I'll start with ten, and you can find more if you like.
Sarcoplasmic reticulum calcium handling and excitation-contraction coupling
Ørtenblad N, Nielsen J, Saltin B, Holmberg HC. Role of glycogen availability in sarcoplasmic reticulum Ca2 kinetics in human skeletal muscle. J Physiol. 2011;589(3):711-25. PMID: 21135051 DOI: 10.1113/jphysiol.2010.195982 Directly shows that depleted muscle glycogen reduces SR Ca2 release rate independent of ATP status.
Ørtenblad N, Westerblad H, Nielsen J. Muscle glycogen stores and fatigue. J Physiol. 2013;591(18):4405-13. PMID: 23652590 DOI: 10.1113/jphysiol.2013.251629 Review by Westerblad's group explicitly arguing that the glycogen-fatigue link operates via E-C coupling, not energy crisis.
Gejl KD, Hvid LG, Frandsen U, Jensen K, Sahlin K, Ørtenblad N. Muscle glycogen content modifies SR Ca2 release rate in elite endurance athletes. Med Sci Sports Exerc. 2014;46(3):496-505. PMID: 24091991 DOI: 10.1249/MSS.0b013e3182a7a435 Demonstrates in elite athletes that lower glycogen reduces calcium release rate, which is a fatigue mechanism independent of ATP.
Subcellular glycogen pool localization
Jensen R, Ørtenblad N, Stausholm MLH, et al. Heterogeneity in subcellular muscle glycogen utilisation during exercise impacts endurance capacity in men. J Physiol. 2020;598(19):4271-92. PMID: 32686845 DOI: 10.1113/JP280247 Shows intramyofibrillar glycogen depletion specifically predicts fatigue, again pointing to a localized E-C coupling mechanism rather than whole-cell ATP failure.
Comprehensive reviews of the mechanisms
Allen DG, Lamb GD, Westerblad H. Skeletal muscle fatigue: cellular mechanisms. Physiol Rev. 2008;88(1):287-332. PMID: 18195089 DOI: 10.1152/physrev.00015.2007 The foundational Physiological Reviews article on muscle fatigue mechanisms. Lays out the multiple peripheral mechanisms (Ca2 release, Pi accumulation, ion handling) without invoking ATP-to-rigor.
Vigh-Larsen JF, Ørtenblad N, Spriet LL, Overgaard K, Mohr M. Muscle glycogen metabolism and high-intensity exercise performance: a narrative review. Sports Med. 2021;51(9):1855-74. PMID: 33900579 DOI: 10.1007/s40279-021-01475-0 Modern review specifically on glycogen and performance, summarizing both direct (calcium kinetics, excitability) and indirect mechanisms.
Vigh-Larsen JF, Ørtenblad N, Nielsen J, Andersen OE, Overgaard K, Mohr M. The role of muscle glycogen content and localization in high-intensity exercise performance: a placebo-controlled trial. Med Sci Sports Exerc. 2022;54(12):2073-86. PMID: 35868015 DOI: 10.1249/MSS.0000000000002967 Placebo-controlled trial showing glycogen content and localization matter for performance.
Economy and substrate-pathway mechanisms
Stellingwerff T, Spriet LL, Watt MJ, et al. Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration. Am J Physiol Endocrinol Metab. 2006;290(2):E380-8. PMID: 16188909 DOI: 10.1152/ajpendo.00268.2005 Shows fat-adapted muscle has downregulated PDH and glycogenolysis, which impairs the capacity to oxidize CHO at high intensity. This is the metabolic-flexibility cost of LCHF that has nothing to do with rigor.
Burke LM, Ross ML, Garvican-Lewis LA, et al. Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers. J Physiol. 2017;595(9):2785-807. PMID: 28012184 DOI: 10.1113/JP273230 The original Supernova study. Performance impairment in elite athletes via loss of exercise economy, not via energy depletion.
Burke LM, Whitfield J, Heikura IA, et al. Adaptation to a low carbohydrate high fat diet is rapid but impairs endurance exercise metabolism and performance despite enhanced glycogen availability. J Physiol. 2021;599(3):771-90. PMID: 32697366 DOI: 10.1113/JP280221 Crucially shows that even when glycogen is restored, the fat-adaptation impairment in CHO oxidation machinery persists. Again, an E-C coupling and economy story, not an ATP-rigor story.
These references collectively establish the modern mechanistic picture: low muscle glycogen impairs performance through sarcoplasmic reticulum calcium release rate, excitation-contraction coupling at the subcellular level, downregulation of the PDH complex and glycogenolytic enzymes, and loss of exercise economy. None of them invokes ATP falling to rigor levels, because no serious researcher in this space has ever claimed it does. Noakes' attack on TAT is an attack on a position the field abandoned decades ago.