men aged 18-26 years completed 3 protocols: 60 minutes of RES, AER, and a resting (CON) condition. The RES was 2 sets of 8 repetitions and a third set to fatigue at 80% 1RM of 8 lifts using all major muscle groups. The AER was 60 minutes of cycling at 70% of VO2peak. On day 1, subjects completed the 60-minute exercise or resting protocol, and on day 2, they completed an oral glucose tolerance test (OGTT). Blood was collected before and after exercise, at 2 and 7 hour postexercise, and before and every 30 minutes during the OGTT and was analyzed for IL-6, glucose and insulin. Postexercise IL-6 was greater in RES (8.01 ± 2.08 pg · mL(-1)) vs. in AER (4.26 ± 0.27 pg · mL(-1)), and both were greater than in CON (1.61 ± 0.18 pg · mL(-1)). During the OGTT, there were no differences in glucose or insulin between conditions for single time points or as area under the curve. The RES caused greater IL-6 levels immediately after exercise that may be related to the greater active muscle mass compared to AER. Neither exercise produced enhanced glucose removal compared to control; thus, despite the greater elevation in IL-6 in RES, for these exercise conditions and this population, this cytokine did not influence glucose tolerance.

Mucosal-Associated Invariant T Cell Response to Acute Exercise and Exercise Training in Older Obese Women.

(1) Background: Obesity is a major global public health concern as it is associated with many of the leading causes of preventable deaths. Exercise reduces obesity-induced inflammation; however, it is unknown how exercise training may impact mucosal associated invariant T (MAIT) cells in overweight/obese (OW) post-menopausal women. Therefore, the purpose of this study was to investigate (i) circulating MAIT-cells at rest in OW vs. Lean women, (ii) the response of MAIT-cells to a single bout of combined aerobic and resistance exercise, and (iii) the effects of 12 weeks of exercise training (EX) or educational program (ED) on the MAIT-cell response in OW. (2) Methods: OW completed an acute exercise session or sitting control, underwent 12 weeks of exercise training or received educational materials, and then repeated the exercise session/sitting control. Lean post-menopausal women provided a baseline comparison. (3) Results: OW had lower circulating MAIT-cells at rest than Lean prior to exercise training; however, after training EX displayed improved MAIT-cell frequency. Additionally, prior to training EX did not exhibit MAIT-cell mobilization/egress, however, both improved after training. (4) Conclusions: Reduced MAIT-cell frequency and ability to mobilize/egress were potentially partially rescued in EX after 12 weeks of exercise training; however, further research is needed to elucidate age or obesity-induced attenuations in MAIT-cells.

Influence of commonly employed resistance exercise protocols on circulating IL-6 and indices of insulin sensitivity.

The purpose of this project was to examine the influence of resistance exercise (RE) intensities, resulting in different total volume loads on circulating interleukin-6 (IL-6), insulin and glucose response (IGR) to a carbohydrate feeding (CHO), and whether RE-induced IL-6 was associated with postexercise IGR. Fourteen men (21.7 +/- 1.7 years, 83 +/- 14.2 kg), performed 2 RE sessions (low-intensity resulting in high volume [65% 1-repetition maximum (1RM)], LO; high intensity resulting in low volume [85% 1RM], HI); and a nonexercise control trial (CON). Resistance exercise included 3 sets (LO = 12 reps, 12 reps, and failure; HI = 8 reps, 8 reps, and failure) of 8 exercises. Blood was obtained pre- (PR) and post (PO) exercise, and 6 hours postexercise (6H). Twenty-three hours after RE or CON, participants consumed 100 g dextrose (CHO) beverage. Blood was collected before (0 minutes) and 60 minutes after CHO (n = 6, phase 1) or every 30 minutes for a 2-hour oral glucose tolerance test (n = 8; phase 2). Circulating IL-6, insulin, and glucose were analyzed via enzyme-linked immunosorbent assay, radioimmunoassay, and enzymatic methods, respectively. Total volume load was higher in LO (17,729 +/- 1,466 kg) compared with HI (13,160 +/- 1,097 kg; p < 0.001). Postexercise IL-6 was elevated (p = 0.003) in LO and HI compared with CON (7.4 +/- 1.3, 5.2 +/- 0.7, and 2.5 +/- 0.7 pg.mL, respectively), with LO IL-6 greater than HI. Areas under the curve for glucose (p = 0.081; CON: 741 +/- 46, LO: 690 +/- 28, and HI: 660 +/- 21 mM.min) and insulin (p = 0.075; CON: 6,818 +/- 1,018, LO: 5,056 +/- 869, and HI: 5,405 +/- 1,076 microIU.mL) were not different among trials (n = 8). When 0- and 60-minute values were compared (n = 14), insulin was lower at 60 minutes in LO and HI compared with CON (55 + 9.1, 83 +/- 13, 105 +/- 13 microIU.mL, respectively) with LO insulin being lower than HI (p < 0.001). No relationship was observed between PO IL-6 and IGR, but PR IL-6 was negatively related to both PR (r = -0.043, p < 0.05) and 60 minutes (r = -0.59, p < 0.01) glucose (n = 14). These results indicate that TVL contributes to RE-induced IL-6 release and that TVL may be more important than RE intensity when improvements in glucose tolerance or IS are the goal.

Behavioral immune system activity predicts downregulation of chronic basal inflammation.

Here, we present a mechanistically grounded theory detailing a novel function of the behavioral immune system (BIS), the psychological system that prompts pathogen avoidance behaviors. We propose that BIS activity allows the body to downregulate basal inflammation, preventing resultant oxidative damage to DNA and promoting longevity. Study 1 investigated the relationship between a trait measure of pathogen avoidance motivation and in vitro and in vivo proinflammatory cytokine production. Study 2 examined the relationship between this same predictor and DNA damage often associated with prolonged inflammation. Results revealed that greater trait pathogen avoidance motivation predicts a) lower levels of spontaneous (but not stimulated) proinflammatory cytokine release by peripheral blood mononuclear cells (PBMCs), b) lower plasma levels of the proinflammatory cytokine interleukin-6 (IL-6), and c) lower levels of oxidative DNA damage. Thus, the BIS may promote health by protecting the body from the deleterious effects of inflammation and oxidative stress.

Chronic resistance exercise training improves natural killer cell activity in older women.

BACKGROUND: Regular exercise has been reported to slow the age-associated declines in natural killer cell activity (NKCA). To evaluate this response, we recruited older, postmenopausal women (65-85 years old) to fill one of two groups: training (10 weeks of resistance exercise; TR) or control. METHODS: Blood samples were collected from an arm vein in the TR group at rest (PRE), immediately following (POST), and 2 hours (2H) following an acute bout of resistance exercise both before (BEFORE) and after (AFTER) training. Leukocytes and NKCA were determined by flow cytometry and a whole blood (51)Cr release assay, respectively. RESULTS: Acute exercise increased total leukocyte (p < .05), CD8 (p < .05), CD4 (p < .05), and CD56 counts (p < .05), but there was no effect of training. NKCA was greater TR-AFTER-PRE (136%), -POST (80%), and -2H (127%) compared to similar values from TR-BEFORE (p < .05). CONCLUSION: Increased resting NKCA after chronic resistance training suggests that immunity has been improved.

Toll-like receptor 4 and CD14 mRNA expression are lower in resistive exercise-trained elderly women.

The purpose of this study was to examine the influence of resistive exercise training and hormone status on mRNA expression of toll-like receptor 4 (TLR4), CD14, IL-1beta, IL-6, and TNF-alpha. Resistive exercise-trained women on "traditional" hormone replacements [hormone replacement therapy (HRT), n = 9], not taking hormones (NHR, n = 6), or taking medications known to influence bone (MIB, n = 7) were compared with untrained subjects not taking supplemental hormones (Con, n = 6). Blood was taken from trained subjects before, immediately after, and 2 h after resistive exercise (same time points for resting Con). TLR4 mRNA expression (RT-PCR) was not different among groups or across time but was significantly (P = 0.044) lower (1.9-fold) when trained groups were collapsed and compared with Con. There was also a significant group effect (P < 0.0001) for TLR4 mRNA when expressed per monocyte. CD14 expression was significantly (P = 0.006) lower (2.3-fold) for training groups collapsed and compared with Con. CD14 mRNA, expressed per monocyte, was significantly lower immediately after resistive exercise for NHR, HRT, and MIB compared with Con. There were few significant effects detected for IL-6, IL-1beta, and TNF-alpha mRNA, but there was a significant group effect (P < 0.0001) for TNF-alpha mRNA expressed per monocyte (Con > HRT, NHR, MIB). These findings suggest that there may be a resistive exercise training-induced reduction in TLR4/CD14 expression in older women. Further research is needed to determine whether lower TLR4/CD14 could explain the lower LPS-stimulated inflammatory cytokines observed in these women.

Resistance training reduces subclinical inflammation in obese, postmenopausal women.

PURPOSE: Aerobic exercise is frequently prescribed to reduce inflammatory-related disease (cardiovascular disease and diabetes) risk. Resistance training (RT), however, may be key to maximizing anti-inflammatory benefits of consistent exercise. We examined the influence of RT on inflammatory biomarkers in obese, postmenopausal women. METHODS: Twenty-three women (65.6 ± 2.6 yr; body mass index, 33 kg·m) underwent 12 wk of RT (3 sets, 10 exercises, 3× per week, 8-12 repetition maximum (RM), resistance exercise (EX), N = 11) or social interaction intervention (SI, stretching, knitting, health lectures, 2× per week, control group (CON), N = 12). Both before (BT) and after (AT) RT or SI, blood was collected before (PR), immediately (PO), 2 h (2H), and 24 h (24H) after a single resistance exercise bout (RE) in EX and at the same time points in nonexercise, resting CON. For all time points, blood was analyzed for IL-6, leptin, and lipopolysaccharide (LPS)-stimulated tumor necrosis factor-α (TNF-α) (LPS-TNF) and IL-10 (LPS-IL10). PR samples were also examined for C-reactive protein, TNF-α, and adiponectin, and mRNA expression of toll-like receptor 4 (TLR4) and MC1R. Subcutaneous adipose tissue was extracted BT and AT and analyzed for mRNA expression of monocyte chemotactic protein-1, leptin, CD68, and TLR4. RESULTS: RT improved strength (44%) and reduced circulating C-reactive protein (-33%), leptin (-18%) and TNF-α (-29%) with no change in body composition. IL-6 decreased after SI in CON (-17%). LPS-TNF increased after SI or RT (CON +26%, EX +67%, respectively), whereas LPS-IL10 decreased in CON (-28%) but increased in EX (+20%). RT did not influence inflammatory biomarker gene expression in whole blood or subcutaneous adipose tissue. A single RE bout augmented LPS-TNF and LPS-IL10 at 24H in EX, particularly AT. CONCLUSION: RT reduced markers of subclinical inflammation in circulation in obese, postmenopausal women in the absence of changes in body composition. Chronic RT also enhanced response to endotoxin challenge both at rest (PR) and 24 h after an acute RE bout (24H).

The melanocortin 3 receptor: a novel mediator of exercise-induced inflammation reduction in postmenopausal women?

The purpose of this study was to determine whether resistance exercise training-induced reductions in inflammation are mediated via melanocortin 3 receptor expression in obese (BMI 32.7 ± 3.7) women (65.6 ± 2.8 yrs) randomized to either a control (N = 11) or resistance training group (N = 12). The resistance trained group performed resistance training 3 days/week for 12 weeks. Resting blood samples were collected before and after the training intervention in both resistance trained and control groups. Resistance training upregulated melanocortin 3 receptor mRNA by 16-fold (P = .035) and decreased monocyte count, without changing leukocyte number, body composition, or body weight. Resistance trained individuals exhibited increased sensitivity to inflammatory stimuli, whereas control individuals exhibited no change. While there was no change in whole blood tumor necrosis factor alpha mRNA between the groups, whole blood interleukin 10 mRNA was higher in the resistance trained group following the intervention period. In summary, it appears that resistance training may modulate melanocortin 3 receptor expression, providing a possible mechanism for the anti-inflammatory effects of exercise training.

Resistance training at eight-repetition maximum reduces the inflammatory milieu in elderly women.

INTRODUCTION/PURPOSE: Inflammatory cytokines are associated with age- and inactivity-related diseases. We examined the influence of moderate- to high-intensity resistance trainings (RT) on inflammatory cytokines (interleukin 6 (IL-6) and 1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha)) in circulation and lipopolysaccharide (LPS)-stimulated whole blood in elderly women. METHOD: Previously sedentary women (72 +/- 6.1 yr) were grouped according to their hormone replacement regimen: traditional estrogen/progesterone (HRT, n = 12), selective estrogen receptor modulator (SER, n = 7), no hormone replacement (NHR, n = 9), or nonexercise control group taking no hormone replacement (CON, n = 7). Participants in the HRT, SER, and NHR groups trained (three sets, 10 exercises at eight-repetition maximum (8RM)) 3 d x wk(-1), whereas participants in the CON group maintained their "normal" activity for 10 wk. Participants performed a bout of resistance exercise (RE at 8RM; HRT, SER, and NHR groups) or sat quietly (CON) before (BT) and after (AT) RT to assess the influence of training on the acute responses to RE. Blood samples were obtained preexercise (PR), postexercise (PO), and 2 h postexercise (2H; same time points for resting CON). RESULTS: Hormone status had no influence on dependent variables, so HRT, SER, and NHR groups were collapsed into one exercise group (EX, n = 28) and compared with CON. RT significantly reduced resting serum TNF-alpha level by 37%. RT also reduced LPS-stimulated production of IL-6, IL-1beta, and TNF-alpha at all time points (PR, PO, and 2H; per monocyte). Acute RE transiently increased plasma TNF-alpha, but blunted the circadian increase in LPS-stimulated inflammatory cytokines observed in CON. The blunting effect in EX was significantly greater AT compared with BT. RE also resulted in an increase in plasma IL-6, which was significantly reduced AT (BT: PR = 1.6 +/- 0.5, PO = 2.8 +/- 0.5; AT: PR = 1.8 +/- 0.3, PO = 2.4 +/- 0.3). CONCLUSIONS: We found that 10 wk of moderate- to high-intensity RT 1) reduced the systemic inflammatory milieu and 2) abrogated exercise-induced circulating IL-6 in previously sedentary elderly women.