Evaluating Airflow Sensor Methods: Precision in Indirect Calorimetry.

This study assesses the impact of three volumetric gas flow measurement methods-turbine (fT); pneumotachograph (fP), and Venturi (fV)-on predictive accuracy and precision of expired gas analysis indirect calorimetry (EGAIC) across varying exercise intensities. Six males (Age: 38 ± 8 year; Height: 178.8 ± 4.2 cm; V ̇ O 2 peak $$ \dot{V}{\mathrm{O}}_2\mathrm{peak} $$ : 42 ± 2.8 mL O2 kg-1 min-1) and 14 females (Age = 44.6 ± 9.6 year; Height = 164.6 ± 6.9 cm; V ̇ O 2 peak $$ \dot{V}{\mathrm{O}}_2\mathrm{peak} $$ = 45 ± 8.6 mL O2 kg-1 min-1) were recruited. Participants completed physical exertion on a stationary cycle ergometer for simultaneous pulmonary minute ventilation ( V ̇ $$ \dot{V} $$ ) measurements and EGAIC computations. Exercise protocols and subsequent conditions involved a 5-min cycling warm-up at 25 W min-1, incremental exercise to exhaustion ( V ̇ O 2 $$ \dot{V}{\mathrm{O}}_2 $$ ramp test), then a steady-state exercise bout induced by a constant Watt load equivalent to 80% ventilatory threshold (80% VT). A linear mixed model revealed that exercise intensity significantly affected V ̇ O 2 $$ \dot{V}{\mathrm{O}}_2 $$ measurements (p < 0.0001), whereas airflow sensor method (p = 0.97) and its interaction with exercise intensity (p = 0.91) did not. Group analysis of precision yielded a V ̇ O 2 $$ \dot{V}{\mathrm{O}}_2 $$ CV % = 21%; SEM = 5 mL O2 kg-1 min-1. Intra- and interindividual analysis of precision via Bland-Altman revealed a 95% confidence interval (CI) precision benchmark of 3-5 mL kg-1 min-1. Agreement among methods decreased at power outputs eliciting V ̇ $$ \dot{V} $$ up to 150 L min-1, indicating a decrease in precision and highlighting potential challenges in interpreting biological variability, training response heterogeneity, and test-retest comparisons. These findings suggest careful consideration of airflow sensor method variance across metabolic cart configurations.

Invited review: Quantifying proton exchange from chemical reactions - Implications for the biochemistry of metabolic acidosis.

Given that the chemistry of lactate production disproves the existence of a lactic acidosis, there is a need to further reveal and explain the importance of the organic and computational chemistry of pH dependent competitive cation fractional (~) proton (H+) exchange (~H+e). An additional importance of this knowledge is that it could potentially contradict the assumption of the Stewart approach to the physico-chemical theory of acid-base balance. For example, Stewart proposed that chemical reaction and pH dependent H+ dissociation and association do not directly influence the pH of cellular and systemic body fluids. Yet at the time of Stewart's work, there were no data that quantified the H+ exchange during chemical reactions, or from pH dependent metabolite H+ association or dissociation. Consequently, the purpose of this review and commentary was three-fold; 1) to provide explanation of pH dependent competitive cation ~H+e exchange; 2) develop a model of and calculate new data of substrate flux in skeletal muscle during intense exercise; and 3) then combine substrate flux data with the now known ~H+e from chemical reactions of non-mitochondrial energy catabolism to quantify chemical reaction and metabolic pathway ~H+e. The results of purpose 3 were that ~H+ release for the totality of cytosolic energy catabolism = -187.2 mmol·L-1, where total glycolytic ~H+te = -85.0 mmol·L-1. ATP hydrolysis had a ~H+te = -43.1 mmol·L-1. Lactate production provided the largest metabolic ~H+ buffering with a ~H+te = 44.5 mmol·L-1. The total ~H+ release to La ratio = 4.25. The review content and research results of this manuscript should direct science towards new approaches to understanding the cause and source of H+e during metabolic acidosis and alkalosis.

Caution using data from triaxial accelerometers housed in player tracking units during running.

Usage of accelerometers within player tracking devices in sport to quantify load, vertical ground reaction force (vGRF) or energy expenditure is contrary to placement guidelines. This study aimed to determine whether trunk-mounted accelerometers were a valid and reliable method to estimate thoracic segment or centre of gravity (COG) acceleration or vGRF, and the whether the elasticised harness contributes to the overestimation of acceleration. Ten male amateur rugby players performed five linear running tasks per lower limb at three speeds, twice, each with a different player tracking unit. Three-dimensional data were recorded and triaxial accelerometers were attached lateral to the device on the harness and skin and both shanks. Accelerometers demonstrated poor reliability (ICC:0.0-0.67), high variability (CV%:14-33%) and change in mean (41-160%), and were not valid to estimate vertical acceleration of the COG and thoracic segment nor vGRF. Caution is advised when utilising trunk-mounted triaxial accelerometer data as it is not a valid or reliable means to estimate peak vertical acceleration for its thoracic location nor whole-body COG acceleration or vGRF during running. To improve player tracking instrument validity and reliability, a new attachment method and/or harness material(s), that reduce or eliminate extraneous acceleration during running, are urgently required.

Optimal loads for a 30-s maximal power cycle ergometer test using a stationary start.

INTRODUCTION: A stationary start modification to the Wingate Anaerobic Test (WAnT) has become increasingly common. The aim of the present study was to determine whether the traditional 85 g kg(-1) body weight (BW) load (TRAD), or an individualized optimal load (OPT), is more suitable for obtaining peak and mean power outputs (PPO and MPO, respectively) for a stationary start. METHODS: Twelve recreationally active males and 10 females (mean age 30 ± 9.1 and 25 ± 5.5 years, respectively) completed three trials. The first determined the OPT load and included a familiarization of the 30-s stationary start test, followed by two randomized sessions testing the OPT and TRAD loads during the 30-s stationary start test on separate days. For each test, measures of power (watts), time, and cadence were collected to determine PPO, MPO, rate of power decline (rPD) and time to peak power (TtPP). All power data were corrected for flywheel moment of inertia. RESULTS: Results revealed significant differences between OPT and TRAD load settings for males (95.1 ± 10.7 and 85.06 ± 0.40 g kg(-1) BW; p = 0.008) but not for females (84.71 ± 8.72 and 85.2 ± 0.61 g kg(-1) BW; p = 0.813). Relative PPO was not different for OPT or TRAD loads for males (p = 0.485) or females (p = 0.488). CONCLUSION: It is not necessary to use an OPT load setting to acquire maximal PO for a 30-s cycle test using a stationary start. Instead, the traditional 85 g kg(-1) BW loading is suitable for both males and females.

Palm Cooling and Heating Delays Fatigue During Resistance Exercise in Women.

We previously reported that cold application to the palms between sets of high-intensity bench press exercise produces an ergogenic effect in men. In this study, we hypothesized that palm cooling (PC) or heating during rest intervals between high-intensity weight training sets will increase total repetitions and exercise volume load (kilograms) in resistance trained female subjects in a thermoneutral (TN) environment. Eight female subjects (mean ± SD, age = 25 ± 6 years, height = 160 ± 6 cm, body mass = 56 ± 7 kg, 1-repetition maximum [1RM] = 52 ± 6 kg, weight training experience = 6 ± 2 years) completed 4 sets of 85% 1RM bench press exercise to failure, with 3-minute rest intervals. Exercise trials were performed in a counterbalanced order on 3 days, separated by at least 3 days in TN, Palm heating (PH), and PC conditions. Heating and cooling were applied by placing both hands in a hand cooling device with the hand plate set to 45° C for heating and 10° C for cooling. Data were analyzed using a 2-factor repeated-measures analysis of variance and Tukey's post hoc tests. Palm cooling repetitions were significantly higher than TN repetitions during the second set, and PH repetitions were significantly higher than those of TN during the fourth set. Total exercise volume load (kilograms) for both PC (1,387 ± 358) and PH (1,349 ± 267) were significantly higher than TN (1,187 ± 262). In women, both heating and cooling of the palms between sets of resistance exercise increased the total exercise volume load performed. This ergogenic response to a peripheral sensory input is consistent with the central governor theory of muscular fatigue.

The missing hydrogen ion, Part-3: Science and the human flaws that compromise it.

The purpose of this research was to use a historical method and core principles from scientific philosophy to explain why mistakes were made in the development of the lactic acidosis construct. On a broader scope, this research explains what science is, why some scientists despite good intention, often get it wrong, and why it takes so long (decades) to correct these errors. Science is a human behaviour that consists of the identification of a problem based on the correct application of prior knowledge, the development of a method to best resolve or test the problem, completion of these methods to acquire results, and then a correct interpretation of the results. If these steps are done correctly there is an increased probability (no guarantee) that the outcome is likely to be correct. Thomas Kuhn proposed that you can understand what science is from how it has been performed, and from his essays he revealed a very dysfunctional form of science that he called 'normal' (due the preponderance of its presence) science. Conversely, Karl Popper was adamant that the practice of 'normal' science revealed numerous flaws that deviate from fundamental principles that makes science, science. Collectively, the evidence reveals that within the sports medicine and health sciences, as with all disciplines, errors in science are more frequent than you might expect. There is an urgent need to improve how we educate and train scientists to prevent the pursuit of 'normal' science and the harm it imparts on humanity.

The missing hydrogen ion, part-2: Where the evidence leads to.

The purpose of this manuscript was to present the evidence for why cells do not produce metabolic acids. In addition, evidence that opposes common viewpoints and arguments used to support the cellular production of lactic acid (HLa) or liver keto-acids have been provided. Organic chemistry reveals that many molecules involved in cellular energy catabolism contain functional groups classified as acids. The two main acidic functional groups of these molecules susceptible to ∼H+ release are the carboxyl and phosphoryl structures, though the biochemistry and organic chemistry of molecules having these structures reveal they are produced in a non-acidic ionic (negatively charged) structure, thereby preventing pH dependent ∼H+ release. Added evidence from the industrial production of HLa further reveals that lactate (La-) is produced followed by an acidification step that converts La- to HLa due to pH dependent ∼H+ association. Interestingly, there is a plentiful list of other molecules that are classified as acids and compared to HLa have similar values for their H+ dissociation constant (pKd). For many metabolic conditions, the cumulative turnover of these molecules is far higher than for La-. The collective evidence documents the non-empirical basis for the construct of the cellular production of HLa, or any other metabolic acid.

Carbohydrate Ingestion before Exercise for Individuals with McArdle Disease: Survey Evidence of Implementation and Perception in Real-World Settings.

In individuals with McArdle disease (IWMD), the ingestion of carbohydrates before exercise has previously been shown in laboratory studies to significantly decrease the exercising symptoms of the condition and increase exercise tolerance during the early stages of exercise. As a result, carbohydrate ingestion pre-exercise is currently included in management guidelines, and often advised by medical professionals treating the condition. The aim of the current study was to determine whether positive lab-based results for the ingestion of carbohydrate before exercise in laboratory studies are being effectively translated into practice and produce perceptions of the same positive outcomes in real-world settings (RWS). An online survey method was used to collect responses from 108 IWMD. Data collected on the amount and type of carbohydrate consumed prior to exercise found that most surveyed participants (69.6%) who supplied qualitative data (n = 45) consumed less than the 37 g currently recommended in management guidelines. Survey data also revealed a large variation in the type and amount of carbohydrate ingested when IWMDs are applying carbohydrate ingestion before exercise in RWS. Consistent with these findings, only 17.5% of participants stated that they found carbohydrate ingestion before exercise relieved or minimised their MD symptoms. Results suggest that positive lab-based findings (increased exercise tolerance) of carbohydrate ingestion before exercise are not being effectively translated to RWS for many IWMD. There is a need for improved patient education of IWMD on the application of carbohydrate ingestion before exercise in RWS.

Effect of local cooling on short-term, intense exercise.

The widespread belief that local cooling impairs short-term, strenuous exercise performance is controversial. Eighteen original investigations involving cooling before and intermittent cooling during short-term, intensive exercise are summarized in this review. Previous literature examining short-term intensive exercise and local cooling primarily has been limited to the effects on muscle performance immediately or within minutes following cold application. Most previous cooling studies used equal and longer than 10 minutes of pre-cooling, and found that cooling reduced strength, performance and endurance. Because short duration, high intensity exercise requires adequate warm-up to prepare for optimal performance, prolonged pre-cooling is not an effective method to prepare for this type of exercise. The literature related to the effect of acute local cooling immediately before short duration, high intensity isotonic exercise such as weight lifting is limited. However, local intermittent cooling during short-term, high intense exercise may provide possible beneficial effects; first, by pain reduction, caused by an "irritation effect" from hand thermal receptors which block pain sensation, or second, by a cooling effect, whereby stimulation of hand thermal receptors or a slight lowering of blood temperature might alter central fatigue.

A rationale for assessing the lower-body power profile in team sport athletes.

Training at the load that maximizes peak mechanical power (Pmax) is considered superior for the development of power. We aimed to identify the Pmax load ('optimal load') in the jump squat and to quantify small, moderate, large, and very large substantial differences in power output across a spectrum of loads to identify loads that are substantially different to the optimal, and lastly, to investigate the nature of power production (load-force-velocity profiles). Professional Australian Rules Football (ARF; n = 16) and highly trained Rugby Union (RU; n = 20) players (subdivided into stronger [SP] vs. weaker [WP] players) performed jump squats across incremental loads (0-60 kg). Substantial differences in peak power (W·kg(-1)) were quantified as 0.2-2.0 of the log transformed between-athlete SD at each load, backtransformed and expressed as a percent with 90% confidence limits (CL). A 0-kg jump squat maximized peak power (ARF: 57.7 ± 10.8 W·kg(-1); RU: 61.4 ± 8.5 W·kg(-1); SP: 64.4 ± 7.5 W·kg(-1); WP: 54.8 ± 9.5 W·kg(-1)). The range for small to very large substantial differences in power output was 4.5-55.9% (CL: ×/÷1.36) and 2.8-32.4% (CL: ×/÷1.31) in ARF and RU players, whereas in SP and WP, it was 3.7-43.1% (CL: ×/÷1.32) and 4.3-51.7% (CL: ×/÷1.36). Power declined per 10-kg increment in load, 14.1% (CL: ±1.6) and 10.5% (CL: ±1.5) in ARF and RU players and 12.8% (CL: ±1.9) and 11.3% (CL: ±1.7) in SP and WP. The use of a 0-kg load is superior for the development of jump squat maximal power, with moderate to very large declines in power output observed at 10- to 60-kg loads. Yet, performance of heavier load jump squats that are substantially different to the optimal load are important in the development of sport-specific force-velocity qualities and should not be excluded.

Influence of rest interval duration on muscular power production in the lower-body power profile.

There is a paucity of evidence-based support for the allocation of rest interval duration between incremental loads in the assessment of the load-power profile. We examined the effect of rest interval duration on muscular power production in the load-power profile and sought to determine if greater rest is required with increasing load (i.e., variable rest interval). Ten physically trained men completed 4 experimental conditions in a crossover balanced design. Participants performed jump squats across incremental loads (0-60 kg) on 4 occasions, with an allocated recovery interval of 1, 2, 3, or 4 minutes. The mean log-transformed power output at each load was used for comparison between conditions (rest intervals). Unloaded jump squats (0 kg) maximized power output at each condition. The maximal mechanical power output was 66.6 ± 6.5 W·kg (1 minute), 66.2 ± 5.2 W·kg (2 minutes), 67.1 ± 5.9 W·kg (3 minutes), and 66.2 ± 6.5 W·kg (4 minutes). Trivial or unclear differences in power output were observed between rest intervals at each incremental load. As expected, power declined per 10 kg increment in load, the magnitude of decrease was 13.9-14.5% (confidence limits [CL]: ±1.3-2.0%) and 13.4-14.6% (CL: ±2.4-3.9%) for relative peak and mean power, respectively, yet differences in power output between conditions were likely insubstantial. The prescription of rest intervals between loads that are longer than 1 minute have a likely negligible effect on muscular power production in the jump squat incremental load-power profile. Practitioners should select either a 1- to 4-minute rest interval to best accommodate the logistical constraints of their monitoring sessions.

The missing hydrogen ion, part-1: Historical precedents vs. fundamental concepts.

The purpose of this review and commentary was to provide an historical and evidence-based account of organic acids and the biochemical and organic chemistry evidence for why cells do not produce metabolites that are acids. The scientific study of acids has a long history dating to the 16th and 17th centuries, and the definition of an acid was proposed in 1884 as a molecule that when in an aqueous solution releases a hydrogen ion (H+). There are three common ionizable functional groups for molecules classified as acids: 1) the carboxyl group, 2) the phosphoryl group and 3) the amine group. The propensity by which a cation will associate or dissociate with a negatively charged atom is quantified by the equilibrium constant (Keq) of the dissociation constant (Kd) of the ionization (Keq â€‹= â€‹Kd), which for lactic acid (HLa) vs. lactate (La-) is expressed as: Keq=Kd=[H+][La-][HLa]= 4 677.351 4 (ionic strength â€‹= â€‹0.01 Mol⋅L-1, T â€‹= â€‹25 â€‹°C). The negative log10 of the dissociation pKd reveals the pH at which half of the molecules are ionized, which for HLa â€‹= â€‹3.67. Thus, knowing the pKd and the pH of the solution at question will reveal the extent of the ionization vs. acidification of molecules that are classified as acids.

The Computational Acid-Base Chemistry of Hepatic Ketoacidosis.

Opposing evidence exists for the source of the hydrogen ions (H+) during ketoacidosis. Organic and computational chemistry using dissociation constants and alpha equations for all pertinent ionizable metabolites were used to (1) document the atomic changes in the chemical reactions of ketogenesis and ketolysis and (2) identify the sources and quantify added fractional (~) H+ exchange (~H+e). All computations were performed for pH conditions spanning from 6.0 to 7.6. Summation of the ~H+e for given pH conditions for all substrates and products of each reaction of ketogenesis and ketolysis resulted in net reaction and pathway ~H+e coefficients, where negative revealed ~H+ release and positive revealed ~H+ uptake. Results revealed that for the liver (pH = 7.0), the net ~H+e for the reactions of ketogenesis ending in each of acetoacetate (AcAc), ß-hydroxybutyrate (ß-HB), and acetone were -0.9990, 0.0026, and 0.0000, respectively. During ketogenesis, ~H+ release was only evident for HMG CoA production, which is caused by hydrolysis and not ~H+ dissociation. Nevertheless, there is a net ~H+ release during ketogenesis, though this diminishes with greater proportionality of acetone production. For reactions of ketolysis in muscle (pH = 7.1) and brain (pH = 7.2), net ~H+ coefficients for ß-HB and AcAc oxidation were -0.9649 and 0.0363 (muscle), and -0.9719 and 0.0291 (brain), respectively. The larger ~H+ release values for ß-HB oxidation result from covalent ~H+ release during the oxidation-reduction. For combined ketogenesis and ketolysis, which would be the metabolic condition in vivo, the net ~H+ coefficient depends once again on the proportionality of the final ketone body product. For ketone body production in the liver, transference to blood, and oxidation in the brain and muscle for a ratio of 0.6:0.2:0.2 for ß-HB:AcAc:acetone, the net ~H+e coefficients for liver ketogenesis, blood transfer, brain ketolysis, and net total (ketosis) equate to -0.1983, -0.0003, -0.2872, and -0.4858, respectively. The traditional theory of ketone bodies being metabolic acids causing systemic acidosis is incorrect. Summation of ketogenesis and ketolysis yield H+ coefficients that differ depending on the proportionality of ketone body production, though, in general, there is a small net H+ release during ketosis. Products formed during ketogenesis (HMG-CoA, acetoacetate, ß-hydroxybutyrate) are created as negatively charged bases, not acids, and the final ketone body, acetone, does not have pH-dependent ionizable groups. Proton release or uptake during ketogenesis and ketolysis are predominantly caused by covalent modification, not acid dissociation/association. Ketosis (ketogenesis and ketolysis) results in a net fractional H+ release. The extent of this release is dependent on the final proportionality between acetoacetate, ß-hydroxybutyrate, and acetone.

Moderate continuous- and high-intensity interval training elicit comparable cardiovascular effect among middle-aged men regardless of recovery mode.

To assess the effect of active and passive intra-interval recovery modes in time-efficient high-intensity interval training (HIT) on cardiorespiratory fitness, autonomic function, and endothelial function in sedentary middle-aged men.Participants (n = 62; age: 49.5 ± 5.8 y; BMI: 29.7 ± 3.7 kg·m-2) completed the assessments of cardiorespiratory fitness, flow-mediated dilation (FMD) and heart rate variability before being randomly allocated to control (CON; n = 14), moderate intensity continuous training (MICT; n = 15), HIT with passive (P-HIT; n-15), or active recovery (A-HIT; n = 15). Participants performed thrice weekly exercise sessions for 12 weeks. MICT completed 50-60 min of continuous cycling at 60-70% heart rate (HR) maximum. HIT completed 30-s work intervals (∼85% HR) interspaced with 2.5 min of active or passive recovery.All exercise modalities increased oxygen uptake (V̇O2) (MD: ≥ 3.1 ml·kg-1·min-1, 95%CI: 1.5-4.7 ml·kg-1·min-1; P < 0.001), power output (MD: ≥ 26 W, 95%CI: 15-37 W; P < 0.001) and cycle duration (MD: ≥ 62 s, 95%CI: 36-88 s; P < 0.001) at 85% HRM. Significant pre-to-post differences were observed among all exercise groups for FMD (MD: ≥ 3.4%, 95%CI: 0.3-6.5%; P < 0.05), while MICT and P-HIT significantly increased the standard deviation of all NN intervals (SDNN) pre-to-post intervention (MD: ≥ 7 ms, 2-13 ms; P ≤ 0.05).Time-efficient HIT elicits significant improvements in cardiorespiratory fitness, FMD and autonomic modulation following a thrice weekly 12-week exercise intervention among sedentary middle-aged men. Active recovery between successive high-intensity intervals provided no additional benefit among this deconditioned cohort.

Exercise duration and blood lactate concentrations following high intensity cycle ergometry.

The aim of this study was to investigate differences in blood lactate accumulation following 10 and 20 sec of maximal cycle ergometer exercise. Body mass, stature, and age of the group was determined prior to testing (82.57 ± 5.94 kg 177 ± 5.94 cm and 21.42 ± 1.61 yrs, respectively). Eight male rugby union players performed two maximal sprints in a random fashion of 10 and 20 sec duration on a cycle ergometer. During the 10 and 20 sec trial, blood lactate levels measured were as follows 1.58 ± 0.78, 4.43 ± 1.4, and 3.5 ± 1.2 mmol.l⁻¹ vs. 1.72 ± 0.65, 6.14 ± 2, and 5.68 ± 2.22 mmol.l⁻¹, respectively. Differences were found (P < 0.01) from rest to 5 and 10 min postexercise in both groups. Differences in concentration also were found between groups at both postexercise stages (P < 0.01). The reduction in blood lactate concentrations observed between the 5 to 10 min recovery stages were 0.91 ± 0.58 mmol.l⁻¹ vs. 0.46 ± 0.48 mmol.l⁻¹ following 10 and 20 sec of maximal exercise, respectively (P > 0.05). The concentrations observed are interesting and may influence recovery time and subsequent exercise performance.

How to be a better scientist: Lessons from scientific philosophy, the historical development of science, and past errors within exercise physiology.

What is science? While a simple question, the answer is complex. Science is a process involving human behaviour, and due to the human influence, science is often not pursued correctly. In fact, one can argue that we still do not know what the "correct" pursuit of science should entail. This is because science remains a work in progress, differs for different questions, and we often are not aware of the mistakes made until years, or decades, later. Such mistakes are common, regardless of the discipline. Within exercise physiology, mistakes have been frequent and led to eventual corrections; the replacement of the post-exercise rate of oxygen consumption (V̇O2) debt concept with that of excess post-exercise V̇O2; the invalidation of the cellular production of lactic acid; improvements to maximal heart rate estimation; and on-going debate over the Central Governor Model. Improved training and education in the historical development of science and the contributions from scientific philosophy are important in providing an understanding of science, and more importantly, how to pursue "better" vs. "inferior" forms of science. The writings of Popper and Kuhn are core to enhanced understanding of how to improve the quality of science pursued. Unfortunately, quality education and training in the historical and philosophical development of science remain poor in most countries. Until inadequate educational training is overcome, there is sustained risk for the pursuit of science to remain inadequate, which in turn has a potential widespread detriment to humanity and the planet we live on.

Effects of whole-body heat acclimation on cell injury and cytokine responses in peripheral blood mononuclear cells.

To test the hypothesis that whole-body heat acclimation (HA) would increase peripheral blood mononuclear cells' (PBMC) tolerance to heat shock (HS) and/or alter the release of cytokines (IL-1ß, IL-6, IL-10 and TNF-α) to bacterial lipopolysaccharide (LPS), we heat acclimated nine subjects by exercising them for 100 min in a hot environment for 10 days. The subjects' PBMC were separated and cultured on days 1 and 10 of HA pre- and post-exercise. Pre-exercise PBMC were allocated to three treatments: control (PRE, 37°C), HS (42.5°C for 2 h), or LPS (1 ng mL(-1) for 24 h). Post-exercise samples were incubated at 37°C. PBMC lactate dehydrogenase release increased (p < 0.05) after HS but it was not different (p > 0.05) between days 1 and 10 (0.100 ± 0.012 and 0.102 ± 0.16 abs., respectively). LPS treatment induced an increased (p < 0.05) release of cytokines but HA did not alter this response (p > 0.05). Pre-exercise intracellular heat shock protein 72 (Hsp72) was higher (p < 0.05) on day 10 compared to day 1 of HA (13 ± 5 and 8 ± 5 ng mL(-1), respectively). HS treatment caused a greater increase (p < 0.05) in Hsp72 than the exercise sessions on HA days 1 and 10. In addition, after HA, the Hsp72 response to HS was reduced (day 1, 129 ± 46; day 10, 80 ± 32 ng mL(-1), p < 0.05). In conclusion, HA increases PBMC Hsp72 but it does not reduce cellular damage to HS or alter cytokine response to LPS. We speculate that the stress applied during HA is not sufficient to modify the PBMC response.