Metabolic instability vs fibre recruitment contribution to the $${\dot{V}O_2}$$ slow component in different exercise intensity domains

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 ($${\dot{V}O_2}$$ V ˙ O 2 ) slow component ($${\dot{V}O_2}{_s}{_c}$$ V ˙ O 2 s c ) in different intensity domains. We hypothesized that (i) after the transient phase, $${\dot{V}O_2}$$ 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 $${\dot{V}O_2}{_s}{_c}$$ 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. $${\dot{V}O_2}$$ 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 $${\dot{V}O_2}$$ V ˙ O 2 after the third min were compared by simple and multiple linear regressions. We found domain-dependent dynamics over time of $${\dot{V}O_2}$$ 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 $${\dot{V}O_2}$$ 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 $${\dot{V}O_2}{_s}{_c}$$ 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 $${\dot{V}O_2}{_s}{_c}$$ V ˙ O 2 s c was explained by [HHb] and RMS.

Power Output Manipulation from Below to Above the Gas Exchange Threshold Results in Exacerbated Performance Fatigability

“…The former hypothesis is not supported in the present study given the stability of VL EMG RMS in the presence of a manifested VO 2SC during supra-GET cycling. Although the limitations of compound EMG might limit the ability to detect subtle increases in motor unit recruitment (31), the lack of temporal association between the EMG RMS and the VO 2SC corroborates numerous other studies (32)(33)(34) but conflicts with others (27,28). Regarding the latter hypothesis, it is interesting to note that in the present study, both heavy-and moderate-intensity exercise elicited impairments in neuromuscular function in contrast to previous results (12).…”

Modeling V̇o2 on-kinetics based on intensity-dependent delayed adjustment and loss of efficiency (DALE)

“…The framework described earlier is corroborated by recent findings from our group (15,18) and others (19), suggesting that, in the heavy domain, a contribution of fast-twitch fibers may suffice to explain the observed slowing of the V _ O 2 kinetics and, possibly, a concomitant increase in gain, without the need for increased recruitment over time as an explanatory mechanism. Moreover, in the heavy domain, the so-called V _ O 2 slow component may not be the result of a loss of efficiency manifesting over time; rather, it may be the result of a slower upregulation of the activity of rate-limiting enzymes and provision of adequate substrates.…”

“…Moreover, in the heavy domain, the so-called V _ O 2 slow component may not be the result of a loss of efficiency manifesting over time; rather, it may be the result of a slower upregulation of the activity of rate-limiting enzymes and provision of adequate substrates. In the severe domain of exercise, however, the bioenergetic approach proposed by Colosio et al (15,18) verified the existence of a true slow component of V _ O 2 (i.e., a loss of efficiency over time), which develops in unison with increased muscle activation. Accordingly, characterization of the V _ O 2 response in this domain should include a delayed onset term, similar to the third phase of the traditional three-phase modeling of V _ O 2 kinetics.…”

The effects of exercise intensity and duration on the relationship between the slow component of V̇O2 and peripheral fatigue

“…4 VȮ 2SC has been mostly related to impairments in contractile function and the development of neuromuscular fatigue (NMF), 5 despite a possible contribution in muscle substrate utilization shift from glycolysis to βoxidation during the submaximal exercise. [6][7][8] This has important physiological and applied connotations, as the development of both the VȮ 2SC and NMF has been linked with exercise tolerance. 9,10 Recent evidence has linked the development of peripheral fatigue to both the time and intensity of exercise that elicits the VȮ 2SC .…”

“…Although the precise mechanisms contributing to the development of the V̇O 2SC remain to be fully elucidated, it is believed that a large portion (~85%) of the V̇O 2SC is because of the changes within the active muscles 4 . V̇O 2SC has been mostly related to impairments in contractile function and the development of neuromuscular fatigue (NMF), 5 despite a possible contribution in muscle substrate utilization shift from glycolysis to β‐oxidation during the submaximal exercise 6‐8 . This has important physiological and applied connotations, as the development of both the V̇O 2SC and NMF has been linked with exercise tolerance 9,10 …”