Most studies focusing on the interaction between IF and motor performance have generally used training paradigms involving endurance exercise [27, 28] or examined changes in physiological capacity elicited by Ramadan fasting . Various factors related to endurance-exercise fatigue (e.g. depletion of carbohydrate stores, increased body temperature and dehydration) are less likely to affect motor performance during physically demanding tasks lasting only a few seconds or a few minutes . Moreover, the negative impact of Ramadan fasting on WnT performance is not relevant to TRF because most people can stay well-hydrated by unrestricted non-caloric fluid ingestion . By showing that WnT performance improved after 4 weeks of TRF (vs. non-TRF) in healthy well-trained young men, our findings are well aligned with this concept. We also found that the mechanistic basis of heightened WnT performance does not depend on altered body composition post-TRF. Finally, our data indicate that short-term TRF (i.e. 1 week) is ineffective for changing individual WnT performance and body composition.
WnT power output is related to athletic performance in sports involving short bouts of supramaximal exercise (e.g., football, tennis, basketball, field hockey, running, rowing, canoeing, swimming, cross training and wrestling) [14, 16, 31–33]. Power output is particularly critical for the fast speeds observed in mid-distance events . We found that, after 4 weeks of TRF, participants improved their total work time by more than 1 s. This magnitude of improvement can be practically meaningful for track and field athletes who compete in running distances of 400/800 m, and may represent the difference between qualifying for a competition or even winning a race (e.g. the difference between the former and new 400 m running distance world record is of 15 centesimal seconds) . This is even more relevant when considering that participants who enrolled in this investigation continued their habitual training throughout the study and exhibited no differences in daily dietary intake before each intervention (TRF vs. non-TRF). Ultimately, the result indicates that enhanced WnT performance was primarily linked with the physiological adaptations elicited by TRF per se. However, given that WnT performance did not improve after 1 week of intervention, it should also be emphasized that the magnitude of interaction between TRF and WnT performance is strongly mediated by the duration of TRF.
The impact of fasting on WnT performance remains poorly understood. According to past research, while short-term TRF has detrimental effects on WnT peak power during the early phase of restriction, performance returns to that seen at baseline after 4 days of dieting . Unfortunately, it is difficult to compare our results with those of Naharudin et al (2018) because their experimental design involved a TRF duration that was limited to 10 days, involved a 40% daily CR and only reported measures of peak power. Nevertheless, as we also did not observe any impact of short- or long-term TRF (i.e. 1 or 4 weeks, respectively) on peak power, it may be concluded that this specific marker of motor performance remains largely unaffected beyond 1 week of TRF and that this occurs similarly either with or without CR. In accordance, it can be concluded that short-term TRF exerts no significant impact on the ability of the lower-limb muscles to produce high mechanical power . Conversely, 4 weeks of TRF led to a positive adaptation in WnT mean power, implying that this nutritional regimen is effective for improving muscular endurance of the lower-limbs (i.e. their ability to sustain extremely high power outputs) . The etiological basis of heightened mean power may relate to increases in the expression of SIRT1 and phosphorylated AMPK with exercise in the fasted state . AMPK has numerous downstream effects on gene expression and is involved in the regulation of mitochondrial biogenesis, in the use of metabolic substrates, and autophagy . On the other hand, SIRT1 is involved in the regulation of metabolic processes primarily related to mitochondrial adaptation via increased peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and SIRT1, suppressing apoptosis and oxidative stress [17, 37]. Given that performance in WnT has been shown to be highly dependent on energy release from both anaerobic and aerobic processes, improved oxidative capacity (e.g. via mitochondrial biogenesis) resulting from 4 weeks of TRF potentially provides a partial explanation for our findings [9, 10].
TRF was as effective as the control condition in increasing FFM after 4 weeks of intervention. Even though we did not control caloric intake during TRF, participants were asked to maintain their habitual food preferences over the course of the study and no weight loss was observed after 4 weeks of intervention. Therefore, our findings further substantiate that long-term TRF does not negatively impact FFM compared to traditional meal timing given a relatively high protein intake (1.9 g.kg− 1.d− 1). Indeed, increases in FFM post-TRF have been reported in two previous studies in which caloric intake was carefully controlled to avoid weight loss [38, 39]. Moreover, TRF may have an adjunctive role in preserving or delaying FFM losses when combined with resistance training [3, 5].
Although significant decreases in FM with TRF have been reported in some previous studies [2, 3, 6], we were unable to replicate such findings. There are many factors that likely explain the lack of reduction in FM with TRF. For one, the magnitude of the caloric deficit elicited by TRF in this study was not sufficient to reduce body fatness to a significant level. Yet, it should be noted that the participants did lose a small percentage of body fat post-TRF (Table 3). Alternatively, the effectiveness of TRF in reducing FM may vary as a function of baseline body fatness. This is supported by past reports showing that FM is more easily lost in individuals with overweight/obesity than in those exhibiting a healthy body composition .
This study has several limitations that should be taken into account. First, energy and macronutrient intake were estimated based on self-report using dietary record over 4 consecutive days and this approach has known limitations foe accurately assessing nutritional intake [3, 40]. Second, our sample size was relatively small, somewhat compromising statistical power. However, the effect size of TRF on WnT mean power was large (partial eta square > 0.14), indicating a large proportion of the variance in the dependent variable was explained by the independent variable. Third, inclusion was limited to young, well-trained male physical education students and thus our findings cannot be generalized to elite athletes, female athletes, or older participants. Fourth, during the free-living period [wash-out before crossing over to the alternate condition (TRF or non-TRF)], participants were instructed to follow their regular dietary habits. This lack of standardization may have influenced the baseline results and lessened our ability to detect differences after 1-week of TRF. Finally, although efforts were made to ensure that the participants followed their habitual training practices throughout the study (i.e. through detailed instruction and weekly follow-up contact), the exercise sessions were not directly supervised by any member of the research team. That said, the crossover design would seemingly account for individual variability in this regard.