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.

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.

Open-ended time durations for stationary start intense cycle ergometer exercise testing.

The study involved application of different applied loads to measure altered test durations, time to peak power, peak power, and peak cadence during intense cycle ergometry exercise. Healthy, physically active male (n = 11) and female (n = 11) subjects (18-45 years) performed the following 3 bouts of intense cycle ergometry at peak cadence to volitional exhaustion on 3 separate days, 48 h to 1 week apart: (i) 85 g·kg(-1) body mass load; (ii) 75 g·kg(-1) body mass load; and (iii) 100 g·kg(-1) body mass load. Trials (ii) and (iii) were performed in random order after trial (i). Exercise consisted of a stationary start, where test termination occurred when cadence decreased to <35 r·min(-1). Mean (±SD) for gender main effects for time to peak power were 7.64 ± 2.76 vs. 9.49 ± 2.76 s (p < 0.001) for males and females, respectively. Relative peak power data for males vs. females for 75, 85, and 100 g·kg(-1) were 10.01 ± 1.371 vs. 7.81 ± 1.25, 10.16 ± 1.61 vs. 7.67 ± 1.35, and 10.91 ± 2.03 vs. 7.31 ± 1.37 W·kg(-1), respectively. The means for test duration for the GENDER × LOAD interaction (p = 0.09) were 68.25 ± 17.80 vs. 56.5 ± 11.56, 63.70 ± 17.21 vs.57.95 ± 10.45, and 51.99 ± 14.59 vs. 49.54 ± 12.45 s for males vs. females for each of 75, 85, and 100 g·kg(-1), respectively. Stepwise multiple regression involving load and gender resulted in an explanation of variance (R(2)) of only 31.2%. Open-ended testing should be performed at a load of 100 g·kg(-1) body mass for males and 85 g·kg(-1) body mass females, causing volitional exhaustion in approximately 60 s and should allow test duration to be another measured variable.

Validation of a new mixing chamber system for breath-by-breath indirect calorimetry.

Limited validation research exists for applications of breath-by-breath systems of expired gas analysis indirect calorimetry (EGAIC) during exercise. We developed improved hardware and software for breath-by-breath indirect calorimetry (NEW) and validated this system as well as a commercial system (COM) against 2 methods: (i) mechanical ventilation with known calibration gas, and (ii) human subjects testing for 5 min each at rest and cycle ergometer exercise at 100 and 175 W. Mechanical calibration consisted of medical grade and certified calibration gas ((4.95% CO(2), 12.01% O(2), balance N(2)), room air (20.95% O(2), 0.03% CO(2), balance N(2)), and 100% nitrogen), and an air flow turbine calibrated with a 3-L calibration syringe. Ventilation was mimicked manually using complete 3-L calibration syringe manouvers at a rate of 10·min(-1) from a Douglas bag reservoir of calibration gas. The testing of human subjects was completed in a counterbalanced sequence based on 5 repeated tests of all conditions for a single subject. Rest periods of 5 and 10 min followed the 100 and 175 W conditions, respectively. COM and NEW had similar accuracy when tested with known ventilation and gas fractions. However, during human subjects testing COM significantly under-measured carbon dioxide gas fractions, over-measured oxygen gas fractions and minute ventilation, and resulted in errors to each of oxygen uptake, carbon dioxide output, and respiratory exchange ratio. These discrepant findings reveal that controlled ventilation and gas fractions are insufficient to validate breath-by-breath, and perhaps even time-averaged, systems of EGAIC. The errors of the COM system reveal the need for concern over the validity of commercial systems of EGAIC.