Effects of sprint interval training on VO2maxand aerobic exercise performance: A systematic review and meta-analysis: Effects of sprint interval training on VO2max

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Abstract

Recently, several studies have examined whether low-volume sprint interval training (SIT) may improve aerobic and metabolic function. The objective of this study was to systematically review the existing literature regarding the aerobic and metabolic effects of SIT in healthy sedentary or recreationally active adults. A systematic literature search was performed (Bibliotek.dk, SPORTDiscus, Embase, PEDro, SveMed+, and Pubmed). Meta-analytical procedures were applied evaluating effects on maximal oxygen consumption (VO2max). Nineteen unique studies [four randomized controlled trials (RCTs), nine matched-controlled trials and six noncontrolled studies] were identified, evaluating SIT interventions lasting 2-8 weeks. Strong evidence support improvements of aerobic exercise performance and VO2max following SIT. A meta-analysis across 13 studies evaluating effects of SIT on VO2max showed a weighted mean effects size of g = 0.63 95% CI (0.39; 0.87) and VO2max increases of 4.2-13.4%. Solid evidence support peripheral adaptations known to increase the oxidative potential of the muscle following SIT, whereas evidence regarding central adaptations was limited and equivocal. Some evidence indicated changes in substrate oxidation at rest and during exercise as well as improved glycemic control and insulin sensitivity following SIT. In conclusion, strong evidence support improvement of aerobic exercise performance and VO2max following SIT, which coincides with peripheral muscular adaptations. Future RCTs on long-term SIT and underlying mechanisms are warranted.

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PGC-1alpha: a key regulator of energy metabolism.

Huiyun Liang, Walter F Ward (2006)

Peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha is a member of a family of transcription coactivators that plays a central role in the regulation of cellular energy metabolism. It is strongly induced by cold exposure, linking this environmental stimulus to adaptive thermogenesis. PGC-1alpha stimulates mitochondrial biogenesis and promotes the remodeling of muscle tissue to a fiber-type composition that is metabolically more oxidative and less glycolytic in nature, and it participates in the regulation of both carbohydrate and lipid metabolism. It is highly likely that PGC-1alpha is intimately involved in disorders such as obesity, diabetes, and cardiomyopathy. In particular, its regulatory function in lipid metabolism makes it an inviting target for pharmacological intervention in the treatment of obesity and Type 2 diabetes.

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Short-term sprint interval versus traditional endurance training: similar initial adaptations in human skeletal muscle and exercise performance.

Martin Gibala, Jonathan Little, Martin van Essen … (2006)

Brief, intense exercise training may induce metabolic and performance adaptations comparable to traditional endurance training. However, no study has directly compared these diverse training strategies in a standardized manner. We therefore examined changes in exercise capacity and molecular and cellular adaptations in skeletal muscle after low volume sprint-interval training (SIT) and high volume endurance training (ET). Sixteen active men (21 +/- 1 years, ) were assigned to a SIT or ET group (n = 8 each) and performed six training sessions over 14 days. Each session consisted of either four to six repeats of 30 s 'all out' cycling at approximately 250% with 4 min recovery (SIT) or 90-120 min continuous cycling at approximately 65% (ET). Training time commitment over 2 weeks was approximately 2.5 h for SIT and approximately 10.5 h for ET, and total training volume was approximately 90% lower for SIT versus ET ( approximately 630 versus approximately 6500 kJ). Training decreased the time required to complete 50 and 750 kJ cycling time trials, with no difference between groups (main effects, P

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A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms.

Jonathan Little, Adeel Safdar, Geoffrey Wilkin … (2010)

High-intensity interval training (HIT) induces skeletal muscle metabolic and performance adaptations that resemble traditional endurance training despite a low total exercise volume. Most HIT studies have employed 'all out', variable-load exercise interventions (e.g. repeated Wingate tests) that may not be safe, practical and/or well tolerated by certain individuals. Our purpose was to determine the performance, metabolic and molecular adaptations to a more practical model of low-volume HIT. Seven men (21 + or - 0.4 years, V(O2peak) = 46 + or - 2 ml kg(-1) min(-1)) performed six training sessions over 2 weeks. Each session consisted of 8-12 x 60 s intervals at approximately 100% of peak power output elicited during a ramp V(O2) peak test (355 + or - 10 W) separated by 75 s of recovery. Training increased exercise capacity, as assessed by significant improvements on both 50 kJ and 750 kJ cycling time trials (P < 0.05 for both). Skeletal muscle (vastus lateralis) biopsy samples obtained before and after training revealed increased maximal activity of citrate synthase (CS) and cytochrome c oxidase (COX) as well as total protein content of CS, COX subunits II and IV, and the mitochondrial transcription factor A (Tfam) (P < 0.05 for all). Nuclear abundance of peroxisome proliferator-activated receptor gamma co-activator 1alpha (PGC-1alpha) was approximately 25% higher after training (P < 0.05), but total PGC-1alpha protein content remained unchanged. Total SIRT1 content, a proposed activator of PGC-1alpha and mitochondrial biogenesis, was increased by approximately 56% following training (P < 0.05). Training also increased resting muscle glycogen and total GLUT4 protein content (both P < 0.05). This study demonstrates that a practical model of low volume HIT is a potent stimulus for increasing skeletal muscle mitochondrial capacity and improving exercise performance. The results also suggest that increases in SIRT1, nuclear PGC-1alpha, and Tfam may be involved in coordinating mitochondrial adaptations in response to HIT in human skeletal muscle.