Author(s): KURUCSAI, G., Institution: DR. KURUCSAI MEDICAL CARE CENTRE, Country: HUNGARY, Abstract-ID: 630

INTRODUCTION:
Classical threshold concepts (VT1/VT2; lactate thresholds) are typically derived from incremental laboratory protocols, yet team-sport reality includes disruptor bouts and a reversed (decreasing-intensity) workload structure. We hypothesized that lactate alone becomes non-informative during field recovery kinetics, whereas acid–base and blood-gas logistics better and faster track substrate switching and recovery biology.
METHODS:
Thirty-eight elite American football players (EFL) completed a standardized postprandial, field-ready performance test: mixed meal + digestion, then an in-lab stepwise warm-up and incremental YMCA protocol, immediately followed by a 1-min “disruptor” all-out bout. The subsequent field phase was intentionally reversed (decremental): high-demand mixed drills/CrossFit-type work transitioned to lower-intensity aerobic running, then stretching and passive recovery, reflecting match-like load followed by progressive unloading. Venous samples were repeatedly obtained via cannula and analyzed point-of-care for pH (H⁺ load), pO₂, pCO₂ and lactate. Indirect calorimetry quantified substrate kinetics (FFA contribution).
RESULTS:
A key marker finding was threshold-equivalent lactate under two physiologically different conditions: YMCA vs the field aerobic-run phase (YMCA: 5.95 ± 1.78 vs aerobic run: 6.24 ± 1.98 mmol·L⁻¹, NS). Despite similar lactate, the accompanying regulatory milieu diverged: Acid–base/H⁺: YMCA H⁺ 5.33 ± 0.82 nmol·dL⁻¹ (≈pH 7.27) vs aerobic run H⁺ 4.59 ± 0.53 (≈pH 7.34), p<0.001. O₂–CO₂ clearance: pO₂/pCO₂ YMCA 0.79 ± 0.37 vs aerobic run 0.97 ± 0.41, p<0.001. Substrate kinetics: FFA utilization YMCA 12.66 ± 11.14% vs aerobic run 31.10 ± 13.66%, p<0.001. CO₂ elimination showed a FEtCO₂ plateau, whereas O₂ availability remained intensity-dependent (as indicated by SmO₂), shaping the pO₂/pCO₂ response and aligning with higher field CHO reliance (HIF-1α–linked) despite unchanged lactate. Insulin increased during passive recovery vs aerobic run (p<0.01) despite a parallel elevation in whole-body FFA utilization, supporting dissociation of hormonal control from substrate oxidation.
CONCLUSION:
In a field-realistic, reversed workload sequence, lactate can remain “high/threshold-like” while pH/H⁺, pO₂/pCO₂, and fat utilization normalize; thus, lactate becomes a false state marker of metabolic readiness after disruptor bouts. Recovery should be interpreted through integrated O₂/CO₂ logistics and acid–base control: intensity-dependent reductions in O₂ availability likely destabilize HIF-1α–linked regulation and promote higher CHO reliance even at similar lactate. Active (low-intensity) vs passive recovery represents a metabolic divergence: active recovery sustains oxidative flux and lactate reutilization in local muscles (via monocarboxylate transporter 1, MCT1) and supports by-product handling, whereas passive recovery favors persistence of uncoupling. This marks the distinction between fatigue accumulation and adaptation.