Commencing some training sessions with reduced carbohydrate (CHO) availability has been shown to enhance skeletal muscle adaptations, but the effect on exercise performance is less clear. We examined whether restricting CHO intake between twice daily sessions of high-intensity interval training (HIIT) augments improvements in exercise performance and mitochondrial content. Eighteen active but not highly trained subjects (peak oxygen uptake [VO2peak] = 44 ± 9 ml/kg/min), matched for age, sex, and fitness, were randomly allocated to two groups. On each of 6 days over 2 weeks, subjects completed two training sessions, each consisting of 5 × 4-min cycling intervals (60% of peak power), interspersed by 2 min of recovery. Subjects ingested either 195 g of CHO (HI-HI group: ~2.3 g/kg) or 17 g of CHO (HI-LO group: ~0.3 g/kg) during the 3-hr period between sessions. The training-induced improvement in 250-kJ time trial performance was greater (p = .02) in the HI-LO group (211 ± 66 W to 244 ± 75 W) compared with the HI-HI group (203 ± 53 W to 219 ± 60 W); however, the increases in mitochondrial content was similar between groups, as reflected by similar increases in citrate synthase maximal activity, citrate synthase protein content and cytochrome c oxidase subunit IV protein content (p > .05 for interaction terms). This is the first study to show that a short-term “train low, compete high” intervention can improve whole-body exercise capacity. Further research is needed to determine whether this type of manipulation can also enhance performance in highly-trained subjects.
Andrew J.R. Cochran, Frank Myslik, Martin J. MacInnis, Michael E. Percival, David Bishop, Mark A. Tarnopolsky and Martin J. Gibala
Andrew J.R. Cochran, Michael E. Percival, Sara Thompson, Jenna B. Gillen, Martin J. MacInnis, Murray A. Potter, Mark A. Tarnopolsky and Martin J. Gibala
Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. β-alanine (β-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic β-ALA supplementation would augment work capacity during SIT and augment training-induced adaptations in skeletal muscle and performance. Twenty-four active but untrained men (23 ± 2 yr; VO2peak = 50 ± 6 mL·kg−1·min−1) ingested 3.2 g/day of β-ALA or a placebo (PLA) for a total of 10 weeks (n = 12 per group). Following 4 weeks of baseline supplementation, participants completed a 6-week SIT intervention. Each of 3 weekly sessions consisted of 4–6 Wingate tests, i.e., 30-s bouts of maximal cycling, interspersed with 4 min of recovery. Before and after the 6-week SIT program, participants completed a 250-kJ time trial and a repeated sprint test. Biopsies (v. lateralis) revealed that skeletal muscle carnosine content increased by 33% and 52%, respectively, after 4 and 10 weeks of β-ALA supplementation, but was unchanged in PLA. Total work performed during each training session was similar across treatments. SIT increased markers of mitochondrial content, including cytochome c oxidase (40%) and β-hydroxyacyl-CoA dehydrogenase maximal activities (19%), as well as VO2peak (9%), repeated-sprint capacity (5%), and 250-kJ time trial performance (13%), but there were no differences between treatments for any measure (p < .01, main effects for time; p > .05, interaction effects). The training stimulus may have overwhelmed any potential influence of β-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.
Martin J. MacInnis, Aaron C.Q. Thomas and Stuart M. Phillips
during their competitive seasons. Indeed, the 60-minute MPO was a better predictor of cycling performance than maximum oxygen uptake or skeletal muscle capillarization, fiber type, or mitochondrial content. 3 The 60-minute TT is reproducible 4 and has been used to assess the effectiveness of various
Sabrina Skorski, Iñigo Mujika, Laurent Bosquet, Romain Meeusen, Aaron J. Coutts and Tim Meyer
and thus possibly augment mitochondrial biogenesis. 45 However, Broatch et al 46 observed only limited effects on exercise-induced mitochondrial biogenesis, changes in mitochondrial content or function, and VO 2 max when administering regular CWI during a 6-week cycling sprint interval training
Guillaume P. Ducrocq, Thomas J. Hureau, Olivier Meste and Grégory M. Blain
.181743 20100740 18. Jacobs RA , Flück D , Bonne TC , et al . Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function . J Appl Physiol . 2013 ; 115 : 785 – 793 . PubMed ID: 23788574 doi: 10
Øyvind Skattebo, Thomas Losnegard and Hans Kristian Stadheim
profiles, mitochondrial content, and enzyme activities of the exceptionally well-trained arm and leg muscles of elite cross-country skiers . Front Physiol . 2018 ; 9 : 1031 . PubMed ID: 30116201 doi:10.3389/fphys.2018.01031 10.3389/fphys.2018.01031 30116201 14. Van Hall G , Jensen-Urstad M
Iñigo Mujika, Shona Halson, Louise M. Burke, Gloria Balagué and Damian Farrow
glycogen stores. 140 These strategies enhance the cellular outcomes of endurance training, such as increased maximal mitochondrial enzyme activities and/or mitochondrial content and increased rates of lipid oxidation. The combination of research and practical experience has led to a paradigm that athletes