Carbohydrate Ingestion Increases Interstitial Glucose and Mitigates Neuromuscular Fatigue During Single-Leg Knee Extensions

• Published in: Medicine and science in sports and exercise
• Main Authors: Elghobashy, Mohamed E, Richards, Andrew J, Malekzadeh, Rohin, Patel, Disha, Turner, Lauren V, Burr, Jamie F, Power, Geoffrey A, Laham, Robert, Riddell, Michael C, Cheng, Arthur J
• Format: Journal Article
• Language: English
• Published: United States 01.08.2024
• ISSN: 1530-0315
• DOI: 10.1249/MSS.0000000000003440

We aimed to investigate the neuromuscular contributions to enhanced fatigue resistance with carbohydrate ingestion, and to identify whether fatigue is associated with changes in interstitial glucose levels assessed using a continuous glucose monitor (CGM). Twelve healthy participants (6 males, 6 females) performed isokinetic single-leg knee extensions (90°/s) at 20% of the maximal voluntary contraction (MVC) torque until MVC torque reached 60% of its initial value (i.e, task failure). Central and peripheral fatigue were evaluated every 15 min during the fatigue task using the interpolated twitch technique (ITT), and electrically evoked torque. Using a single-blinded cross-over design, participants ingested carbohydrates (CHO) (85 g sucrose/h), or a placebo (PLA), at regular intervals during the fatigue task. Minute-by-minute interstitial glucose levels measured via CGM, and whole blood glucose readings were obtained intermittently during the fatiguing task. CHO ingestion increased time to task failure over PLA (113 ± 69 vs. 81 ± 49 min; mean ± SD; p < 0.001) and was associated with higher glycemia as measured by CGM (106 ± 18 vs 88 ± 10 mg/dL, p < 0.001) and whole blood glucose sampling (104 ± 17 vs 89 ± 10 mg/dL, p < 0.001). When assessing the values in the CHO condition at a similar timepoint to those at task failure in the PLA condition (i.e., ~81 min), MVC torque, % voluntary activation, and 10 Hz torque were all better preserved in the CHO vs. PLA condition (p < 0.05). Exogenous CHO intake mitigates neuromuscular fatigue at both the central and peripheral levels by raising glucose concentrations rather than by preventing hypoglycemia.