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The present investigation examined the ability of two threshold detection analyses (maximum distance, Dmax; modified maximum distance, mDmax) in identifying the near-infrared spectroscopy (NIRS) threshold, a lactate threshold (LT) estimate, from exercising tissue oxygen saturation (StO(2)) responses. Additionally, the test-retest reliability of exercising StO(2) and total hemoglobin concentration (THC) responses were examined at moderate and peak cycling intensities. Fourteen healthy, recreationally active participants performed maximal incremental step cycling tests (+25 W / 3 minutes) to volitional fatigue on two separate occasions while StO(2) and THC of the vastus lateralis were monitored. Exercising blood [lactate] was collected during Session One. LT and NIRS thresholds (NIRS1, NIRS2) were then determined using Dmax and mDmax threshold analyses. Significant (p < 0.05), moderate correlations were detected between LT and NIRS1 when using Dmax (LT = 130 ± 49 W, NIRS1 = 136 ± 34 W, r = 0.690), but not for mDmax (r = 0.487). No significant test-retest reliability for the NIRS thresholds were observed for Dmax (ICC = 0.351) or mDmax (ICC = 0.385). Exercising StO(2) responses demonstrated good reliability (ICC = 0.841–0.873) while exercising THC responses demonstrated moderate-good reliability (ICC = 0.720–0.873) at moderate and peak exercise intensities. The results of this study suggest that neither the Dmax nor mDmax threshold analyses should be used to estimate the LT due to the unreliable detection of the NIRS threshold from session to session.

The purpose of this study was to determine how differences in hydration states and ion content of hydrating fluids affected bioelectrical impedance (BI) and hydrostatic weighing (HW) measurements.Fifteen athletic subjects aged 19-56 yr were recruited. Relative body fat (%), fat-weight (FW), and fat-free weight (FFW) were assessed using BI and HW under normal conditions (N), hypohydration (HPO), rehydration (RHY), and superhydration (SHY) states. During the RHY and SHY trial periods, subjects were hydrated with either distilled water or an electrolyte solution (ELS). HPO and SHY levels were set at 3% of each person's normally hydrated body weight.Comparison between the distilled water and the ELS trials indicated that hydration solution had no effect on BI or HW. Thus, the results presented are the trial means of both hydration solutions combined. Both BI and HW were shown to be highly test-retest reliable (r-values: 0.96 and 0.99, respectively). The effects of exercise induced HPO followed by RHY on body composition values indicated that HW was very stable across measurement periods while BI was not. From N to the HPO state, BI %BF declined from 14.4 +/- 5.3% to 12.3 +/- 5.3%, respectively. After RHY, BIA %BF increased to 15.5 +/- 5.8%. Similar findings occurred when subjects were superhydrated (N-BI = 13.2 +/- 5.3%; SHY-BI = 15.4 +/- 5.6%). With a comparison of the intercepts and slopes of HW and BIA for the N and SHY states, it was clear hydration status significantly affected the intercepts (HW: 0.37 vs. BI: 1.85) and not the slopes (HW: 1.00 vs BI: 0.99). As a result, a majority of all fluid changes were interpreted as FW by BI. During HPO, 82% of the weight loss was considered FW while during RHY or SHY, 128% and 85% of the water weight regain/gain was considered FW.These results indicate that BI is not a valid technique in athletes, especially when wanting to determine body composition effects of training/detraining. This study indicates that even small fluid changes such as those that occur with endurance training may be interpreted incorrectly as changes in an athlete's body fat content.

This study's purpose was to determine the validity of near-infrared interactance (NIR) and bioelectric impedance (BIA) in tracking changes in body composition over 12 wk of either a high intensity endurance (ET) or resistance (RT) training program in nondieting weight-stable untrained males. Prior to and following the control or training period, each subject completed a series of body composition analyses including hydrostatic weighing (HW) with a measurement of residual volume: anthropometric measurements including height, weight, skinfold, and girth: BIA measurement: and NIR measurements. Based on the HW results, there were no significant body composition changes in the control group. For the ET group, a significant decline in relative body fat resulted from a reduction in fat weight (FW) with no change in fat-free weight (FFW). In the RT group, both a significant decline in FW and an increase in FFW contributed to this group's decline in relative body fat. Tracking changes in relative body fat, FW, and FFW, skinfolds agree reasonably well with HW in all groups while BIA and NIR did not always track body composition changes well. For example, SF and BIA were significantly correlated with the changes in FFW (HW = +4.1%, SF = +4.5%. BIA = +3.1%. NIR = -0.7%) observed in the RT group compared to HW (SF: r-value = 0.45, SEE = 2.5; BIA: r = 0.33, SEE = 3.4) while the NIR measurements were nonsignificant (r = 0.09, SEE = 5.0). Interestingly, NIR underestimated the gain in FFW in the resistance trained group while BIA underestimated the changes in relative body fat. FW, and FFW in the endurance trained group. Based on these results, BIA and NIR appear not to be appropriate measurement tools for tracking body composition changes in endurance and resistance training individuals respectively.

To investigate the influence of intensity versus total energy expenditure on neutrophilia and blood oxidative stress to acute exercise.Nine males (18-30 yr) completed one maximal (Max) and three submaximal exercise sessions: 1) 45 min at 10% above (LT+) lactate threshold (LT), 2) 45 min at 10% below (LT-) LT, and 3) 10% below LT until caloric expenditure equaled the 10%+ trial (LT-kcal). Blood was sampled before (PRE), immediately (POST), 1 h, and 2 h after exercise to measure neutrophils, myeloperoxidase, superoxide (O(2)-), neutrophil activation (O(2)-/neutrophils), ascorbic acid, uric acid, malondialdehyde, and lipid hydroperoxides.Intensity-dependent neutrophilia occurred POST exercise with significant increases (Por= 0.05) after Max and LT+. A second neutrophilia wave occurred 2 h postexercise. Superoxide was elevated POST (Max) and 2 h post (Max and LT+). In contrast, O(2)-/neutrophils was increased at 2 h only (Max and LT+). These data indicate that immediately postexercise, total neutrophil number rather than activation best represents neutrophil-generated reactive species within blood. POST Max, ascorbic acid and uric acid were decreased indicating a blood oxidative stress occurred. Alternately, total energy expenditure was not related to any marker of neutrophilia or oxidative stress.Exercise intensity plays a major role in postexercise blood oxidative stress, whereas total exercise energy expenditure does not. Further, neutrophils recruited into circulation during exercise may impose a threshold dependent oxidative stress in blood plasma after exercise.

Background Since the passage of The Dietary Supplement Health and Education Act in 1994, there has been a flood of new "dietary" supplements promoting anti-aging benefits such as the enhancement of growth hormone or testosterone levels. Androstenediol and androstenedione are such products. This study's purpose was to elucidate the physiological and hormonal effects of 200 mg/d of oral androstenediol and androstenedione supplementation in men aged 35 to 65 years while participating in a 12-week high-intensity resistance training program. Methods Fifty men not consuming any androgenic-enhancing substances and with normal total testosterone levels, prostate-specific antigen, hemoglobin, and hematocrit, and with no sign of cardiovascular or metabolic diseases participated. Subjects were randomly assigned to a placebo, androstenediol (diol), or androstenedione (dione) group using a double-blind study design. Main outcomes included serum sex hormone profile, body composition assessment, muscular strength, and blood lipid profiles. Results During the 12 weeks of androstenedione or androstenediol use, a significant increase in the aromatization by-products estrone and estradiol was observed in both groups ( P = .03). In the dione group, total testosterone levels significantly increased 16% after 1 month of use, but by the end of 12 weeks, they returned to pretreatment levels. This return to baseline levels resulted from increases in aromatization and down-regulation in endogenous testosterone synthesis based on the fact that luteinizing hormone was attenuated 18% to 33% during the treatment period. Neither androstenediol nor androstenedione enhanced the adaptations to resistance training compared with placebo for body composition or muscular strength. However, both androstenediol and androstenedione supplementation adversely affected high-density lipoprotein cholesterol (HDL-C) levels, coronary heart disease risk (representing a 6.5% increase), and each group's respective (low-density lipoprotein cholesterol [LDL-C]/HDL-C)/(apolipoprotein A/apolipoprotein B) lipid ratio (diol: +5.2%; dione: +10.5%; P = .05). In contrast, the placebo group's HDL-C levels increased 5.1%, with a 12.3% decline in the (LDL-C/HDL-C)/(apolipoprotein A/apolipoprotein B) lipid ratio. These negative and positive lipid effects occurred despite no significant alterations in body composition or dietary intakes in the supplemental groups or placebo group, respectively. Conclusions Testosterone precursors do not enhance adaptations to resistance training when consumed in dosages recommended by manufacturers. Testosterone precursor supplementation does result in significant increases in estrogen-related compounds, dehydroepiandrosterone sulfate concentrations, down-regulation in testosterone synthesis, and unfavorable alterations in blood lipid and coronary heart disease risk profiles of men aged 35 to 65 years.