Systemic LPS and inflammatory response during consecutive days of exercise in heat.

This investigation studied circulating LPS activity, potential intestinal damage, and the systemic inflammatory response (SIR) during the exercise heat acclimation process. 8 healthy males (Age=24±3 years) ran in a hot environment on 5 consecutive days until core temperature (Tc) was elevated 2°C above rest. Plasma was obtained pre-, post-, 1 h post-, and 3 h post-exercise on the 1(st), 3(rd), and 5(th) day of exercise and analyzed for TNF-α, IL-6, IL-10, IL-1ra, LPS, and intestinal fatty acid-binding protein (I-FABP). Plasma LPS (1.1 EU·ml(-1)±0.1 vs. 0.7 EU·ml(-1)±0.03; P<0.01) and I-FABP (930.7 pg·ml(-1)±149.0 vs. 640.2 pg·ml(-1)±125.0; P<0.001) were significantly increased post-exercise each. The SIR remained largely unchanged during the study except for TNF-α. Plasma TNF-α was significantly lower on Day 5 at 1 h (3.2 pg·ml(-1)±0.6 vs. 4.5 pg·ml(-1)±0.8; P=0.01) and 3 h (3.6 pg·ml(-1)±0.8 vs. 4.8 pg·ml(-1)±0.9; P=0.05) post-exercise as compared to Day 1. Findings indicate that adaptations to exercise in the heat resulting in reductions of intestinal damage and plasma LPS activity require longer time periods in moderately trained males.

Acute regulation of IGF-I by alterations in post-exercise macronutrients.

This investigation sought to examine the contributions of exercise and nutrient replenishment on in vivo regulation of the insulin-like growth factor-I (IGF-I) axis components. Eight college-aged males completed three high-intensity interval training (HIIT) protocols followed by three post-exercise nutritional protocols: (1) placebo (EX); (2) carbohydrate only (CHO); and (3) essential amino acid/carbohydrate (EAA/CHO). Samples were analyzed for growth hormone (GH), free IGF-I, IGFBP-1, IGFBP-2, insulin, hematocrit, hemoglobin, serum leucine, matrix metalloproteinase-9 (MMP-9) proteolytic activity, and presence of IGFBP-3 protease activity. No evidence for IGFBP-3 proteolysis was observed. Significant increases in [free IGF-I] and [leucine] were observed in the EAA/CHO group only. Significant differences were noted in [IGFBP-1] and [IGFBP-2] across conditions. Significant increases in [GH] and MMP-9 activity were observed in all groups. These results indicate that post-exercise macronutrient ratio is a determinant of [free IGF-I], [IGFBP-1 and -2] and may play a role in modulating the IGF-I axis in vivo.

Muscle glycogenolysis during differing intensities of weight-resistance exercise.

Skeletal muscle glycogen metabolism was investigated in eight male subjects during and after six sets of 70% one repetition maximum (1 RM, I-70) and 35% 1 RM (I-35) intensity weight-resistance leg extension exercise. Total force application to the machine lever arm was determined via a strain gauge and computer interfaced system and was equated between trials. Compared with the I-70 trial, the I-35 trial was characterized by almost double the repetitions (13 +/- 1 vs. 6 +/- 0) and half the peak concentric torque for each repetition (12.4 +/- 0.5 vs. 24.2 +/- 1.0 Nm). After the sixth set, muscle glycogen degradation was similar between I-70 and I-35 trials (47.0 +/- 6.6 and 46.6 +/- 6.0 mmol/kg wet wt, respectively), as was muscle lactate accumulation (13.8 +/- 0.7 and 16.7 +/- 4.2 mmol/kg wet wt, respectively). After 2 h of passive recovery without caloric intake, muscle glycogen increased by 22.2 +/- 6.8 and 14.2 +/- 2.5 mmol/kg wet wt in the I-70 and I-35 trials, respectively. Optical absorbance measurement of periodic acid-Schiff-stained muscle sections after the 2 h of recovery revealed larger absorbance increases in fast-twitch than in slow-twitch fibers (0.119 +/- 0.024 and 0.055 +/- 0.024, P = 0.02). Data indicated that when external work was constant, the absolute amount of muscle glycogenolysis was the same regardless of the intensity of resistance exercise. Nevertheless the rate of glycogenolysis during the I-70 trial was approximately double that of the I-35 trial.

Impaired muscle glycogen resynthesis after eccentric exercise.

Eight men performed 10 sets of 10 eccentric contractions of the knee extensor muscles with one leg [eccentrically exercised leg (EL)]. The weight used for this exercise was 120% of the maximal extension strength. After 30 min of rest the subjects performed two-legged cycling [concentrically exercised leg (CL)] at 74% of maximal O2 uptake for 1 h. In the 3 days after this exercise four subjects consumed diets containing 4.25 g CHO/kg body wt, and the remainder were fed 8.5 g CHO/kg. All subjects experienced severe muscle soreness and edema in the quadriceps muscles of the eccentrically exercised leg. Mean (+/- SE) resting serum creatine kinase increased from a preexercise level of 57 +/- 3 to 6,988 +/- 1,913 U/l on the 3rd day of recovery. The glycogen content (mmol/kg dry wt) in the vastus lateralis of CL muscles averaged 90, 395, and 592 mmol/kg dry wt at 0, 24, and 72 h of recovery. The EL muscle, on the other hand, averaged 168, 329, and 435 mmol/kg dry wt at these same intervals. Subjects receiving 8.5 g CHO/kg stored significantly more glycogen than those who were fed 4.3 g CHO/kg. In both groups, however, significantly less glycogen was stored in the EL than in the CL.

Influence of carbohydrate dosage on exercise performance and glycogen metabolism.

This study was undertaken to examine the effects of ingestion of carbohydrate (CHO) solutions of 0 (WP), 6 (CHO-6), 12 (CHO-12), and 18 g CHO/100 ml (CHO-18) on performance and muscle glycogen use. Ten trained cyclists performed five 120-min cycling trials. The first 105 min of each trial was at 70% of maximal O2 consumption (VO2max), and the final 15 min was an all-out performance ride on an isokinetic cycle ergometer equipped to measure total work output. In one of the trials (CHO-12I) the submaximal portion of the ride consisted of seven 15-min rides at 70% of VO2max with a 3-min rest between each ride. Every 15 min the men consumed 8.5 ml.kg-1.h-1 (approximately 150 ml) of one of the four test solutions. Venous blood samples were obtained every 15 min for glucose and insulin. Muscle biopsies were obtained from the vastus lateralis at 0 and 105 min in the WP and the CHO-12 continuous and intermittent trials. Biopsy samples were assayed for glycogen and sectioned and stained for myosin adenosinetriphosphatase and glycogen for single fiber depletion measurements. There were no differences in glycogen use (86.7 +/- 6.0, 75.5 +/- 7.9, and 83.5 +/- 5.5 mmol/kg for the WP, CHO-12C, and CHO-12I, respectively) or depletion patterns between the WP and the two CHO-12 trials. Blood glucose was significantly elevated in both the CHO-12 trials and in the CHO-18 trial compared with the WP trial.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscle glycogen resynthesis after short term, high intensity exercise and resistance exercise.

Typical rates of muscle glycogen resynthesis after short term, high intensity exercise (15.1 to 33.6 mmol/kg/h) are much higher than glycogen resynthesis rates following prolonged exercise (approximately 2 mmol/kg/h), even when optimal amounts of oral carbohydrate are supplied (approximately mmol/kg/h). Several factors differ during post-exercise recovery from short term, high intensity exercise compared with prolonged exercise. The extremely fast rate of muscle glycogen resynthesis following short term, high intensity exercise may originate from these differences. First, peak blood glucose levels range from 6.6 to 8.9 mmol/L during recovery from short term, high intensity exercise. This is markedly higher than the blood glucose values of 2 to 3.4 mmol/L after prolonged exercise. In response to this elevation in plasma glucose levels, insulin levels increase to approximately 60 microU/ml, a 2-fold increase over resting values. Both glucose and insulin regulate glycogen synthase activity, and higher levels of them improve muscle glycogen synthesis. Secondly, high intensity exercise produces high levels of glycolytic intermediates in muscle, as well as high lactate levels ([La]) in muscle and blood. Finally, fast-twitch glycolytic muscle fibres are more heavily used in short term, high intensity exercise. This promotes greater glycogen depletion in the fast-twitch fibres, which have a higher level of glycogen synthase activity than slow-twitch fibres. While the exact contribution of each of these factors is unknown, they may act in combination to stimulate rapid muscle glycogen resynthesis rates. Muscle glycogen resynthesis rates following resistance exercise (1.3 to 11.1 mmol/kg/h) are slower than the rates observed after short term, high intensity exercise. This may be caused by slightly lower muscle and blood [La] after resistance exercise. In addition, a greater eccentric component in the resistance exercise may cause some interference with glycogen resynthesis.

Clothing and exercise. I: Biophysics of heat transfer between the individual, clothing and environment.

Despite large environmental variations, the human body maintains a tightly regulated core temperature. Effective thermoregulation must balance the interaction between skin surface, clothing and ambient air. Indices of thermal stress (wet bulb globe temperature, heat stress index, maximum evaporation rate, required evaporative rate and wind chill) provide valuable information concerning the heat exchange between the individual and the environment, and serve as protective guidelines while working in environmental extremes. The role of clothing, as an interactive barrier, greatly affects thermal balance. Clothing is varied according to prevailing environmental conditions, metabolic heat production, gender and age differences, fabric thermal properties, garment design and intended use. Models (static, dynamic and human) have investigated the biophysical transfer of heat between the skin surface area, clothing and ambient air. Additionally, the role of metabolic heat production during exercise can greatly influence tolerance to thermal stress during a variety of environmental conditions.

Clothing and exercise. II. Influence of clothing during exercise/work in environmental extremes.

Thermoregulatory studies often investigate thermal responses without considering the influences of clothing. These studies have expanded our understanding of basic human responses to various environmental conditions. However, human thermoregulation is variable and modified by heat transfer interactions between skin surface area, clothing and environment. Much of the original work on the influence of clothing on work performance was the result of ergonomic concerns. Currently, the importance of clothing and the influence of new clothing technology aimed at minimising thermal stress has spawned a new interest. For hot climates, new fabrics have been developed with improved wicking properties to keep the wearer cooler and drier, and to enhance heat transfer from the body while providing greater comfort. In contrast, the challenge of cold environments requires a different approach to clothing, which tries to minimise the free movement of air and water along the skin surface of the body. The materials used should also be able to absorb radiant heat from the environment and be nonconductive. In a cold climate, the wearer needs to balance the need for a clothing barrier for warmth with the potential for accumulating too much heat as the result of metabolic heat production from exercise. To counteract this potential problem, it is suggested that cold-weather clothing be worn in layers that can be removed during exercise and replaced during less active periods. Protective clothing for firefighters, hazardous waste workers and astronauts, and athletic protective gear, have specialised design requirements which may be influenced by considerations, for example, of environmental conditions, garment weight, the need for durability, impact forces.

Influence of muscle glycogen depletion on the rate of resynthesis.

In an effort to determine what effect the degree of muscle glycogen depletion has on the rate of resynthesis, six male cyclists completed an exercise protocol that involved both one- and two-legged cycling. One leg completed 30 min of single-leg cycling, ten one-min sprints, and 30 min cycling with both legs. This resulted in a large degree of depletion (LD). The contralateral leg completed only 30 min of double-leg cycling and experienced a small amount of depletion (SD). Following the exercise, the subjects rested quietly for 6 h and were fed a 24% carbohydrate (CHO) solution every 20 min in order to achieve a CHO intake of 0.7 g.kg-1.h-1. Biopsies taken from the vastus lateralis muscle immediately after exercise revealed that the glycogen content of the LD leg decreased 93.9 (+/- 11.6) mmol.kg-1 w.w., whereas the SD leg used 49.3 (+/- 5.7) mmol.kg-1 w.w. (P less than 0.01). Subsequent biopsies taken at 2 and 6 h of recovery demonstrated that the rate of muscle glycogen resynthesis was significantly greater in the LD leg, averaging 8.8 (+/- 2.4) mmol.kg-1.h1 w.w, while the SD leg restored glycogen at a rate of 3.0 (+/- 1.0) mmol.kg-1.h-1 w.w. (P less than 0.05). Glycogen synthase activity, expressed as its activity ratio (I/D), was also greater (P less than 0.01) in the LD leg both immediately after exercise (0.45 +/- 0.05 vs 0.24 +/- 0.04) and at 2 h of recovery (0.54 +/- 0.06 vs 0.27 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Lactate distribution in the blood during progressive exercise.

The purpose of this study was to examine the effect of increment durations of 1-min and 4-min during progressive incremental exercise tests on: 1) the distribution of lactate between plasma and red blood cells (RBCs), and 2) lactate threshold (LT) detection via three conventional methods using whole blood lactate concentration ([La]) or plasma [La]. Eight males (age, 22.5 +/- 0.6 yr: height, 170.6 +/- 2.3 cm, weight, 76.0 +/- 3.1 kg, and VO2peak, 42.8 +/- 2.0 mL.kg-1.min-1) performed two progressive load tests to volitional fatigue on a cycle ergometer. Work rate was increased 30 W at 1-min or 4-min intervals. All data were normalized to individual LT work rates. For both protocols, whole blood [La], plasma [La], RBC [La], and [La] gradient increased significantly (P < 0.05) after exercise intensity exceeded LT. However, the RBC:plasma [La] ratio remained at the resting value throughout the progressive exercise tests. The increase in [La] gradient after LT, with no change in the RBC:plasma lactate ratio, suggests that given an incremental work rate increase of 30 W, 1 min is adequate for equilibration of lactate between the plasma and RBCs. Also, under the conditions of this investigation, neither blood fraction analyzed nor exercise protocol had any effect on estimations of LT (in terms of VO2) by the Visual and Log-Log methods. However, LT determined by a fixed [La] of 2 mM may underestimate LT when plasma samples are used.

Lactate distribution in the blood during steady-state exercise.

PURPOSE: The purpose of this investigation was to examine the plasma to red blood cell (RBC) lactate concentration ([La]) gradient and RBC:plasma [La] ratio during 30 min of steady-state cycle ergometer exercise at work rates below lactate threshold ( LT. Blood samples were taken from a heated forearm vein, immediately cooled to 4 degrees C in a dry-ice ethanol slurry, and centrifuged at 4 degrees C to separate plasma and RBCs. RESULTS: During >LT, plasma [La] rose to 8.8+/-1.1 mM after 10 min and remained above 6 mM. RBC [La] (4.9+/-0.7 mM) was significantly lower than plasma [La] at 10 min and remained lower throughout exercise. As a result, there was a sizable [La] gradient (approximately 3.5 mM) from plasma to RBC during most of >LT. In LT, the ratio of RBC [La]:plasma [La] was the same for both (0.58+/-0.02) and not significantly different from rest. CONCLUSIONS: These results refuted our hypothesis that the RBC:plasma [La] ratio would decrease at the onset of >LT exercise because of muscle lactate release exceeding the ability of RBCs to take up the lactate. Instead, there appears to be an equilibrium between plasma [La] and RBC [La] in arterialized venous blood from a resting muscle group as evidenced by the constant RBC [La]:plasma [La] ratio.

Glycogen resynthesis in skeletal muscle following resistive exercise.

The purpose of this investigation was to determine the influence of post-exercise carbohydrate (CHO) intake on the rate of muscle glycogen resynthesis after high intensity weight resistance exercise in subjects not currently weight training. In a cross-over design, eight male subjects performed sets (mean = 8.8) of six single leg knee extensions at 70% of one repetition max until 50% of full knee extension was no longer possible. Total force application was equated between trials using a strain gauge interfaced to a computer. The subjects exercised in the fasted state. Post-exercise feedings were administered at 0 and 1 h consisting of either a 23% CHO solution (1.5 g.kg-1) or an equal volume of water (H2O). Total force production, preexercise muscle glycogen content, and degree of depletion (-40.6 and -44.3 mmol.kg-1 wet weight) were not significantly different between H2O and CHO trials. As anticipated during the initial 2-h recovery, the CHO trial had a significantly greater rate of muscle glycogen resynthesis as compared with the H2O trial. The muscle glycogen content was restored to 91% and 75% of preexercise levels when water and CHO were provided after 6 h, respectively.

Effects of exercise mode on muscle glycogen restorage during repeated days of exercise.

The purpose of this study was to examine differences in muscle glycogen storage during three successive days of running or cycling. In a crossover design, seven male subjects performed two 3-d trials of either running (trial R) or cycling (trial C) for 60 min at 75% VO2max. Biopsy samples were obtained before and after each day's exercise from the gastrocnemius (trial R) or vastus lateralis (trial C) muscle. Diets in the 2 d preceding and during each trial contained 5 g carbohydrate.kg-1.d-1 and 14,475 +/- 402 kJ.d-1. Mean pre-exercise glycogen content (mmol.kg-1 wet wt.) was significantly reduced in both trials on day 3 (103.4 +/- 6.0) when compared to day 1 and day 2 (119.9 +/- 6.8 and 116.4 +/- 5.7, respectively). Day 1 glycogen reduction was significantly greater in trial C (P less than 0.03), and glycogen restorage was greater (P less than 0.02) only in trial C between the 1st and 2nd d. On day 3, spectrophotometric analysis of PAS strains showed that pre-exercise glycogen content in either muscle group was significantly (P less than 0.01) less in Type I as compared to Type II fibers. This difference in fiber glycogen storage did not appear to be attributable to muscle damage as negligible leukocyte infiltration and low blood CK levels were obtained. No difference between modes were observed for CK values throughout the trials. These data suggest that the depressed glycogen storage before the 3rd d of exercise was due to the moderate carbohydrate intake.

The influence of exercise intensity on heat acclimation in trained subjects.

Low-intensity exercise (less than or equal to 50% VO2max) has been demonstrated to produce heat acclimation (HA) in trained subjects. The purpose of this study was to determine whether shorter-duration, moderate-intensity exercise would also result in HA. Nine trained runners performed two 9-d exercise heat-stress protocols. Each protocol consisted of a 90-min heat tolerance test on days 1 (HTT1) and 9 (HTT2). On days 2-8 the subjects exercised at 50% VO2max for 60 min.d-1 (T50) or at 75% VO2max for 30-35 min.d-1 (T75). Final HTT2 heart rate and rectal temperature (Tr) were significantly (P less than 0.001) reduced, as compared to HTT1, with no differences between T50 and T75. Both protocols resulted in significant (P less than 0.05) reductions in HTT2 pre-exercise Tr and total exercising caloric expenditure, both of which are known to contribute to HA. No changes in resting plasma volume, osmolality, protein, post-HTT aldosterone, and exercising sweat rate were observed. These results demonstrate that equal levels of HA were obtained with T50 and T75, which suggests that moderate-intensity, short-duration exercise in the heat can produce HA in trained subjects.

Comparison of the BOD POD with the four-compartment model in adult females.

PURPOSE: This study was designed to compare the accuracy and bias in estimates of total body density (Db) by hydrostatic weighing (HW) and the BOD POD, and percent body fat (%fat) by the BOD POD with the four-compartment model (4C model) in 42 adult females. Furthermore, the role of the aqueous and mineral fractions in the estimation of body fat by the BOD POD was examined. METHODS: Total body water was determined by isotope dilution ((2)H(2)0) and bone mineral was determined by dual-energy x-ray absorptiometry. Db and %fat were determined by the BOD POD and HW. The 4C model of Baumgartner was used as the criterion measure of body fat. RESULTS: HW Db (1.0352 g x cm(-3)) was not statistically different (P = 0.35) from BOD POD Db (1.0349 g x cm(-3)). The regression between Db by HW and the BOD POD significantly deviated from the line of identity (Db by HW = 0.90 x Db by BOD POD + 0.099; R(2) = 0.94). BOD POD %fat (28.8%) was significantly lower (P < 0.01) than %fat by the 4C model (30.6%). The regression between %fat by the 4C model and the BOD POD significantly deviated from the line of identity (%fat by 4C model = 0.88 x %fat by BOD POD + 5.41%; R(2) = 0.92). BOD POD Db and %fat showed no bias across the range of fatness. Only the aqueous fraction of the fat-free mass (FFM) had a significant correlation with the difference in %fat between the 4C model and the BOD POD. CONCLUSION: These data indicate that the BOD POD underpredicted body fat as compared with the 4C model, and the aqueous fraction of the FFM had a significant effect on estimates of %fat by the BOD POD.

Effects of warm-up on muscle glycogenolysis during intense exercise.

This study investigated the effects of preliminary exercise (warm-up) on glycogen degradation and energy metabolism during intense cycle ergometer exercise. After determination of VO2max, six male subjects were randomly assigned to perform warm-up (WU) and no warm-up (NWU) trials incorporating a 2 min standardized sprint ride (SR) at 120% of the power output attained at VO2max (POmax). Muscle biopsies and temperature (Tm) recordings were obtained from the vastus lateralis muscle. Tm was elevated above the resting level prior to the SR during the WU trial (37.7 +/- 0.1 vs 35.4 +/- 0.4 degrees C; P less than 0.05) and remained higher than the NWU trial after the SR (38.6 +/- 0.2 vs 37.1 +/- 0.4 degrees C; P less than 0.05). Similar trends existed for rectal temperature (Tr). The increases in Tm and Tr during the SR were both greater in the NWU trial (P less than 0.05). Muscle glycogen degradation was similar for the WU and NWU trials (30.8 +/- 3.7 vs 25.6 +/- 3.7 mmol.kg-1, respectively). When blood and muscle lactate concentrations after the SR were expressed relative to values before the SR, the WU trial resulted in a lower accumulation of blood lactate (6.5 +/- 0.9 vs 10.7 +/- 0.8 mEq.l-1; P less than 0.01) and muscle lactate (20.1 +/- 0.1 vs 23.4 +/- 2.2 mEq.kg-1 wet wt.; P less than 0.05). Furthermore, oxygen consumption during the 1st min of the SR was higher in the WU trial (2.3 +/- 0.2 vs 1.9 +/- 0.2 l.min-1; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of induced alkalosis on exhaustive leg press performance.

PURPOSE: Fifteen males were studied before, during, and in recovery from exhaustive resistance exercise 105 min after ingesting 0.3 g.kg-1 of either a placebo (white flour) or sodium bicarbonate (NaHCO3). METHODS: The exercise consisted of five maximal sets on a leg press machine, The load was adjusted to maintain the number of repetitions per set for each subject at approximately 12 repetitions. A significant (P < 0.05) increase in pH (7.40 to 7.47), oxygenated base excess (OxyBE) (-1.3 to 4.0 mEq.L-1), and bicarbonate concentration ([HCO3-]) (22.8 to 27.4 mM) was achieved before exercise with the ingestion of NaHCO3. RESULTS: The exercise protocol produced significant changes in acid base status consistent with metabolic acidosis for both trials (pH sets 1-5: placebo, 7.4 to 7.26; NaHCO3, 7.47 to 7.33), (OxyBE sets 1-5: placebo, -1.3 to -12.3 mEq.L-1; NaHCO3, 4.0 to -6.9 mEq.L-1) and ([HCO3-] sets 1-5: placebo, 22.9 to 14.0 mM; NaHCO3, 27.4 to 17.6 mM). After every set; pH, OxyBE, and [HCO3-] were significantly higher in the NaHCO3 trial. Blood lactate concentration ([La-]) significantly increased throughout exercise for both trials ([La-] sets 1-5: placebo, 4.6 to 11.3 mM; NaHCO3, 4.8 to 13.4 mM). After sets 4 and 5, blood [La-] was significantly higher in the NaHCO3 trial. Bicarbonate ingestion did not improve performance (total repetitions: NaHCO3 = 59 +/- 3; placebo = 60 +/- 2). CONCLUSIONS: This may be a result of a lower demand on the whole body metabolic system in comparison with that for other modes of exercise in which ergogenic effects have been found.

Force patterns of heel strike and toe off on different heel heights in normal walking.

This study investigated the changes of force patterns of the heel strike and toe off phases at different heel heights during normal walking. Ten healthy female college students wore running shoes, flat leather shoes and high heeled shoes while walking on a Kistler force platform at their self-comfortable paces. It was found that the high heeled shoes and the leather shoes generated significantly greater vertical impact forces and anterior-posterior forces in the toe off phase than those in the heel strike phase. Accumulated impulses did not show significant increase while the heel heights increased and total support time while wearing the high heeled shoes was significantly longer than while wearing the running shoes.

Lymphocyte enzymatic antioxidant responses to oxidative stress following high-intensity interval exercise.

The purposes of this study were to 1) examine the immune and oxidative stress responses following high-intensity interval training (HIIT); 2) determine changes in antioxidant enzyme gene expression and enzyme activity in lymphocytes following HIIT; and 3) assess pre-HIIT, 3-h post-HIIT, and 24-h post-HIIT lymphocyte cell viability following hydrogen peroxide exposure in vitro. Eight recreationally active males completed three identical HIIT protocols. Blood samples were obtained at preexercise, immediately postexercise, 3 h postexercise, and 24 h postexercise. Total number of circulating leukocytes, lymphocytes, and neutrophils, as well as lymphocyte antioxidant enzyme activities, gene expression, cell viability (CV), and plasma thiobarbituric acid-reactive substance (TBARS) levels, were measured. Analytes were compared using a three (day) × four (time) ANOVA with repeated measures on both day and time. The a priori significance level for all analyses was P < 0.05. Significant increases in superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities were observed in lymphocytes following HIIT. No significant increases in lymphocyte SOD, CAT, or GPX gene expression were found. A significant increase in TBARS was found immediately post-HIIT on days 1 and 2. Lymphocyte CV in vitro significantly increased on days 2 and 3 compared with day 1. Additionally, there was a significant decrease in CV at 3 h compared with pre- and 24 h postexercise. These findings indicate lymphocytes respond to oxidative stress by increasing antioxidant enzyme activity. Additionally, HIIT causes oxidative stress but did not induce a significant postexercise lymphocytopenia. Analyses in vitro suggest that lymphocytes may become more resistant to subsequent episodes of oxidative stress. Furthermore, the analysis in vitro confirms that lymphocytes are more vulnerable to cytotoxic molecules during recovery from exercise.

Hyperthermia increases exercise-induced oxidative stress.

The purpose of this investigation was to examine oxidative markers after exercise in a hyperthermic environment (35 degrees C, 70 % RH) (Hot) versus a neutral environment (25 degrees C, 40 % RH) (Con). Hyperthermia may exacerbate oxidative stress by uncoupling the mitochondrial respiratory chain or by inhibiting antioxidant defense mechanisms, but this has not been assessed in vivo. Six male subjects performed low-intensity exercise (50 % VO(2max)) on a treadmill in Hot until a core temperature of 39.5 degrees C was reached, and for an equivalent time in Con. Blood samples were drawn before and immediately after exercise and at 8 min and 15 min following exercise. Samples were analyzed for F2 isoprostanes (FIP), lipid hydroperoxides (LPO), and lactate. A 2 x 4 repeated measures ANOVA was used to test for treatment, time, and interaction effects for FIP, LPO, and lactate. Differences in VO(2) were tested with Student's t-test. Significance was set at p < 0.05. Oxygen consumption was not significantly different between Hot and Con. The pattern of change of FIP and lactate in Hot was significant versus exercise in Con. LPO was significantly elevated over time in both Hot and Con, but the pattern of change was not significantly different. Ending core temperatures and heart rates were significantly elevated in Hot versus Con. These data indicate that hyperthermia increases oxidative stress and selectively affects specific lipid markers, independent of oxygen consumption.