The major novel finding from the present study was that six sessions of either low volume SIT or traditional high volume ET induced similar improvements in muscle oxidative capacity, muscle buffering capacity and exercise performance. To our knowledge this is the first study to directly compare interval versus continuous training using a research design that matched groups with respect to exercise mode (cycling), training frequency (3 × per week) and training duration (2 weeks), but differed in terms of total training volume and time commitment. Several previous studies have examined muscle metabolic and/or performance adaptations to interval versus continuous training (Henriksson & Reitman, 1976; Saltin et al. 1976; Eddy et al. 1977; Fournier et al. 1982; Gorostiaga et al. 1991; Edge et al. 2006), but the data are equivocal and in all cases the total volume of work was similar between groups. The present study was unique because, by design, the total training volume for the SIT group was only ∼10% that of the ET group (i.e. 630 versus 6500 kJ). In addition, the total training time commitment over 2 weeks was ∼2.5 h for the SIT group (including the work intervals and the recovery periods between intervals), whereas the ET group performed continuous exercise each training day for a total of ∼10.5 h. Thus, while previously speculated by others (Coyle, 2005), to our knowledge this is the first study to demonstrate that SIT is indeed a very ‘time efficient’ training strategy.
Effect of short-term sprint or endurance training on exercise performance
We are aware of only one previous study that examined changes in volitional exercise performance after continuous or interval training. Eddy et al. (1977) had subjects perform cycle exercise training, 4 days per week for 7 weeks, using either a continuous (70% of ) or interval method (repeated 1 min bouts at 100% followed by 1 min of rest). The daily workload was matched between groups and increased progressively from ∼100 kJ per session during week 1 to ∼275 kJ per session during week 7. After training, subjects in both groups showed similar improvements during a matched-work exercise test, such that cycling time to exhaustion at 90% of increased by an almost identical amount (∼26 min) in both the continuous and interval groups. In the present study, subjects performed 50 and 750 kJ cycling time trials, which demanded work intensities equivalent to ∼120 and ∼65% of peak power output elicited during the tests. Consistent with the work of Eddy et al. (1977), subjects in the interval and continuous training groups showed remarkably similar improvements in exercise performance. However, whereas Eddy et al. (1977) employed matched-work training protocols, the SIT group in the present study performed only 2–3 min of intense exercise per training session (which lasted 18–27 min in total, including recovery periods between intervals), whereas the ET group performed 90–120 min of continuous exercise per session. While there was no control group in the present study, recent work from our laboratory has shown that control subjects drawn from the same population show no change in cycle endurance capacity (Burgomaster et al. 2005) or time trial performance (Burgomaster et al. 2006) when tested ∼2 weeks apart with no training intervention.
Rapid muscle adaptations induced by sprint or endurance training
Obviously, the factors responsible for training-induced improvements in exercise capacity are extremely complex and determined by numerous physiological (e.g. cardiovascular, muscle metabolic, neural, respiratory, thermoregulatory) and psychological attributes (e.g. mood, motivation, perception of effort). We assessed changes in two parameters – muscle oxidative capacity and muscle buffering capacity – that are related to exercise tolerance (Hawley, 2002) and thus may have contributed to the observed improvement in time trial performance. Surprisingly, only a few previous studies have directly compared changes in mitochondrial capacity after interval or continuous training, and all employed matched-work training protocols that lasted several weeks (Henriksson & Reitman, 1976; Saltin et al. 1976; Fournier et al. 1982; Gorostiaga et al. 1991). The results from these studies are equivocal, with two studies reporting similar increases in the maximal activities of mitochondrial enzymes after interval and continuous training (Henriksson & Reitman, 1976; Saltin et al. 1976), while two others reported increases after continuous training only (Fournier et al. 1982; Gorostiaga et al. 1991). The present study is the first to directly compare changes in muscle oxidative capacity after low-volume SIT and high-volume ET.
In accordance with one of our hypotheses, we observed a training-induced increase in the maximal activity of COX and the protein contents of COX subunits II and IV, but there were no differences between groups despite the marked differences in training volume. The present findings are consistent with recent work from our laboratory that showed muscle oxidative capacity was increased after a SIT protocol similar to that used in the present study, or ∼15 min of intense exercise over six training sessions in 2 weeks (Burgomaster et al. 2005, 2006). While the time course for mitochondrial adaptations after short-term aerobic exercise training is equivocal (Green et al. 1992; Putman et al. 1998), our results are consistent with data from many laboratories showing increases in oxidative enzymes after six to seven sessions of prolonged moderate intensity exercise (Spina et al. 1996; Chesley et al. 1996; Green et al. 1999; Starrit et al. 1999; Youngren et al. 2001). Finally, while the design of the present human study was unique, our data are supported by previous work on rats that examined muscle adaptations to various forms of exercise training (Dudley et al. 1982; Terada et al. 2001). Dudley et al. (1982) reported similar increases in COX maximal activity after 6 weeks of training with either short bouts of intense running or prolonged periods of continuous running at lower work intensities. Given the large difference in training volume between groups, the authors concluded: ‘the typical endurance-training response of a biochemical change in mitochondrial content can be achieved at relatively intense exercise (i.e. exceeding ) maintained for relatively short durations … for the same adaptive response, the length of daily exercise necessary to bring about the change becomes less as the intensity of training increases’ (Dudley et al. 1982). More recently, Terada et al. (2001) showed that 8 days of high-intensity, intermittent swim training (lasting < 5 min per day) increased citrate synthase maximal activity in rat skeletal muscle to a level similar to that induced by 6 h of daily low-intensity training.
In spite of a significant increase in both COX enzyme activity and protein content for COX subunits encoded by nuclear (COX IV) and mitochondrial (COX II) DNA, we did not find a corresponding increase in mRNA content. Previously, some groups have reported increased mRNA abundance for components of the electron transport chain and/or fatty acid metabolism following endurance training in humans (Tunstall et al. 2002; Schmitt et al. 2003; Timmons et al. 2005). There is also evidence that both the intensity and duration of exercise affect the transcriptional regulation of metabolic genes in a fibre type-specific manner, possibly reflecting the relative stress imposed by the exercise bout (Hildebrandt et al. 2003). Various factors including the specific mRNA species being studied, the duration of the training program, as well as the time of the biopsy following the last bout of exercise can influence skeletal muscle mRNA content. For example, after 9 days of endurance training, baseline mRNA content for fatty acid translocase (FAT/CD36) and carnitine palmitoyltransferase 1(CPT1) was elevated, yet plasma membrane associated FA-binding protein (FABPpm) and β-hydroxyacyl-CoA dehydrogenase (β-HAD) mRNA content was unchanged (Tunstall et al. 2002). Schmitt et al. (2003) observed higher CPTI mRNA content in endurance trained athletes compared with sedentary controls and Short et al. (2003) reported a 66% increase in COX IV mRNA abundance after 16 weeks of endurance exercise training, which suggests longer term training can influence mRNA content. Finally, our laboratory has previously found that the mRNA for several proteins involved in mitochondrial biogenesis and metabolism were elevated 3 h after an acute bout of endurance exercise, but not at 48 h (Mahoney et al. 2005). These data are consistent with the concept that initial signalling events associated with acute exercise induce transient pulses of increased mRNA abundance that eventually lead to an increase in protein content and enzyme activity, and that with longer term training there are increases in mRNA abundance for some but not all mitochondrial proteins (Hood, 2001; Mahoney & Tarnopolsky, 2005; Hawley et al. 2006).
The potency of SIT to elicit rapid changes in oxidative capacity comparable to ET is no doubt related to its high level of muscle fibre recruitment, and the potential to stress type II fibres in particular (Gollnick et al. 1973; Dudley et al. 1982). Contraction-induced metabolic disturbances in muscle activate several kinases and phosphatases involved in signal transduction; in particular, the adenosine monophosphate-activated protein kinase (AMPK), calcium–calmodulin-dependent protein kinase (CAPK), and mitogen-activated protein kinase (MAPK) cascades have been shown to play a role in promoting specific co-activators involved in mitochondrial biogenesis and metabolism (Hood, 2001; Hawley et al. 2006; Koulmann & Bigard, 2006). Studies in animals have shown that different exercise or stimulation protocols result in selective activation of specific intracellular signalling pathways, which may determine the specific adaptations induced by different forms of exercise training (Nader & Esser, 2001; Lee et al. 2002; Atherton et al. 2005; Terada et al. 2005). Recently, Terada et al. (2005) examined the effect of exercise intensity on exercise-induced expression of peroxisome proliferator-activated receptor γ co-activator-1 (PGC-1α) protein in rat skeletal muscle. PGC-1α has emerged as a critical factor coordinating the activation of metabolic genes required for substrate utilization and mitochondrial biogenesis, possibly via its interaction with several DNA binding transcription factors (Knutti & Kralli, 2001). Terada et al. (2005) measured PGC-1α protein content after a single session of exercise that consisted of either high intensity swimming (14 × 20 s intervals while carrying a load equivalent to 14% of body mass, with 10 s of rest between intervals), or low intensity swimming (2 × 3 h with no load, separated by 45 min of rest). Epitrochlearis muscle samples harvested after 2, 6 and 18 h following exercise revealed that PGC-1α increased to a similar extent in both groups (by 126–140% in the high intensity group and 67–95% in the low intensity group) compared with resting control muscle. Given their previous observation that 8 days of swim training using either the high-intensity or low-intensity protocol produced similar increased in muscle oxidative capacity (Terada et al. 2001), the authors concluded ‘high-intensity exercise is a potent tool to increase mitochondrial biogenesis, probably through enhancing PGC-1α expression in rat skeletal muscle.’ With regards to human muscle, several groups have described changes in the expression of PGC-1α and other metabolic transcriptional co-activators and transcription factors after acute exercise (Pilegaard et al. 2003; Russell et al. 2005; Coffey et al. 2006); however, no studies have directly compared adaptations induced by different types of exercise training.
With respect to our other marker of exercise tolerance, both the SIT and ET protocols induced similar increases in skeletal muscle buffering capacity, which was in contrast to one of our hypotheses. Previous studies have yielded equivocal data with respect to exercise training and buffering capacity (Nevill et al. 1989; Bell & Wenger, 1988; Weston et al. 1997) and to our knowledge only one group has specifically examined the issue of training intensity (Edge et al. 2006). Recently, Edge et al. (2006) studied the effect of 5 weeks of interval (4–10 repeats × 2 min at ∼90–100%) or continuous training (∼20 min at ∼60–75%) on muscle buffering capacity in recreationally active women. Following training, buffering capacity in the interval training group increased by ∼25% but there was no change in the group that performed continuous exercise. While these data (Edge et al. 2006) are in contrast to the present results, there are marked differences between studies in terms of the training stimulus. Edge et al. (2006) matched the interval and continuous training groups in terms of the total work performed during each session, which meant that the continuous training group performed only 20 min of moderate intensity exercise per session. The training stimulus in that study (Edge et al. 2006) was therefore modest compared with the exercise bouts performed by the ET group in the present study (90–120 min of cycling at ∼65% per session). The present study is the first to report improvements in muscle buffering capacity after short-term exercise training (<4 week) and we speculate that changes in this parameter might represent a relatively rapid muscle adaptation that contributes to the observed improvement in exercise capacity. It should be noted that the in vitro method employed in this study isolates for the physico-chemical buffering capacity of skeletal muscle, which is dominated by cytosolic phosphates and proteins/peptides. Histidine-related compounds appear to be the most important determinant of muscle buffering capacity, particularly across the physiological pH range (Abe, 2000), and thus in theory any protein or peptide with histidine residues that are exposed to the cytosol could contribute to buffering capacity.
Perspective: limitations and implications of the present work
The adaptive response to physical training is obviously influenced by a multitude of complex molecular, cellular and physiological changes, and the present data should not be interpreted to suggest that SIT is necessarily adequate preparation for prolonged endurance-type activities. The duration of the training program in the present study was relatively short (6 sessions over 2 weeks) and it remains to be determined whether similar adaptations are manifest after many weeks or months of interval and continuous training. It is possible that the time course for physiological adjustments differs between training protocols; the very intense nature of the SIT protocol may stimulate rapid changes, whereas the adaptations induced by lower intensity ET may occur more slowly. The present study examined only a few specific muscle parameters, and future studies should examine whether low volume SIT induces other physiological adjustments typically associated with high volume ET (e.g. increased maximal capacity for lipid oxidation, improvements in cardiorespiratory function, changes in blood health status markers, potential for weight loss, etc.). Although pulmonary oxygen uptake remains high during recovery between intervals, energy expenditure during a 20–30 min SIT session is nonetheless lower than a 90–120 min bout of endurance exercise. We estimate, based on calculations of heart rate reserve, that during Wingate-based interval training averages ∼65–70% of over the course of each 30 s sprint and subsequent 4 min recovery period. Thus, based on the average duration of each training session in the present study, absolute energy expenditure in the SIT group was ≤25% of the ET group. A detailed discussion of the potential health benefits of various training strategies is beyond the scope of this paper; however, obesity experts have recognized a role for high intensity exercise in body weight management (Hunter et al. 1998). There is also a growing appreciation of the potential for intense, interval-based training to stimulate cardiovascular and muscular adaptations in various populations, including disease states (e.g. Rognmo et al. 2004; Vogiatzis et al. 2005).
In conclusion, the most striking finding from the present study was that two very diverse forms of training induced remarkably similar changes in exercise capacity and selected muscle adaptations that are related to exercise tolerance. Given the markedly lower training volume in the SIT group, our results suggest that intense interval training is indeed a time-efficient strategy to induce rapid muscle and performance adaptations comparable to traditional endurance training. Additional research is warranted to clarify the effect of different acute exercise ‘impulses’ on molecular signalling events in human skeletal muscle, and the precise time course and mechanisms responsible for the contraction-induced changes that facilitate the training adaptation.