It is well established that different types of exercise can provide a powerful stimulus for mitochondrial biogenesis. However, there are conflicting findings in the literature, and a consensus has not been reached regarding the efficacy of high-intensity exercise to promote mitochondrial biogenesis in humans. The purpose of this review is to examine current controversies in the field and to highlight some important methodological issues that need to be addressed to resolve existing conflicts.

The present paper endeavored to elucidate the topic on the effects of morning versus evening resistance training on muscle strength and hypertrophy by conducting a systematic review and a meta-analysis of studies that examined time of day-specific resistance training. This systematic review was performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines with searches conducted through PubMed/MEDLINE, Scopus, and SPORTDiscus databases. The Downs and Black checklist was used for the assessment of the methodological quality of the included studies. Studies that examined the effects of time of day-specific resistance training (while equating all other training variables, such as training frequency and volume, between the groups) on muscle strength and/or muscle size were included in the present review. The random effects model was used for the meta-analysis. Meta-analyses explored (1) the differences in strength expression between morning and evening hours at baseline; (2) the differences in strength within the groups training in the morning and evening by using their post-intervention strength data from the morning and evening strength assessments; (3) the overall differences between the effects of morning and evening resistance training (with subgroup analyses conducted for studies that assessed strength in the morning hours and for the studies that assessed strength in the evening hours). Finally, a meta-analysis was also conducted for studies that assessed muscle hypertrophy. Eleven studies of moderate and good methodological quality were included in the present review. The primary findings of the review are as follows: (1) at baseline, a significant difference in strength between morning and evening is evident, with greater strength observed in the evening hours; (2) resistance training in the morning hours may increase strength assessed in the morning to similar levels as strength assessed in the evening; (3) training in the evening hours, however, maintains the general difference in strength across the day, with greater strength observed in the evening hours; (4) when comparing the effects between the groups training in the morning versus in the evening hours, increases in strength are similar in both groups, regardless of the time of day at which strength assessment is conducted; and (5) increases in muscle size are similar irrespective of the time of day at which the training is performed.

Key points: Sleep restriction has previously been associated with the loss of muscle mass in both human and animal models. The rate of myofibrillar protein synthesis (MyoPS) is a key variable in regulating skeletal muscle mass and can be increased by performing high‐intensity interval exercise (HIIE), although the effect of sleep restriction on MyoPS is unknown. In the present study, we demonstrate that participants undergoing a sleep restriction protocol (five nights, with 4 h in bed each night) had lower rates of skeletal muscle MyoPS; however, rates of MyoPS were maintained at control levels by performing HIIE during this period. Our data suggest that the lower rates of MyoPS in the sleep restriction group may contribute to the detrimental effects of sleep loss on muscle mass and that HIIE may be used as an intervention to counteract these effects. The present study aimed to investigate the effect of sleep restriction, with or without high‐intensity interval exercise (HIIE), on the potential mechanisms underpinning previously‐reported sleep‐loss‐induced reductions to muscle mass. Twenty‐four healthy, young men underwent a protocol consisting of two nights of controlled baseline sleep and a five‐night intervention period. Participants were allocated into one of three parallel groups, matched for age, , body mass index and habitual sleep duration; a normal sleep (NS) group [8 h time in bed (TIB) each night], a sleep restriction (SR) group (4 h TIB each night), and a sleep restriction and exercise group (SR+EX, 4 h TIB each night, with three sessions of HIIE). Deuterium oxide was ingested prior to commencing the study and muscle biopsies obtained pre‐ and post‐intervention were used to assess myofibrillar protein synthesis (MyoPS) and molecular markers of protein synthesis and degradation signalling pathways. MyoPS was lower in the SR group [fractional synthetic rate (% day^–1), mean ± SD, 1.24 ± 0.21] compared to both the NS (1.53 ± 0.09) and SR+EX groups (1.61 ± 0.14) (P < 0.05). However, there were no changes in the purported regulators of protein synthesis (i.e. p‐AKT^ser473 and p‐mTOR^ser2448) and degradation (i.e. Foxo1/3 mRNA and LC3 protein) in any group. These data suggest that MyoPS is acutely reduced by sleep restriction, although MyoPS can be maintained by performing HIIE. These findings may explain the sleep‐loss‐induced reductions in muscle mass previously reported and also highlight the potential therapeutic benefit of HIIE to maintain myofibrillar remodelling in this context.

Sleep loss has emerged as a risk factor for the development of impaired glucose tolerance. The mechanisms underpinning this observation are unknown; however, both mitochondrial dysfunction and circadian misalignment have been proposed. Because exercise improves glucose tolerance and mitochondrial function, and alters circadian rhythms, we investigated whether exercise may counteract the effects induced by inadequate sleep. To minimize between-group differences of baseline characteristics, 24 healthy young males were allocated into one of the three experimental groups: a Normal Sleep (NS) group (8 h time in bed (TIB) per night, for five nights), a Sleep Restriction (SR) group (4 h TIB per night, for five nights), and a Sleep Restriction and Exercise group (SR+EX) (4 h TIB per night, for five nights and three high-intensity interval exercise (HIIE) sessions). Glucose tolerance, mitochondrial respiratory function, sarcoplasmic protein synthesis (SarcPS), and diurnal measures of peripheral skin temperature were assessed pre- and post-intervention. We report that the SR group had reduced glucose tolerance post-intervention (mean change ± SD, P value, SR glucose AUC: 149 ± 115 A.U., P = 0.002), which was also associated with reduction in mitochondrial respiratory function (SR: -15.9 ± 12.4 pmol O2.s-1.mg-1, P = 0.001), a lower rate of SarcPS (FSR%/day SR: 1.11 ± 0.25%, P < 0.001), and reduced amplitude of diurnal rhythms. These effects were not observed when incorporating three sessions of HIIE during this period (SR+EX: glucose AUC 67 ± 57, P = 0.239, mitochondrial respiratory function: 0.6 ± 11.8 pmol O2.s-1.mg-1, P = 0.997, and SarcPS (FSR%/day): 1.77 ± 0.22%, P = 0.971). A five-night period of sleep restriction leads to reduction in mitochondrial respiratory function, SarcPS, and amplitude of skin temperature diurnal rhythms, with concurrent reduction in glucose tolerance. We provide novel data demonstrating that these same detrimental effects are not observed when HIIE is performed during the period of sleep restriction. These data therefore provide evidence in support of the use of HIIE as an intervention to mitigate the detrimental physiological effects of sleep loss.

Endurance exercise begun with reduced muscle glycogen stores seems to potentiate skeletal muscle protein abundance and gene expression. However, it is unknown whether this greater signaling responses is due to performing two exercise sessions in close proximity—as a first exercise session is necessary to reduce the muscle glycogen stores. In the present study, we manipulated the recovery duration between a first muscle glycogen‐depleting exercise and a second exercise session, such that the second exercise session started with reduced muscle glycogen in both approaches but was performed either 2 or 15 hours after the first exercise session (so‐called “twice‐a‐day” and “once‐daily” approaches, respectively). We found that exercise twice‐a‐day increased the nuclear abundance of transcription factor EB (TFEB) and nuclear factor of activated T cells (NFAT) and potentiated the transcription of peroxisome proliferator‐activated receptor‐ɣ coactivator 1‐alpha (PGC‐1α), peroxisome proliferator‐activated receptor‐alpha (PPARα), and peroxisome proliferator‐activated receptor beta/delta (PPARβ/δ) genes, in comparison with the once‐daily exercise. These results suggest that part of the elevated molecular signaling reported with previous “train‐low” approaches might be attributed to performing two exercise sessions in close proximity. The twice‐a‐day approach might be an effective strategy to induce adaptations related to mitochondrial biogenesis and fat oxidation.