Sarcopenic obesity necessitates a multifaceted exercise prescription combining aerobic and resistance training to restore metabolic flexibility and counteract muscle wasting. However, classical sports physiology dictates an "interference effect," where AMP-activated protein kinase (AMPK) activated by aerobic energy stress inhibits the mechanistic target of rapamycin complex 1 (mTORC1) anabolism via the TSC2 complex. This perspective argues that applying this mutually exclusive paradigm primarily derived from young, elite athletes to geriatric populations is physiologically unsound and creates a massive translational gap. Aging muscle operates under a distinct pathological microenvironment characterized by chronic basal AMPK activation and pre-existing anabolic resistance. Despite these theoretical blockades, clinical evidence demonstrates that older adults consistently exhibit dual positive functional adaptations to concurrent training. To resolve this paradox, we propose the "Metabolic Re-synchronization" model. We hypothesize that AMPK-mTOR crosstalk is a manipulable continuum governed by temporal kinetics and chrononutrition. By employing optimal inter-session recovery windows (6–24 hours), the initial aerobic bout acts as an anabolic primer via intracellular calcium dynamics, allowing subsequent resistance training to deploy specific hypertrophic transcripts like PGC-1α4 without cross-interference. Furthermore, targeted post-exercise essential amino acid interventions act as a biochemical override to bypass the lingering TSC2 blockade. Ultimately, this framework provides a mechanistically grounded strategy to optimize exercise dosage, clear dysfunctional organelles, and preserve neuromuscular junction (NMJ) integrity in the management of sarcopenic obesity.
Muhamad Dwi Putra (Sun,) studied this question.