Low-volume 'sprint' interval training (SIT) stimulates rapid improvements in muscle oxidative capacity that are comparable to levels reached following traditional endurance training (ET) but no study has examined metabolic adaptations during exercise after these different training strategies. We hypothesized that SIT and ET would induce similar adaptations in markers of skeletal muscle carbohydrate (CHO) and lipid metabolism and metabolic control during exercise despite large differences in training volume and time commitment. Active but untrained subjects (23 ± 1 years) performed a constant-load cycling challenge (1 h at 65% of peak oxygen uptake (V O 2 peak ) before and after 6 weeks of either SIT or ET (n = 5 men and 5 women per group). SIT consisted of four to six repeats of a 30 s 'all out' Wingate Test (mean power output ∼500 W) with 4.5 min recovery between repeats, 3 days per week. ET consisted of 40-60 min of continuous cycling at a workload that elicited ∼65%V O 2 peak (mean power output ∼150 W) per day, 5 days per week. Weekly time commitment (∼1.5 versus ∼4.5 h) and total training volume (∼225 versus ∼2250 kJ week −1 ) were substantially lower in SIT versus ET. Despite these differences, both protocols induced similar increases (P < 0.05) in mitochondrial markers for skeletal muscle CHO (pyruvate dehydrogenase E1α protein content) and lipid oxidation (3-hydroxyacyl CoA dehydrogenase maximal activity) and protein content of peroxisome proliferator-activated receptor-γ coactivator-1α. Glycogen and phosphocreatine utilization during exercise were reduced after training, and calculated rates of whole-body CHO and lipid oxidation were decreased and increased, respectively, with no differences between groups (all main effects, P < 0.05). Given the markedly lower training volume in the SIT group, these data suggest that high-intensity interval training is a time-efficient strategy to increase skeletal muscle oxidative capacity and induce specific metabolic adaptations during exercise that are comparable to traditional ET.

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,V O 2 peak = 4.0 ± 0.21 min −1 ) 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 ∼250%V O 2 peak with 4 min recovery (SIT) or 90-120 min continuous cycling at ∼65%V O 2 peak (ET). Training time commitment over 2 weeks was ∼2.5 h for SIT and ∼10.5 h for ET, and total training volume was ∼90% lower for SIT versus ET (∼630 versus ∼6500 kJ). Training decreased the time required to complete 50 and 750 kJ cycling time trials, with no difference between groups (main effects, P ≤ 0.05). Biopsy samples obtained before and after training revealed similar increases in muscle oxidative capacity, as reflected by the maximal activity of cytochrome c oxidase (COX) and COX subunits II and IV protein content (main effects, P ≤ 0.05), but COX II and IV mRNAs were unchanged. Training-induced increases in muscle buffering capacity and glycogen content were also similar between groups (main effects, P ≤ 0.05). Given the large difference in training volume, these data demonstrate that SIT is a time-efficient strategy to induce rapid adaptations in skeletal muscle and exercise performance that are comparable to ET in young active men.

Parra et al. (Acta Physiol. Scand 169: 157-165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change "anaerobic" work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (Vo(2 peak)), no study has examined the effect of SIT on "aerobic" exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1-2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at approximately 80% Vo(2 peak). Eight recreationally active subjects [age = 22 +/- 1 yr; Vo(2 peak) = 45 +/- 3 ml.kg(-1).min(-1) (mean +/- SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven "all-out" 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 +/- 1.0 vs. 4.0 +/- 0.7 mmol.kg protein(-1).h(-1)) and resting muscle glycogen content increased by 26% (614 +/- 39 vs. 489 +/- 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 +/- 11 vs. 26 +/- 5 min; P < 0.05), despite no change in Vo(2 peak). The coefficient of variation for the cycle test was 12.0%, and a control group (n = 8) showed no change in performance when tested approximately 2 wk apart without SIT. We conclude that short sprint interval training (approximately 15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.

Our laboratory recently showed that six sessions of sprint interval training (SIT) over 2 wk increased muscle oxidative potential and cycle endurance capacity (Burgomaster KA, Hughes SC, Heigenhauser GJF, Bradwell SN, and Gibala MJ. J Appl Physiol 98: 1895-1900, 2005). The present study tested the hypothesis that short-term SIT would reduce skeletal muscle glycogenolysis and lactate accumulation during exercise and increase the capacity for pyruvate oxidation via pyruvate dehydrogenase (PDH). Eight men [peak oxygen uptake (VO2 peak)=3.8+/-0.2 l/min] performed six sessions of SIT (4-7x30-s "all-out" cycling with 4 min of recovery) over 2 wk. Before and after SIT, biopsies (vastus lateralis) were obtained at rest and after each stage of a two-stage cycling test that consisted of 10 min at approximately 60% followed by 10 min at approximately 90% of VO2 peak. Subjects also performed a 250-kJ time trial (TT) before and after SIT to assess changes in cycling performance. SIT increased muscle glycogen content by approximately 50% (main effect, P=0.04) and the maximal activity of citrate synthase (posttraining: 7.8+/-0.4 vs. pretraining: 7.0+/-0.4 mol.kg protein -1.h-1; P=0.04), but the maximal activity of 3-hydroxyacyl-CoA dehydrogenase was unchanged (posttraining: 5.1+/-0.7 vs. pretraining: 4.9+/-0.6 mol.kg protein -1.h-1; P=0.76). The active form of PDH was higher after training (main effect, P=0.04), and net muscle glycogenolysis (posttraining: 100+/-16 vs. pretraining: 139+/-11 mmol/kg dry wt; P=0.03) and lactate accumulation (posttraining: 55+/-2 vs. pretraining: 63+/-1 mmol/kg dry wt; P=0.03) during exercise were reduced. TT performance improved by 9.6% after training (posttraining: 15.5+/-0.5 vs. pretraining: 17.2+/-1.0 min; P=0.006), and a control group (n=8, VO2 peak=3.9+/-0.2 l/min) showed no change in performance when tested 2 wk apart without SIT (posttraining: 18.8+/-1.2 vs. pretraining: 18.9+/-1.2 min; P=0.74). We conclude that short-term SIT improved cycling TT performance and resulted in a closer matching of glycogenolytic flux and pyruvate oxidation during submaximal exercise.

Low-volume sprint interval training (SIT), or repeated sessions of brief, intense intermittent exercise, elicits metabolic adaptations that resemble traditional high-volume endurance training (ET). The effects of these different forms of exercise training on vascular structure and function remain largely unexplored. To test the hypothesis that SIT and ET would similarly improve peripheral artery distensibility and endothelial function and central artery distensibility, we recruited 20 healthy untrained subjects (age: 23.3 +/- 2.8 yr) and had them perform 6 wk of SIT or ET (n = 5 men and 5 women per group). The SIT group completed four to six 30-s "all-out" Wingate tests separated by 4.5 min of recovery 3 days/wk. The ET group completed 40-60 min of cycling at 65% of their peak oxygen uptake (Vo2peak) 5 days/wk. Popliteal endothelial function, both relative and normalized to shear stimulus, was improved after training in both groups (main effect for time, P < 0.05). Carotid artery distensibility was not statistically altered by training (P = 0.29) in either group; however, popliteal artery distensibility was improved in both groups to the same degree (main effect, P < 0.05). We conclude that SIT is a time-efficient strategy to elicit improvements in peripheral vascular structure and function that are comparable to ET. However, alterations in central artery distensibility may require a longer training stimuli and/or greater initial vascular stiffness than observed in this group of healthy subjects.

Skeletal muscle primarily relies on carbohydrate (CHO) for energy provision during high-intensity exercise. We hypothesized that sprint interval training (SIT), or repeated sessions of high-intensity exercise, would induce rapid changes in transport proteins associated with CHO metabolism, whereas changes in skeletal muscle fatty acid transporters would occur more slowly. Eight active men (22 ± 1 yr; peak oxygen uptake = 50 ± 2 ml·kg−1·min−1) performed 4–6 × 30 s all-out cycling efforts with 4-min recovery, 3 days/wk for 6 wk. Needle muscle biopsy samples (vastus lateralis) were obtained before training (Pre), after 1 and 6 wk of SIT, and after 1 and 6 wk of detraining. Muscle oxidative capacity, as reflected by the protein content of cytochrome c oxidase subunit 4 (COX4), increased by ∼35% after 1 wk of SIT and remained higher compared with Pre, even after 6 wk of detraining ( P < 0.05). Muscle GLUT4 content increased after 1 wk of SIT and remained ∼20% higher compared with baseline during detraining ( P < 0.05). The monocarboxylate tranporter (MCT) 4 was higher after 1 and 6 wk of SIT compared with Pre, whereas MCT1 increased after 6 wk of training and remained higher after 1 wk of detraining ( P < 0.05). There was no effect of training or detraining on the muscle content of fatty acid translocase (FAT/CD36) or plasma membrane associated fatty acid binding protein (FABPpm) ( P > 0.05). We conclude that short-term SIT induces rapid increases in skeletal muscle oxidative capacity but has divergent effects on proteins associated with glucose, lactate, and fatty acid transport.

Low-intensity (approximately 50% of a single repetition maximum-1 RM) resistance training combined with vascular occlusion results in increases in muscle strength and cross-sectional area [Takarada et al. (2002) Eur J Appl Physiol 86:308-331]. The mechanisms responsible for this hypertrophy and strength gain remain elusive and no study has assessed the contribution of neuromuscular adaptations to these strength gains. We examined the effect of low-intensity training (8 weeks of unilateral elbow flexion at 50% 1 RM) both with (OCC) and without vascular occlusion (CON) on neuromuscular changes in the elbow flexors of eight previously untrained men [19.5 (0.4) years]. Following training, maximal voluntary dynamic strength increased (P<0.05) in OCC (22%) and CON (23%); however, isometric maximal voluntary contraction (MVC) strength increased in OCC only (8.3%, P<0.05). Motor unit activation, assessed by interpolated twitch, was high (approximately 98%) in OCC and CON both pre- and post-training. Evoked resting twitch torque decreased 21% in OCC (P<0.05) but was not altered in CON. Training resulted in a reduction in the twitch:MVC ratio in OCC only (29%, P<0.01). Post-activation potentiation (PAP) significantly increased by 51% in OCC (P<0.05) and was not changed in CON. We conclude that low-intensity resistance training in combination with vascular occlusion produces an adequate stimulus for increasing muscle strength and causes changes in indices of neuromuscular function, such as depressed resting twitch torque and enhanced PAP.

A quantitative and dynamic analysis of skeletal muscle structure and function can guide training protocols and optimize interventions for rehabilitation and disease. While technologies exist to measure body composition, techniques are still needed for quantitative, long-term functional imaging of muscle at the bedside. We evaluate whether diffuse optical spectroscopic imaging (DOSI) can be used for long-term assessment of resistance training (RT). DOSI measures of tissue composition were obtained from 12 adults before and after 5 weeks of training and compared to lean mass fraction (LMF) from dual-energy X-ray absorptiometry (DXA). Significant correlations were detected between DXA LMF and DOSI-measured oxy-hemo/myoglobin, deoxy-hemo/myoglobin, total-hemo/myoglobin, water, and lipid. RT-induced increases of ∼6% in oxy-hemo/myoglobin (3.4 AE 1.0 μM, p ¼ 0.00314) and total-hemo/myoglobin (4.9 AE 1.1 μM, p ¼ 0.00024) from the medial gastrocne-mius were detected with DOSI and accompanied by ∼2% increases in lean soft tissue mass (36.4 AE 12.4 g, p ¼ 0.01641) and ∼60% increases in 1 rep-max strength (41.5 AE 6.2 kg, p ¼ 1.9E-05). DOSI measures of vascular and/or muscle changes combined with correlations between DOSI and DXA suggest that quantitative diffuse optical methods can be used to evaluate body composition, provide feedback on long-term interventions, and generate new insight into training-induced muscle adaptations.