Abstract
Manipulating dietary macronutrient intake may modulate adaptive responses to exercise, and improve endurance performance. However, there is controversy as to the impact of short-term dietary modification on athletic performance. In a parallel-groups, repeated measures study, 16 trained endurance runners (maximal oxygen uptake (O2max): 64.2 ± 5.6 mL·kg−1·min−1) were randomly assigned to, and provided with, either a high-protein, reduced-carbohydrate (PRO) or a high-carbohydrate (CHO) isocaloric-matched diet. Participants maintained their training load over 21-consecutive days with dietary intake consisting of 7-days habitual intake (T1), 7-days intervention diet (T2) and 7-days return to habitual intake (T3). Following each 7-day dietary period (T1–T3), a micro-muscle biopsy was taken for assessment of gene expression, before participants underwent laboratory assessment of a 10 km treadmill run at 75% O2max, followed by a 95% O2max time to exhaustion (TTE) trial. The PRO diet resulted in a modest change (1.37-fold increase, p = 0.016) in AMPK expression, coupled with a significant increase in fat oxidation (0.29 ± 0.05 to 0.59 ± 0.05 g·min−1, p < 0.0001). However, a significant reduction of 23.3% (p = 0.0003) in TTE post intervention was observed; this reverted back to pre levels following a return to the habitual diet. In the CHO group, whilst no change in sub-maximal fuel utilisation occurred at T2, a significant 6.5% increase in TTE performance (p = 0.05), and a modest, but significant, increase in AMPK (p = 0.042) and PPAR (p = 0.029) mRNA expression compared to T1 were observed; with AMPK (p = 0.011) and PPAR (p = 0.044) remaining significantly elevated at T3. In conclusion, a 7-day isocaloric high protein diet significantly compromised high intensity exercise performance in trained runners with no real benefit on gene markers of training adaptation. A significant increase in fat oxidation during submaximal exercise was observed post PRO intervention, but this returned to pre levels once the habitual diet was re-introduced, suggesting that the response was driven via fuel availability rather than cellular adaptation. A short-term high protein, low carbohydrate diet in combination with endurance training is not preferential for endurance running performance.
Highlights
A number of factors can influence endurance performance, including body mass, aerobic and anaerobic capacity, running efficiency, fuel utilisation and energy metabolism [1].The manipulation of dietary intake has become a popular intervention to target a number of these determinates
It has since been established that a series of transcriptional genes play an essential role in the activation of mitochondrial biogenesis and fatty acid oxidation including: 50 adenosine monophosphate-activated protein kinase (AMPK), silent information regulator (SIRT1), peroxisome proliferator-activated receptors (PPAR) and PGC-1α [4,5,6]
No significant group interactions or time point differences were observed in habitual dietary intake, body mass, lean mass or fat mass (p > 0.05), demonstrating energy intake matched energy requirement during both the dietary intervention and habitual intake weeks
Summary
A number of factors can influence endurance performance, including body mass, aerobic and anaerobic capacity, running efficiency, fuel utilisation and energy metabolism [1].The manipulation of dietary intake has become a popular intervention to target a number of these determinates. A number of factors can influence endurance performance, including body mass, aerobic and anaerobic capacity, running efficiency, fuel utilisation and energy metabolism [1]. 1-alpha (PGC-1α) as having a key functional role in the regulation of mitochondrial processes. It has since been established that a series of transcriptional genes play an essential role in the activation of mitochondrial biogenesis and fatty acid oxidation including: 50 adenosine monophosphate-activated protein kinase (AMPK), silent information regulator (SIRT1), peroxisome proliferator-activated receptors (PPAR) and PGC-1α [4,5,6]. Nutritional interventions (such as increasing energy expenditure [7,8] and manipulating carbohydrate availability [9]), targeting these transcriptional genes have been developed to improve mitochondrial function
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