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O-49 Muscle oxygenation normalised to intensity domains during incremental stress testing
  1. Diana Ferreira1,
  2. João Beckert1,
  3. Joana Reis2,
  4. Ricardo Minhalma3,
  5. Alberto Prata1,
  6. Francisco Alves3
  1. 1High Performance Sports Centre of Jamor, IPDJ, Lisbon, Portugal
  2. 2Universidade Europeia, Lisbon, Portugal
  3. 3CIPER, FMH-UL, Lisbon, Portugal


Introduction Incremental protocols for cardiopulmonary exercise testing (CPET) are the gold standard in determining intensity domains (IntDom) for exercise prescription. In CPET, gas analysis provides proxy of muscular metabolism during exercise, but a delay between the end-expiratory gases analysed and the myocyte can be attributed to the buffering of metabolites, fluid convection and gas exchanges.

PO2 at the venous end of a muscle capillary reflects the balance of O2 consumed and

the O2 made available by muscle blood flow, via oxyhemoglobin and plasma dissolved O2. As PO2 decreases, and upon reaching a critical value, O2 is no longer available to ensure ATP regeneration solely from aerobic sources, increasing lactate. The pattern of VCO2 alters, and heavy intensity exercise ensues.

The transcutaneous determination of muscle O2 bound to haemoglobin and myoglobin (HbO2), through near-infrared spectroscopy (NIRS), reflects PO2, and could be an alternative to monitoring local changes in muscle metabolism. Given that in the original time series, the IntDom duration varies from individual to individual, comparing the muscular oxygenation behaviours according to IntDom can be problematic, which is the aim of this work.

Methods Well-trained 45 athletes (37 males and 8 females), aged 28.1 ± 9.3 years, performed a maximal incremental stress test (IncST), twenty-seven in a cycle-ergometer and 18 in a treadmill, with gas-exchange and tissue oxygenation monitoring. The IntDom were determined after estimation of first and second ventilatory thresholds (VT1 and VT2). Oxyhemoglobin (HbO2), deoxyhemogobin (HHb), total haemoglobin (tHb) concentrations were paired into each IntDom. Time series for each IntDom were modified by linear interpolation, so that IntDom for all subjects were the same length. HbO2 and HHb were also represented as the percentage of their own average (HbO2% and HHb%), to assess variation throughout the entirety of the IncST. Statistical significance was set at p < 0.05. A repeated-measures ANOVA was conducted to evaluate changes between different IntDom.

Results A linear increase in HHb was observed throughout the IncST, with significant differences between each IntDom. HbO2 remained stable during moderate and heavy IntDom, but declined significantly in the severe IntDom. tHb concentration increased linearly from moderate to heavy IntDom, and after reaching VT2 decreased, with significant differences between each of the domains. Tissue oxygenation index (TOI) decreased significantly between IntDom.The tHb in the exercising muscle increased throughout the moderate and heavy IntDom.

Abstract O-49 Figure 1

Mean TOI (%) in IntDom

Discussion When critical PO2 is reached, the fine regulation of tissue oxygenation seems to be able to maintain HbO2 despite the increasing VO2. This represents an adequate regulatory response, attributed to the diminished peripheral vascular resistances, and increase in cardiac output.In the severe IntDom, notwithstanding the continuing HHb increase, tHb decreases. We hypothesise that the severe IntDom is characterised by a shortage of the muscular O2 content, thus accentuating anaerobic metabolism, up to maximum individual tolerance.

Conclusion The control mechanisms that regulate O2 delivery are able to maintain normal local oxygenation in moderate and heavy exercise, albeit reaching critical muscular PO2.In severe intensity exercise, a shortage in O2 content ultimately impairs performance.

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