Abstract

Key points Continuous high‐intensity constant‐power exercise is unsustainable, with maximal oxygen uptake (V˙O2 max ) and the limit of tolerance attained after only a few minutes.Performing the same power intermittently reduces the O2 cost of exercise and increases tolerance. The extent to which this dissociation is reflected in the intramuscular bioenergetics is unknown.We used pulmonary gas exchange and 31P magnetic resonance spectroscopy to measure whole‐body V˙O2, quadriceps phosphate metabolism and pH during continuous and intermittent exercise of different work:recovery durations.Shortening the work:recovery durations (16:32 s vs. 32:64 s vs. 64:128 s vs. continuous) at a work rate estimated to require 110% peak aerobic power reduced V˙O2, muscle phosphocreatine breakdown and muscle acidification, eliminated the glycolytic‐associated contribution to ATP synthesis, and increased exercise tolerance.Exercise intensity (i.e. magnitude of intramuscular metabolic perturbations) can be dissociated from the external power using intermittent exercise with short work:recovery durations. Compared with work‐matched high‐intensity continuous exercise, intermittent exercise dissociates pulmonary oxygen uptake (V˙O2) from the accumulated work. The extent to which this reflects differences in O2 storage fluctuations and/or contributions from oxidative and substrate‐level bioenergetics is unknown. Using pulmonary gas‐exchange and intramuscular 31P magnetic resonance spectroscopy, we tested the hypotheses that, at the same power: ATP synthesis rates are similar, whereas peak V˙O2 amplitude is lower in intermittent vs. continuous exercise. Thus, we expected that: intermittent exercise relies less upon anaerobic glycolysis for ATP provision than continuous exercise; shorter intervals would require relatively greater fluctuations in intramuscular bioenergetics than in V˙O2 compared to longer intervals. Six men performed bilateral knee‐extensor exercise (estimated to require 110% peak aerobic power) continuously and with three different intermittent work:recovery durations (16:32, 32:64 and 64:128 s). Target work duration (576 s) was achieved in all intermittent protocols; greater than continuous (252 ± 174 s; P < 0.05). Mean ATP turnover rate was not different between protocols (∼43 mm min−1 on average). However, the intramuscular phosphocreatine (PCr) component of ATP generation was greatest (∼30 mm min−1), and oxidative (∼10 mm min−1) and anaerobic glycolytic (∼1 mm min−1) components were lowest for 16:32 and 32:64 s intermittent protocols, compared to 64:128 s (18 ± 6, 21 ± 10 and 10 ± 4 mm min−1, respectively) and continuous protocols (8 ± 6, 20 ± 9 and 16 ± 14 mm min−1, respectively). As intermittent work duration increased towards continuous exercise, ATP production relied proportionally more upon anaerobic glycolysis and oxidative phosphorylation, and less upon PCr breakdown. However, performing the same high‐intensity power intermittently vs. continuously reduced the amplitude of fluctuations in V˙O2 and intramuscular metabolism, dissociating exercise intensity from the power output and work done.

Highlights

  • The coupling of internal to external O2 exchange during dynamic exercise is dependent on muscular oxidativeATP synthesis, the dynamics of the circulation, and volume of the intervening O2 stores, predominantly in the form of oxyhaemoglobin in the venous blood

  • The O2 deficit is associated with accumulation of products linked to muscle fatigue, such as intramuscular inorganic phosphate (Pi) and H+ (Allen et al 2008), and V O2 kinetics are strongly associated with exercise tolerance

  • During the shortest work:recovery duration of intermittent exercise, we found that the peak and nadir of the V O2 and PCr fluctuations remained below values associated with the lactate threshold and there were no net contributions from anaerobic glycolysis to meet the cellular demands for ATP turnover, despite power exceeding that achieved at V maximal oxygen uptake (O2max) in the ramp-incremental exercise test (RIT)

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Summary

Introduction

The coupling of internal (capillary-to-myocyte) to external (capillary-to-alveolus) O2 exchange during dynamic exercise is dependent on muscular oxidativeATP synthesis, the dynamics of the circulation, and volume of the intervening O2 stores, predominantly in the form of oxyhaemoglobin in the venous blood. At the onset of continuous constant-power exercise, the kinetics of pulmonary oxygen uptake (V O2) are supplemented by contributions to energy transfer from utilization of O2 stores and, proportionally more significant, from substrate-level phosphorylation [phosphocreatine (PCr) breakdown, glycolysis/glycogenolysis accumulating lactate]; termed the O2 deficit. Critical power (the asymptote of the relationship between power and tolerable duration, which occurs between ß60% and 80% V O2max; Poole et al 1988; van der Vaart et al 2014) marks the individual threshold in the rate of metabolic power production below which the bodily demands for ATP resynthesis are met by wholly-aerobic energy transfer (Poole et al 1988; Jones et al 2008). During continuous exercise exceeding critical power, V O2 continues to rise (through the action of the dsloowwncaonmdpPoinaenndt;HV+Oa2ScCc)u, manudlaitniotnraamreupscruolgarresPsCivre break(Poole et al 1988; Jones et al 2008; Vanhatalo et al 2010)

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