Abstract

BackgroundThe severity of performance fatigability and the capacity to recover from activity are profoundly influenced by skeletal muscle energetics, specifically the ability to buffer fatigue-inducing ions produced from anaerobic metabolism. Mechanisms responsible for buffering these ions result in the production of excess carbon dioxide (CO2) that can be measured as expired CO2 ( dot{mathrm{V}} CO2) during cardiopulmonary exercise testing (CPET). The primary objective of this study was to assess the feasibility of select assessment procedures for use in planning and carrying out interventional studies, which are larger interventional studies investigating the relationships between CO2 expiration, measured during and after both CPET and submaximal exercise testing, and performance fatigability.MethodsCross-sectional, pilot study design. Seven healthy subjects (30.7±5.1 years; 5 females) completed a peak CPET and constant work-rate test (CWRT) on separate days, each followed by a 10-min recovery then 10-min walk test. Oxygen consumption ( dot{mathrm{V}} O2) and dot{mathrm{V}} CO2 on- and off-kinetics (transition constant and oxidative response index), excess- dot{mathrm{V}} CO2, and performance fatigability severity scores (PFSS) were measured. Data were analyzed using regression analyses.ResultsAll subjects that met the inclusion/exclusion criteria and consented to participate in the study completed all exercise testing sessions with no adverse events. All testing procedures were carried out successfully and outcome measures were obtained, as intended, without adverse events. Excess- dot{mathrm{V}} CO2 accounted for 61% of the variability in performance fatigability as measured by dot{mathrm{V}} O2 on-kinetic ORI (ml/s) (R2=0.614; y = 8.474x − 4.379, 95% CI [0.748, 16.200]) and 62% of the variability as measured by PFSS (R2=0.619; y = − 0.096x + 1.267, 95% CI [−0.183, −0.009]). During CPET, dot{mathrm{V}} CO2 -off ORI accounted for 70% (R2=0.695; y = 1.390x − 11.984, 95% CI [0.331, 2.449]) and dot{mathrm{V}} CO2 -off Kt for 73% of the variability in performance fatigability measured by dot{mathrm{V}} O2 on-kinetic ORI (ml/s) (R2=0.730; y = 1.818x − 13.639, 95% CI [0.548, 3.087]).ConclusionThe findings of this study suggest that utilizing dot{mathrm{V}} CO2 measures may be a viable and useful addition or alternative to dot{mathrm{V}} O2 measures, warranting further study. While the current protocol appeared to be satisfactory, for obtaining select cardiopulmonary and performance fatigability measures as intended, modifications to the current protocol to consider in subsequent, larger studies may include use of an alternate mode or measure to enable control of work rate constancy during performance fatigability testing following initial CPET.

Highlights

  • The severity of performance fatigability and the capacity to recover from activity are profoundly influenced by skeletal muscle energetics, the ability to buffer fatigue-inducing ions produced from anaerobic metabolism

  • While the current protocol appeared to be satisfactory, for obtaining select cardiopulmonary and performance fatigability measures as intended, modifications to the current protocol to consider in subsequent, larger studies may include use of an alternate mode or measure to enable control of work rate constancy during performance fatigability testing following initial cardiopulmonary exercise testing (CPET)

  • If oxidative capacity is insufficient for meeting this demand entirely or if buffering of the ionic by-products of anaerobic metabolism is insufficient for maintaining an optimal intracellular pH, a competitive environment emerges in which an increase in glycolytic by-product accumulation tends to inhibit cross-bridge formation and metabolic pump activity [6, 18]

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Summary

Introduction

The severity of performance fatigability and the capacity to recover from activity are profoundly influenced by skeletal muscle energetics, the ability to buffer fatigue-inducing ions produced from anaerobic metabolism. Gross muscle function impairment, reduced cardiorespiratory capacity, decreased exercise tolerance, and increased performance fatigability follow [13, 20, 32, 33] Mechanisms such as lactate formation and the carbonic anhydrase-bicarbonate system buffer these fatigue-inducing hydrogen ions (H+) resulting in what is often called “nonmetabolic or excess carbon dioxide (CO2)” production [4, 6, 22]. This accumulation can be observed in concomitance with a departure of the rise of expired CO2 (V CO2) plotted on oxygen consumption (V O2) or time from linearity during a cardiopulmonary exercise test (CPET) [4]. The V CO2 deflection point is designated by the terms anaerobic threshold (AT), gas exchange threshold, or ventilatory threshold other terms may be appropriate, and all are often used interchangeably

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