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.

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.

Increases in the incremental exercise mean response time across the steady state domain: Implications for exercise testing & prescription.

We hypothesized that slowed oxygen uptake ( V ˙ O 2 ) kinetics for exercise transitions to higher power outputs (PO) within the steady state (SS) domain would increase the mean response time (MRT) with increasing exercise intensity during incremental exercise. Fourteen highly trained cyclists (mean ±â€¯standard deviation [SD]; age (39 ±â€¯6) years [yr]; and V ˙ O 2 peak = (61 ±â€¯9) mL/kg/min performed a maximal, ramp incremental cycling test and on separate days, four 6-min bouts of cycling at 30%, 45%, 65% & 75% of their incremental peak PO (Wpeak). SS trial data were used to calculate the MRT and verified by mono-exponential and linear curve fitting. When the ramp protocol attained the value from SS, the PO, in Watts (W), was converted to time (min) based on the ramp function W to quantify the incremental MRT (iMRT). Slope analyses for the V ˙ O 2 responses of the SS versus incremental exercise data below the gas exchange threshold (GET) revealed a significant difference (p = 0.003; [0.437 ±â€¯0.08] vs. [0.382 ±â€¯0.05] L⋅min-1). There was a significant difference between the 45% Wpeak steady state V ˙ O 2 (ss V ˙ O 2 ) ([3.08 ±â€¯0.30] L⋅min-1, respectively), and 30% Wpeak ss V ˙ O 2 (2.26 ±â€¯0.24) (p < 0.0001; [3.61 ±â€¯0.80] vs. [2.20 ±â€¯0.39] L⋅min-1) and between the iMRT for 45% and 30% Wpeak ss V ˙ O 2 values ([50.58 ±â€¯36.85] s vs. [32.20 ±â€¯43.28] s). These data indicate there is no single iMRT, which is consistent with slowed V ˙ O 2 kinetics and an increasing V ˙ O 2 deficit for higher exercise intensities within the SS domain.

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 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.

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.

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.

Hydration, thermoregulation, and performance effects of two sport drinks during soccer training sessions.

In the present study, we aimed to compare the thermoregulatory response and soccer-specific training performance aspects of two commercially available sport drinks, both of similar carbohydrate concentration, but one containing 5.2% glycerol. Ten players participated in two similar outdoor training sessions and were randomly assigned to each of two drinks: a carbohydrate (C) beverage or a carbohydrate-glycerol (CG) beverage. Players consumed 500 mL of C or CG 30 minutes pre-exercise and at half-time. Pre- and postexercise body mass, core temperature (CT), and heart rate (HR) were recorded, and urine and blood samples were taken. No difference was observed between days for wet bulb globe temperature (session 1: 17.0 +/- 1.1 degrees C, session 2: 16.9 +/- 1.1 degrees C; P = 0.944). The degree of dehydration (% Delta BM) was greater after the C trial (P = 0.041). Similarly, percent change in plasma volume was greater in the C trial (P = 0.049). No overall main affect was observed between CT and mean exercise HRs during either training session (CT: P = 0.350; mean HR: P = 0.256), and there was no difference observed between groups in time to failure during the session-ending fatigue test (P = 0.547). Ingestion of a CG beverage provided players with better hydration than C alone. However, if training sessions are short (<75 minute), with adequate time for recovery, both drinks are sufficient for maintaining performance intensities during soccer-specific training.

Failure of Rhodiola rosea to alter skeletal muscle phosphate kinetics in trained men.

Rhodiola rosea is an herbal supplement purported to improve resistance to stressors and to enhance physical performance, potentially by improving adenosine triphosphate (ATP) turnover. Phosphocreatine (PCr) kinetics serves as a reflection of ATP turnover. The purpose of this investigation was to examine the effect of R rosea ingestion on human skeletal muscle PCr recovery after exhaustive exercise. Twelve resistance-trained men, aged 19 to 39 years, completed incremental forearm wrist flexion exercise to volitional fatigue, once after ingesting 1500 mg R rosea per day for 4 days, and once after ingesting an equivalent placebo dose. During exercise and recovery from exercise, muscle phosphates were examined using phosphorus 31 nuclear magnetic resonance spectroscopy. [PCr] during recovery was fit with a monoexponential function, and the resulting rate constants (k) were compared between groups. Rating of perceived exertion per stage and time to exhaustion were also compared between groups. For R rosea, k=0.3744+/-0.1532, whereas for placebo, k=0.3956+/-0.2238. Although rating of perceived exertion significantly increased within groups as workload increased, it did not differ between conditions, nor did time to exhaustion (R rosea, 10.71+/-0.54 minutes; placebo, 10.48+/-0.68 minutes). Estimates of [PCr] at time 0, 5, 10, 15, and 20 minutes of recovery were nearly identical between groups. In summary, there were no significant differences between groups for any of theparameters measured. Based on these results, we conclude that R rosea ingestion does not improve ATP turnover during or immediately after exercise.

Exploring the potential ergogenic effects of glycerol hyperhydration.

During athletic competition or recreational pursuits, a body's hydration level can become compromised, resulting in a decrement in performance. Glycerol (1,2,3-propanetriol) has been used to induce hyperhydration in an attempt to offset the deleterious effects of dehydration. When glycerol is consumed orally, it is rapidly absorbed primarily in the small intestine. It is reported to be evenly distributed among all fluid compartments, with the exception of the cerebral spinal fluid and aqueous humour, and promotes hyperhydration by inducing an osmotic gradient. Through an increase in the kidney's medullary concentration gradient, water absorption in the nephron is enhanced. When glycerol is consumed, the plasma glycerol concentration increases in proportion to the dose ingested, which easily exceeds the glycerol saturation point resulting in urinary glycerol excretion. Thus, without supplemental glycerol ingestion, there will be a decrease in the osmotic gradient resulting in a loss of hyperhydration. The ergogenic nature of glycerol has been investigated as to its effect on fluid retention, thermoregulation, cardiovascular responses and performance. While many studies provide evidence of hyperhydration, others do not. Only two studies reviewed showed a thermoregulatory advantage. Furthermore, the preponderance of evidence neither weighed for or against cardiovascular or performance advantages. What makes one study provide favourable results while another study does not is unclear. Possible explanations may include subject characteristics, environmental factors, research design, whether fluids with or without glycerol were given during exercise, the rate at which fluids are initially given to induce hyperhydration, the time between peak hyperhydration/peak plasma glycerol concentration and the trial (i.e. exercise), the glycerol dose (i.e. 1.0 g/kg body mass) and what it is based upon, the percentage glycerol solution (i.e. 5%, 20%), the variation of time between the end of the hydration protocol and the beginning of exercise, or perhaps the intensity of exercise (fixed, variable, percentage maximum oxygen uptake). What is clear is that glycerol has the capacity to enhance fluid retention. In so doing, glycerol hyperhydration may be a logistically preferred method due to concomitant decrease in urine output and free-water clearance, which may give a performance advantage by offsetting dehydration. Future research should focus on maintaining plasma glycerol concentrations at levels necessary to maintain osmotic forces required to support continued hyperhydration. Potential benefits of glycerol should be further explored to identify the circumstances or factors that may contribute to an ergogenic effect.

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.

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.