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.

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.

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.

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.

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.

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.

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.

Quantifying H+ exchange from muscle cytosolic energy catabolism using metabolite flux and H+ coefficients from multiple competitive cation binding: New evidence for consideration in established theories.

The purpose of this investigation was to present calculations of fractional H+ exchange (~H+e ) from the chemical reactions of non-mitochondrial energy catabolism. Data of muscle pH and metabolite accumulation were based on published research for intense exercise to contractile failure within ~3 min, from which capacities and time profiles were modeled. Data were obtained from prior research for multiple competitive cation dissociation constants of metabolites and the chemical reactions of non-mitochondrial energy catabolism, and pH dependent calculations of ~H+e from specific chemical reactions. Data revealed that the 3 min of intense exercise incurred a total ATP turnover of 142.5 mmol L-1 , with a total intramuscular ~H+ exchange (-'ve = release) of -187.9 mmol L-1 . Total ~H+ metabolic consumption was 130.6 mmol L-1 , revealing a net total ~H+e (~H+te ) of -57.3 mmol L-1 . Lactate production had a ~H+te of 44.2 mmol L-1 (for a peak accumulation = 45 mmol L-1 ). The net ~H+te for the sum of the CK, AK, and AMPD reactions was 36.33 mmol L-1 . The ~H+te from ATP turnover equaled -47.5 mmol L-1 . The total ~H+ release to lactate ratio was 4.3 (187.9/44). Muscle ~H+ release during intense exercise is up to ~4-fold larger than previously assumed based on the lactic acid construct.

The effects of concurrent training order on body composition and serum concentrations of follistatin, myostatin and GDF11 in sarcopenic elderly men.

BACKGROUND: Due to the important role of follistatin (FLST), myostatin (MSTN) and growth differentiation factor 11 (GDF11) in muscle mass regulation; alterations in the FLST to MSTN ratio (F:M) may result in muscle mass changes in response to different concurrent training (CT) order. This study investigated the influence of 8 weeks of CT order on body composition and serum concentrations of FLST, MSTN, their ratio (F:M) and GDF11 in sarcopenic elderly men. METHODS: Thirty sarcopenic elderly men (age = 64.3 ± 3.5 years) were randomly assigned into one of three groups, endurance followed by resistance training (E + R; n = 10), resistance followed by endurance training (R + E; n = 10) or control (C; n = 10). Serum concentrations of muscle regulatory markers, body composition, maximum rate of oxygen consumption (VO2max), and upper and lower body strength were evaluated at baseline and after 8 weeks. The training protocol consisted of three training sessions per week for eight weeks. RESULTS: There were significant group-by-time interactions (P < 0.05) for FLST, MSTN, GDF11 and F:M ratio. FLST (E + R = 187 pg/mL and R + E = 292 pg/mL) and F:M ratio (E + R = 0.20 and R + E = 0.27) significantly increased (P < 0.05) while MSTN (E + R = -308 pg/mL and R + E = -294 pg/mL) and GDF11 (E + R = -12 pg/mL and R + E = -10 pg/mL) significantly decreased (P < 0.05) following eight weeks in the E + R and R + E compared to no changes in the C group. In addition, there were significant group x time interactions (P < 0.01) for weight, BMI, body fat percentage (BFP), skeletal muscle mass (SMM), VO2max, upper body strength, and lower body strength. BFP (E + R = -1.5% and R + E = -2%) significantly decreased (P < 0.01) while weight (E + R = 2.4 kg and R + E = 1.1 kg), BMI (E + R = 0.8 kg/m2 and R + E = 0.3 kg/m2), SMM (E + R = 0.7 kg and R + E = 0.5 kg), VO2max (E + R = 2.0 mL/kg/min and R + E = 1.8 mL/kg/min), upper body strength (E + R = 6.9 kg and R + E = 2.3 kg), and lower body strength (E + R = 9.8 kg and R + E = 4.4 kg) significantly increased (P < 0.01) in the E + R and R + E compared to no changes in the C group. CONCLUSIONS: CT increases the F:M ratio and FLST as well as reducing MSTN and GDF11 in sarcopenic elderly men. Additionally, CT improved weight, body composition, muscle mass, function, and aerobic fitness. Notably, these results after CT were achieved irrespective of endurance and resistance exercise order in this population.

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.

Competitive cation binding computations of proton balance for reactions of the phosphagen and glycolytic energy systems within skeletal muscle.

Limited research and data has been published for the H+ coefficients for the metabolites and reactions involved in non-mitochondrial energy metabolism. The purpose of this investigation was to compute the fractional binding of H+, K+, Na+ and Mg2+ to 21 metabolites of skeletal muscle non-mitochondrial energy metabolism, resulting in 104 different metabolite-cation complexes. Fractional binding of H+ to these metabolite-cation complexes were applied to 17 reactions of skeletal muscle non-mitochondrial energy metabolism, and 8 conditions of the glycolytic pathway based on the source of substrate (glycogen vs. glucose), completeness of glycolytic flux, and the end-point of pyruvate vs. lactate. For pH conditions of 6.0 and 7.0, respectively, H+ coefficients (-'ve values = H+ release) for the creatine kinase, adenylate kinase, AMP deaminase and ATPase reactions were 0.8 and 0.97, -0.13 and -0.02, 1.2 and 1.09, and -0.01 and -0.66, respectively. The glycolytic pathway is net H+ releasing, regardless of lactate production, which consumes 1 H+. For glycolysis fueled by glycogen and ending in either pyruvate or lactate, H+ coefficients for pH 6.0 and 7.0 were -3.97 and -2.01 (pyruvate), and -1.96 and -0.01 (lactate), respectively. When starting with glucose, the same conditions result in H+ coefficients of -3.98 and -2.67, and -1.97 and -0.67, respectively. The most H+ releasing reaction of glycolysis is the glyceraldehyde-3-phosphate dehydrogenase reaction, with H+ coefficients for pH 6.0 and 7.0 of -1.58 and -0.76, respectively. Incomplete flux of substrate through glycolysis would increase net H+ release due to the absence of the pyruvate kinase and lactate dehydrogenase reactions, which collectively result in H+ coefficients for pH 6.0 and 7.0 of 1.35 and 1.88, respectively. The data presented provide an extensive reference source for academics and researchers to accurately profile the balance of protons for all metabolites and reactions of non-mitochondrial energy metabolism, and reveal the greater role of glycolysis in net H+ release than previously assumed. The data can also be used to improve the understanding of the cause of metabolic acidosis, and reveal mechanistic connections between H+ release within and from muscle and the electrochemical neutrality concepts that further refine acid-base balance in biological solutions.

New Methods for Processing and Quantifying VO2 Kinetics to Steady State: VO2 Onset Kinetics.

Current methods of oxygen uptake (VO2) kinetics data handling may be too simplistic for the complex physiology involved in the underlying physiological processes. Therefore, the aim of this study was to quantify the VO2 kinetics to steady state across the full range of sub-ventilatory threshold work rates, with a particular focus on the VO2 onset kinetics. Ten healthy, moderately trained males participated in five bouts of cycling. Each bout involved 10 min at a percentage of the subject's ventilation threshold (30, 45, 60, 75, 90%) from unloaded cycling. The VO2 kinetics was quantified using the conventional mono-exponential time constant (tau, τ), as well as the new methods for VO2 onset kinetics. Compared to linear modeling, non-linear modeling caused a deterioration of goodness of fit (main effect, p < 0.001) across all exercise intensities. Remainder kinetics were also improved using a modified application of the mono-exponential model (main effect, p < 0.001). Interestingly, the slope from the linear regression of the onset kinetics data is similar across all subjects and absolute exercise intensities, and thereby independent of subject fitness and τ. This could indicate that there are no functional limitations between subjects during this onset phase, with limitations occurring for the latter transition to steady state. Finally, the continuing use of mono-exponential modeling could mask important underlying physiology of more instantaneous VO2 responses to steady state. Consequently, further research should be conducted on this new approach to VO2 onset kinetics.

Lessons from Popper for science, paradigm shifts, scientific revolutions and exercise physiology.

A connection has been made to the possible role of the central governor model (CGM) to be a paradigm shift within the exercise sciences. Unfortunately, very little evidence was presented to support this notion, and a narrow view of scientific philosophy was used to reflect on the role of the CGM in understanding exercise physiology and the pursuit of a more ideal scientific method. When contrasting the scientific philosophies of Kuhn to Popper, and applying the tenant of falsification to the research and commentary on the CGM, it is probable that the scholarship pertaining to the CGM adheres more to pseudoscience than science. To improve the scientific contributions of research on the CGM, fellow scientists need to adopt a more critical platform where questions are raised and research designs are employed in efforts to refute the theory. The inability to falsify a theory is the most meaningful way to prove that it is likely to be correct. To support this development, the CGM needs to be more carefully worded to form a theory that clearly reveals key features that can be researched and potentially falsified. In addition, the wording of the CGM needs to allow scientists to make predictions that can then be tested in controlled experimental research studies. Until this happens for the CGM and all other pertinent paradigms within exercise physiology, the discipline will never rise out of the abyss of normal science to extraordinary science involving paradigm shifts and scientific revolutions.

Limited Effects of Endurance or Interval Training on Visceral Adipose Tissue and Systemic Inflammation in Sedentary Middle-Aged Men.

Purpose. Limited data exists for the effects of sprint-interval training (SIT) and endurance training (ET) on total body composition, abdominal visceral adipose tissue, and plasma inflammation. Moreover, whether "active" or "passive" recovery in SIT provides a differential effect on these measures remains uncertain. Methods. Sedentary middle-aged men (n = 62; 49.5 ± 5.8 y; 29.7 ± 3.7 kg·m2) underwent abdominal computed tomography, dual-energy X-ray absorptiometry, venepuncture, and exercise testing before and after the interventions, which included the following: 12 wks 3 d·wk-1 ET (n = 15; 50-60 min cycling; 80% HRmax), SIT (4-10 × 30 s sprint efforts) with passive (P-SIT; n = 15) or active recovery (A-SIT; n = 15); or nonexercise control condition (CON; n = 14). Changes in cardiorespiratory fitness, whole-body and visceral fat mass, and plasma systemic inflammation were examined. Results. Compared to CON, significant increases in interpolated power output (P-SIT, P < 0.001; ET, P = 0.012; A-SIT, P = 0.041) and test duration (P-SIT, P = 0.001; ET, P = 0.012; A-SIT, P = 0.046) occurred after training. Final VO2 consumption was increased after P-SIT only (P < 0.001). Despite >90% exercise compliance, there was no change in whole-body or visceral fat mass or plasma inflammation (P > 0.05). Conclusion. In sedentary middle-aged men, SIT was a time-effective alternative to ET in facilitating conditioning responses yet was ineffective in altering body composition and plasma inflammation, and compared to passive recovery, evidenced diminished conditioning responses when employing active recovery.