Abstract

This study focused on the steady-state phase of exercise to evaluate the relative contribution of metabolic instability (measured with NIRS and haematochemical markers) and muscle activation (measured with EMG) to the oxygen consumption ({dot{V}O_2}) slow component ({dot{V}O_2}{_s}{_c}) in different intensity domains. We hypothesized that (i) after the transient phase, {dot{V}O_2}, metabolic instability and muscle activation tend to increase differently over time depending on the relative exercise intensity and (ii) the increase in {dot{V}O_2}{_s}{_c} is explained by a combination of metabolic instability and muscle activation. Eight active men performed a constant work rate trial of 9 min in the moderate, heavy and severe intensity domains. {dot{V}O_2}, root mean square by EMG (RMS), deoxyhaemoglobin by NIRS ([HHb]) and haematic markers of metabolic stability (i.e. [La−], pH, HCO3−) were measured. The physiological responses in different intensity domains were compared by two-way RM-ANOVA. The relationships between the increases of [HHb] and RMS with {dot{V}O_2} after the third min were compared by simple and multiple linear regressions. We found domain-dependent dynamics over time of {dot{V}O_2}, [HHb], RMS and the haematic markers of metabolic instability. After the transient phase, the rises in [HHb] and RMS showed medium–high correlations with the rise in {dot{V}O_2} ([HHb] r = 0.68, p < 0.001; RMS r = 0.59, p = 0.002). Moreover, the multiple linear regression showed that both metabolic instability and muscle activation concurred to the {dot{V}O_2}{_s}{_c} (r = 0.75, [HHb] p = 0.005, RMS p = 0.042) with metabolic instability possibly having about threefold the relative weight compared to recruitment. Seventy-five percent of the dynamics of the {dot{V}O_2}{_s}{_c} was explained by [HHb] and RMS.

Highlights

  • During constant work rate exercise (CWR), oxygen consumption (V O2 ) response is linearly related to the workload with a ratio of around ~ 10 ml*min−1*W–1 [23]

  • We tested the following hypotheses: (i) after the initial 3 min, V O2, metabolic instability and muscle activation display a different tendency to increase over time depending on the relative exercise intensity and (ii) the increase in V O2sc is explained by a combination of metabolic instability and muscle activation

  • gas exchange threshold (GET) and RCP were identified at a V O2 respectively of 2418 ± 385 and 3094 ± 377 ml*min−1, while the V O2 targets in the moderate, heavy and severe exercise domains were identified at 1935 ± 308 ml*min−1, 2743 ± 348 ml*min−1 and 3154 ± 408 ml*min−1.V O2 values recorded in the last 30 s of exercise were 1973 ± 478 ml*min−1 for moderate, 3013 ± 365 ml*min−1 for heavy and 3640 ± 514 ml*min−1 for severe, highlighting a clear contribution of the V O2 slow component in the rise of V O2 over time both in the heavy and severe domains

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Summary

Introduction

During constant work rate exercise (CWR), oxygen consumption (V O2 ) response is linearly related to the workload with a ratio of around ~ 10 ml*min−1*W–1 [23]. Given that the V O2sc may not entail a loss of efficiency of locomotion in heavy but only in severe [10], a study aimed at testing its muscular contributors at different intensities would add valuable information to the ongoing debate In this context, near-infrared spectroscopy (NIRS) provides a non-invasive index of oxygen extraction that reflects the imbalance between delivery and utilization within the working muscle [18, 19] and in turn may be associated with metabolic instability [17]. We tested the following hypotheses: (i) after the initial 3 min, V O2 , metabolic instability and muscle activation display a different tendency to increase over time depending on the relative exercise intensity (i.e. no changes occur in the moderate domain and increasing dynamics are observed in the heavy and severe intensity domains) and (ii) the increase in V O2sc is explained by a combination of metabolic instability and muscle activation

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