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Purpose τ of the primary phase of $$\dot{V}{\text{O}}_{{2{\text{A}}}}$$ V ˙ O 2 A kinetics during square-wave, moderate-intensity exercise mirrors that of PCr splitting (τPCr). Pre-exercise [PCr] and the absolute variations of PCr (∆[PCr]) occurring during transient have been suggested to control τPCr and, in turn, to modulate $$\dot{V}{\text{O}}_{{2{\text{A}}}}$$ V ˙ O 2 A kinetics. In addition, $$\dot{V}{\text{O}}_{{2{\text{A}}}}$$ V ˙ O 2 A kinetics may be slower when exercise initiates from a raised metabolic level, i.e., from a less-favorable energetic state. We verified the hypothesis that: (i) pre-exercise [PCr], (ii) pre-exercise metabolic rate, or (iii) ∆[PCr] may affect the kinetics of muscular oxidative metabolism and, therefore, τ. Methods To this aim, seven active males (23.0 yy ± 2.3; 1.76 m ± 0.06, $$\dot{V}{\text{O}}_{2\max }$$ V ˙ O 2 max : 3.32 L min−1 ± 0.67) performed three repetitions of series consisting of six 6-min step exercise transitions of identical workload interspersed with different times of recovery: 30, 60, 90, 120, 300 s. Results Mono-exponential fitting was applied to breath-by-breath $$\dot{V}{\text{O}}_{{2{\text{A}}}}$$ V ˙ O 2 A , so that τ was determined. τ decays as a first-order exponential function of the time of recovery (τ = 109.5 × e(−t/14.0) + 18.9 r2 = 0.32) and linearly decreased as a function of the estimated pre-exercise [PCr] (τ = − 1.07 [PCr] + 44.9, r2 = 0.513, P Conclusions Our results in vivo do not confirm the positive linear relationship between τ and pre-exercise [PCr] and ∆[PCr]. Instead, $$\dot{V}{\text{O}}_{{2{\text{A}}}}$$ V ˙ O 2 A kinetics seems to be influenced by the pre-exercise metabolic rate and the altered intramuscular energetic state. |
