Abstract
"Sleep Low-Train Low" is a training-nutrition strategy intended to purposefully reduce muscle glycogen availability around specific exercise sessions, potentially amplifying the training stimulus via augmented cell signalling. The aim of this study was to assess the feasibility of a 3-week home-based "sleep low-train low" programme and its effects on cycling performance in trained athletes. Fifty-five trained athletes (Functional Threshold Power [FTP]: 258 ± 52W) completed a home-based cycling training program consisting of evening high-intensity training (6 × 5 min at 105% FTP), followed by low-intensity training (1 hr at 75% FTP) the next morning, three times weekly for three consecutive weeks. Participant's daily carbohydrate (CHO) intake (6 g·kg-1·d-1) was matched but timed differently to manipulate CHO availability around exercise: no CHO consumption post- HIT until post-LIT sessions [Sleep Low (SL), n = 28] or CHO consumption evenly distributed throughout the day [Control (CON), n = 27]. Sessions were monitored remotely via power data uploaded to an online training platform, with performance tests conducted pre-, post-intervention. LIT exercise intensity reduced by 3% across week 1, 3 and 2% in week 2 (P < 0.01) with elevated RPE in SL vs. CON (P < 0.01). SL enhanced FTP by +5.5% vs. +1.2% in CON (P < 0.01). Comparable increases in 5-min peak power output (PPO) were observed between groups (P < 0.01) with +2.3% and +2.7% in SL and CON, respectively (P = 0.77). SL 1-min PPO was unchanged (+0.8%) whilst CON improved by +3.9% (P = 0.0144). Despite reduced relative training intensity, our data demonstrate short-term "sleep low-train low" intervention improves FTP compared with typically "normal" CHO availability during exercise. Importantly, training was completed unsupervised at home (during the COVID-19 pandemic), thus demonstrating the feasibility of completing a "sleep low-train low" protocol under non-laboratory conditions.
Highlights
Muscle glycogen can mediate cell signalling pathways associated with endurance training adaptation [1], inducing an augmented muscle transcriptional response when exercise is completed under conditions of reduced muscle glycogen availability [2,3,4,5,6]
Participant’s daily carbohydrate (CHO) intake (6 g kg-1 d-1) was matched but timed differently to manipulate CHO availability around exercise: no CHO consumption post- high-intensity training (HIT) until post-low-intensity training (LIT) sessions [Sleep Low (SL), n = 28] or CHO consumption evenly distributed throughout the day [Control (CON), n = 27]
LIT exercise intensity reduced by 3% across week 1, 3 and 2% in week 2 (P < 0.01) with elevated RPE in SL vs. CON (P < 0.01)
Summary
Muscle glycogen can mediate cell signalling pathways associated with endurance training adaptation [1], inducing an augmented muscle transcriptional response when exercise is completed under conditions of reduced muscle glycogen availability [2,3,4,5,6]. AMPK acts as a cellular energy sensor, upregulating peroxisome proliferator-activated receptor 1 coactivator alpha (PGC-1α) activity and expression [1, 9, 10], a transcriptional co-activator often touted as the master regulator of mitochondrial biogenesis [11,12,13], a key hallmark of endurance training adaptation [14,15,16] Concomitant with these adaptations, the increased body fat mobilisation for energy supply during exercise with low glycogen availability, upregulates peroxisome proliferator-activated receptor (PPARδ) transcription factor [17], increasing the expression of proteins involved in lipid metabolism. Despite growing evidence of the molecular adaptation triggered by such “train low” strategies, the translation to improved physical performance remains limited [20, 22, 26, 27]
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