Six sessions of sprint interval training increases muscle
oxidative potential and cycle endurance capacity in

Kirsten A. Burgomaster, Scott C. Hughes, George J. F. Heigenhauser, Suzanne N.
Bradwell and Martin J. Gibala

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J Appl Physiol 98: 1985–1990, 2005.
First published February 10 2005; doi:10.1152/japplphysiol.01095.2004.
Six sessions of sprint interval training increases muscle oxidative potential Kirsten A. Burgomaster,1 Scott C. Hughes,1 George J. F. Heigenhauser,2
Suzanne N. Bradwell,1 and Martin J. Gibala1
1Exercise Metabolism Research Group, Department of Kinesiology, and
2Department of Medicine, McMaster University, Hamilton, Ontario, Canada
Submitted 1 October 2004; accepted in final form 1 February 2005 Burgomaster, Kirsten A., Scott C. Hughes, George J. F.
cently, two studies reported large increases in citrate synthase Heigenhauser, Suzanne N. Bradwell, and Martin J. Gibala.
maximal activity, as well as peak oxygen uptake (V Six sessions of sprint interval training increases muscle oxida- after only 2 wk of daily sprint training (30, 33). These data tive potential and cycle endurance capacity in humans. J Appl suggest that improvements in aerobic energy metabolism can Physiol 98: 1985–1990, 2005. First published February 10 2005; be rapidly stimulated by brief bouts of very intense exercise; doi:10.1152/japplphysiol.01095.2004.—Parra et al. (Acta Physiol. however, the effect of fewer sprint training sessions is not Scand 169: 157–165, 2000) showed that 2 wk of daily sprint interval known. In addition, aside from changes in V training (SIT) increased citrate synthase (CS) maximal activity but did not change “anaerobic” work capacity, possibly because of chronic aware of no data that suggest sprint training leads to an fatigue induced by daily training. The effect of fewer SIT sessions on increased ability to perform exercise that is primarily “aerobic” muscle oxidative potential is unknown, and aside from changes in in nature, e.g., an endurance test to fatigue at a fixed submaxi- 2 peak), no study has examined the effect of SIT on “aerobic” exercise capacity. We tested the hypothesis that six The primary purpose of the present study, therefore, was to sessions of SIT, performed over 2 wk with 1–2 days rest between examine the effect of six sessions of sprint interval training on sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at ϳ80% V fatigue during cycling at an intensity equivalent to ϳ80% recreationally active subjects [age ϭ 22 Ϯ 1 yr; V ˙ O2 peak. On the basis of pilot work in our laboratory that ml ⅐ kgϪ1 ⅐ minϪ1 (mean Ϯ SE)] were studied before and 3 days after showed modest performance improvements after 6 consecutive SIT. Each training session consisted of four to seven “all-out” 30-s days of sprint training, we decided to employ a 2-wk training Wingate tests with 4 min of recovery. After SIT, CS maximal activity intervention, such that 1–2 days of rest were permitted between increased by 38% (5.5 Ϯ 1.0 vs. 4.0 Ϯ 0.7 mmol ⅐ kg proteinϪ1 ⅐ hϪ1)and resting muscle glycogen content increased by 26% (614 Ϯ 39 vs.
training sessions, in an effort to promote recovery and facilitate 489 Ϯ 57 mmol/kg dry wt) (both P Ͻ 0.05). Most strikingly, cycle performance adaptations. The importance of rest days between endurance capacity increased by 100% after SIT (51 Ϯ 11 vs. 26 Ϯ sprint training sessions was emphasized in a recent study (30) 5 min; P Ͻ 0.05), despite no change in V that showed peak and mean power elicited during a Wingate variation for the cycle test was 12.0%, and a control group (n ϭ 8) test were unchanged after 14 consecutive days of sprint train- showed no change in performance when tested ϳ2 wk apart without ing; however, when subjects performed the same number of SIT. We conclude that short sprint interval training (ϳ15 min of training sessions over 6 wk (i.e., with 1–2 days of rest between intense exercise over 2 wk) increased muscle oxidative potential and training sessions), power output improved significantly. Al- doubled endurance capacity during intense aerobic cycling in recre- though numerous mechanisms could potentially be involved, the importance of rest days between training sessions may be Wingate test; citrate synthase; muscle glycogen related in part to the fact that strenuous exercise leads toinactivation of muscle cation pumps (23, 36), and it has beenspeculated that up to several days may be required for normal- PERFORMING REPEATED BOUTS of high-intensity “sprint”-type ex- ization of sarcoplasmic reticulum Ca2ϩ pump function (41).
ercise over several weeks or months induces profound changes Thus the mode and intensity of sprint efforts in the present in skeletal muscle. A wide range of muscle metabolic and study was similar to two recent studies that incorporated 2-wk morphological adaptations have been described (25, 34); how- training interventions (30, 33); however, the overall volume ever, the magnitude and direction of change in many variables was reduced by approximately two-thirds and in total depend on the nature of the training protocol, i.e., the fre- amounted to only ϳ15 min of exercise over 2 wk. We hypoth- quency, intensity, and duration of sprint efforts as well as the esized that our short sprint training protocol would increase recovery between bouts. Given the significant contribution muscle oxidative potential and cycle endurance capacity. We from aerobic energy metabolism during repeated sprinting (3, also measured resting muscle glycogen concentration because 26, 29, 40), it is not surprising that an increase in muscle only a few sprint training studies have done so and these have oxidative potential, as indicated by changes in the maximal yielded conflicting results (14, 27, 30, 33, 28). Our experimen- activities of “marker” enzymes such as citrate synthase, has tal design included a control group who completed the exercise been reported after 6 – 8 wk of sprint training (19, 25). Re- performance tests ϳ2 wk apart with no training intervention, Address for reprint requests and other correspondence: M. J. Gibala, The costs of publication of this article were defrayed in part by the payment Exercise Metabolism Research Group, Dept. of Kinesiology, McMaster Univ., of page charges. The article must therefore be hereby marked “advertisement” Hamilton, Ontario, Canada L8S 4K1 (E-mail:
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
8750-7587/05 $8.00 Copyright 2005 the American Physiological Society ADAPTATIONS TO SHORT SPRINT INTERVAL TRAINING and all subjects performed extensive familiarization trials be-fore baseline testing.
Sixteen healthy individuals volunteered to take part in the experi- ment (Table 1). Eight subjects (2 women) were assigned to a traininggroup and performed exercise tests before and after a 2-wk sprinttraining intervention. Eight other men served as a control group andperformed the exercise performance tests ϳ2 wk apart with notraining intervention. We also obtained needle biopsy samples fromthe training group to examine potential training-induced adaptationsin resting skeletal muscle. We did not obtain biopsies from the control Fig. 1. Overview of experimental protocol. V group for ethical reasons, because other studies have shown no change PRE, preexercise; POST, postexercise; SIT, sprint interval training. Numbers in resting muscle metabolite concentrations or the maximal activities in boxes denote number of Wingate tests completed during each of 6 trainingsessions over a 2-wk period.
of mitochondrial enzymes when control subjects are tested severalweeks apart with no sprint training intervention (1, 28). All subjectswere recreationally active individuals from the McMaster Universitystudent population who participated in some form of exercise two to of ventilation rate, oxygen uptake, carbon dioxide production, and three times per week (e.g., jogging, cycling, aerobics), but none was respiratory exchange ratio were collected and averaged over the 6- to engaged in any sort of structured training program. After routine medical screening, the subjects were informed of the procedures to be Reproducibility of exercise performance tests. Ten individuals who employed in the study and associated risks, and all provided written, were not subjects in the present study performed a V informed consent. The experimental protocol was approved by the cycle endurance capacity test on separate days at least 1 wk apart, and McMaster University and Hamilton Health Sciences Research Ethics method error reproducibility was calculated as described by Sale (35).
capacity test was 3.7 and 12.0%, respectively.
Before taking part in any experimental trial (i.e., before baseline measurements), all subjects performed familiarization trials to become The experimental protocol consisted of 1) baseline testing (i.e., oriented with all testing procedures and training devices. Specifically, after familiarization procedures described above); 2) a 2-wk sprint ˙ O2 peak test; 2) a “practice ride” to training intervention or similar period without sprint training (control establish a workload that elicited ϳ80% of V group); and 3) posttesting, as described further below.
endurance capacity test that consisted of cycling to volitional fatigue Baseline testing. Baseline measurements for all subjects consisted ˙ O2 peak on at least two separate occasions.
˙ O2 peak test and a cycle endurance capacity test. Each baseline Details of Exercise Performance Tests test was conducted on a separate day with 24 h between tests. Subjectsin the training group also underwent a muscle biopsy procedure 3 days after the baseline cycle endurance capacity test and several days 2 peak test. Subjects performed an incremental test to exhaustion on an electronically braked cycle ergometer (Excalibur Sport V2.0, before the start of the training intervention. For the biopsy procedure, Lode, Groningen, The Netherlands) to determine V the area over the lateral portion of one thigh was anesthetized (2% online gas collection system (Moxus modular oxygen uptake system, lidocaine, AstraZeneca Canada, Ontario, Canada), and a small inci- AEI technologies, Pittsburgh, PA). The initial three stages of the test sion was made through the skin and underlying fascia to permit a consisted of 2-min intervals at 50, 100, and 150 W, respectively, and tissue sample (50 –100 mg) to be obtained from the vastus lateralis the workload was then increased by 25 W every minute until voli- muscle (1). Details regarding the experimental protocol are summa- highest value achieved over a 30-s collection period.
Training. Training was initiated 3–5 days after the baseline muscle Cycle endurance capacity test. Subjects cycled to volitional ex- biopsy procedure and consisted of six sessions of sprint interval haustion on an electronically braked cycle ergometer (Lode) at a training spread over 14 days. Each training session consisted of repeated 30-s “all-out” efforts on an electronically braked cycle were conducted in the absence of temporal, verbal, or physiological ergometer (Lode) against a resistance equivalent to 0.075 kg/kg body feedback. The test was terminated when pedal cadence fell below 40 mass (i.e., a Wingate test). Subjects were instructed to begin pedaling rpm (according to the manufacturer’s specifications, the power output as fast as possible against the ergometer’s inertial resistance, ϳ2 s displayed may not have been valid below this cadence), and exercise before the appropriate load was applied by a computer interfaced with duration was recorded. Expired breath samples for the determination the ergometer and loaded with appropriate software (Wingate soft-ware version 1.11, Lode). Subjects were verbally encouraged tocontinue pedaling as fast as possible throughout the 30-s test. Peakpower, mean power and fatigue index were subsequently determined using an online data acquisition system. During the 4-min recoveryperiod between tests, subjects remained on the bike and either rested or were permitted to cycle at a low cadence (Ͻ50 rpm) against a light resistance (Ͻ30 W) to reduce venous pooling in the lower extremities and minimize feelings of light-headedness or nausea. The training protocol consisted of exercise performed three times per week on alternate days (i.e., Monday, Wednesday, Friday) for 2 wk. The number of Wingate tests performed each day during training increased J Appl Physiol • VOL 98 • JUNE 2005 • ADAPTATIONS TO SHORT SPRINT INTERVAL TRAINING from 4 to 7 over the first five training sessions, and on the final session power output during the first vs. last sprint training session (training subjects completed four intervals, as summarized in Fig. 1.
group only), the factors were trial (pretraining, posttraining) and sprint Posttesting. A second muscle biopsy sample was obtained 3 days bout (1– 4). All muscle data were analyzed using paired (2-tailed) after the final training session to examine training-induced changes in t-tests. The level of significance for analyses was set at P Ͻ 0.05, and resting muscle, and a second battery of performance tests was initiated significant interactions and main effects were subsequently analyzed 2 days after the biopsy procedure (Fig. 1). The control group per- using Tukey’s honestly significant difference post hoc test. All data formed a second set of tests ϳ2 wk after the baseline tests. The nature of the posttesting exercise performance measurements were identicalin all respects to the baseline tests.
Cycle endurance capacity. After training, the individual improvements in cycle endurance capacity ranged from 81 to In an attempt to minimize any potential diet-induced variability in 169% compared with baseline, with the exception of one exercise metabolism and the resting metabolic profile of skeletal subject (16% decrease) who, on completion of the study, muscle, subjects were instructed to consume the same types and disclosed that he had sustained a minor ankle injury (unrelated quantities of food during the baseline and posttesting phases. The to the experiment) on the day before his posttraining ride. Even subjects in the training group were particularly encouraged to keep with the inclusion of this subject’s data (Fig. 2), the mean their diet as similar as possible during the 24 h before the pre- and increase in cycle endurance time to fatigue for the training posttraining biopsy procedures. Subjects were asked to record all foodintake during these periods, and compliance was assessed by perform- group (n ϭ 8) was 100% compared with baseline (51 Ϯ 11 vs.
ing dietary analyses on the individual food records maintained by the 26 Ϯ 5 min; P Ͻ 0.05), and this was higher (P Ͻ 0.05) subjects. Pre- and posttraining food diaries were analyzed for total compared with the control group, who showed no change in energy intake and proportion of energy derived from carbohydrates, performance (Fig. 2). Oxygen uptake during exercise was not fats, and protein (Nutritionist Five, First Data Bank, San Bruno, CA).
different between the first and second rides in either group; These analyses confirmed that there was no difference between trials however, expired ventilation (posttraining: 91 Ϯ 7 vs. pretrain- in the total amount of energy consumed or macronutrient proportions.
ing: 104 Ϯ 9 l/min) and respiratory exchange ratio (posttrain-ing: 1.18 vs. pretraining: 1.24) were lower (P Ͻ 0.05) after training in the sprint-training group (P Ͻ 0.05). V On removal from the leg, each muscle biopsy sample was imme- not change in either group over the course of the study.
diately frozen by plunging the biopsy needle into liquid nitrogen. The Anaerobic work capacity. Peak power output during each of samples were subsequently divided into two pieces while still frozen, the four consecutive Wingate tests performed during the last and one piece was kept in liquid nitrogen for the determination of (sixth) training session was higher (P Ͻ 0.05) compared with muscle enzyme activities. The remainder of each sample was freeze- the first training session (Fig. 3). However, fatigue index was dried, powdered, dissected free of blood and connective tissue, and also higher (P Ͻ 0.05) posttraining, and thus there were no stored at Ϫ86°C before metabolite analyses.
differences in mean power output for each of the four Wingate Citrate synthase. Frozen wet muscle samples were initially homog- tests during the first compared with the last training session.
enized using methods described by Henriksson and Reitman (17) to a50-fold dilution. The maximal activity of citrate synthase was deter- Citrate synthase activity and resting muscle metabolite con- mined on a spectrophotometer (Ultrospec 3000 pro UV/Vis) using a centrations. The maximal activity of citrate synthase increased method described by Carter et al. (6). The intra-assay coefficient of (P Ͻ 0.05) by 38% after training (Fig. 4). Resting muscle variation for the citrate synthase assay, based on 10 repeats of the glycogen concentration increased (P Ͻ 0.05) by 26% after same sample, was 4.9%. Protein content of the homogenate was training (Fig. 5); however, there were no training-induced determined by the method of Bradford (5) using a commercial assay changes in the resting muscle concentrations of ATP, phos- kit (Quick Start, Bio-Rad Laboratories, Hercules, CA), and enzyme data are expressed as moles per kilogram of protein per hour.
Metabolites. An aliquot of freeze-dried muscle was extracted on ice DISCUSSION
using 0.5 M perchloric acid (containing 1 mM EDTA), neutralizedwith 2.2 M KHCO The primary novel finding from the present study was that 3, and the resulting supernatant was used for the determination of all metabolites except glycogen. ATP, phosphocre- six bouts of sprint interval training performed over 14 days atine and creatine were measured using enzymatic assays adapted forfluorometry (Hitachi F-2500, Hitachi Instruments, Tokyo, Japan) (15,31). For glycogen analysis, an ϳ2-mg aliquot of freeze-dried musclewas incubated in 2.0 N HCl and heated for 2 h at 100°C to hydrolyzethe glycogen to glucosyl units. The solution was subsequently neu-tralized with an equal volume of 2.0 N NaOH and analyzed forglucose by using an enzymatic assay adapted for fluorometry (31).
The intra-assay coefficient of variation for all muscle metaboliteassays, based on 10 repeats of the same sample, ranged from 2 to 3%.
All muscle metabolite measurements were corrected to the peak totalcreatine concentration for a given subject.
All exercise performance data were analyzed by using a two-factor Fig. 2. Cycle endurance time to fatigue before and after a 2-wk sprint training repeated-measures ANOVA. For the single Wingate test, endurance protocol (training group; SIT) or equivalent period without training (control; ˙ O2 peak test, the factors were trial (pretraining, Con). Values are means Ϯ SE for 8 subjects. Individual data are also plotted posttraining) and condition (training, control). For the comparison of for all subjects in each group. *P Ͻ 0.05.
J Appl Physiol • VOL 98 • JUNE 2005 • ADAPTATIONS TO SHORT SPRINT INTERVAL TRAINING Fig. 3. Peak anaerobic power elicited during 4 consecutive Wingate tests Fig. 5. Muscle glycogen concentration measured in resting biopsy samples performed during the first and last sprint training session. Values are means Ϯ obtained before and after a 2-wk sprint training protocol. Values are means Ϯ SE for 8 subjects. *P Ͻ 0.05.
SE for 8 subjects. dw; Dry weight. *P Ͻ 0.05.
increased muscle oxidative potential and doubled endurance tive potential, and other investigators have justified their se- time to fatigue during cycling at ϳ80% V lection of this enzyme because it exists in constant proportion ally active subjects. The validity of this latter observation is with other mitochondrial enzymes (e.g., Ref. 13). There are bolstered by the fact that all subjects performed extensive equivocal data regarding the effect of sprint training on the familiarization trials before testing and that a control group maximal activity of this enzyme; however, studies that have showed no change in endurance performance when tested 2 wk failed to observe an increase in citrate synthase generally used apart with no sprint training intervention. We also detected very short sprints lasting Ͻ10 s (8, 24) or sprints that were not increases in resting muscle glycogen content after sprint train- all-out maximal efforts (10). In contrast, all studies that have ing. The present data therefore demonstrate that short, repeated reported increases in citrate synthase activity incorporated bouts of 30-s all-out cycling efforts, amounting to ϳ15 min of maximal effort sprint bouts that lasted 15–30 s (19, 25, 30, 33).
total exercise over 2 wk, dramatically increased cycle endur- Another relevant consideration is the fact that acute exercise ance capacity and favorably altered the resting metabolic per se may elevate citrate synthase activity, potentially con- profile of human skeletal muscle. Although increases in citrate founding the interpretation of training-induced effects, and synthase activity and glycogen content have been previously thus the timing of muscle sampling relative to the last exercise reported after several weeks of sprint interval training (19, 25, session is critical when measuring the activity of this enzyme 30, 33), the data are equivocal (8, 10, 14, 24, 27), and we show (22, 39). In the present study, we allowed 72 h of recovery here that the total training volume necessary to stimulate these before any biopsy sampling procedure (i.e., after baseline metabolic adaptations is substantially lower than previously testing and after the final training session) to minimize the potential confounding effects of acute prior exercise on citrate Muscle Oxidative Potential and Glycogen Content After synthase activity (22). Our data clearly show that the maximal activity of citrate synthase was increased after only six sessionsof sprint interval training. Notably, the magnitude of the We measured the maximal activity of citrate synthase in increase was similar to that reported in other studies that resting muscle biopsies before and after training, because this incorporated a substantially greater number of sprint training is arguably the most commonly used marker of muscle oxida- bouts (19, 25, 30, 33). Moreover, the increase in citrate syn-thase activity in the present study is comparable to that re-ported by some authors after 6 –7 days of traditional enduranceexercise training (i.e., 2 h/day at ϳ65% V whereas others have reported no change in muscle oxidativepotential after short endurance training (e.g., Ref. 12). Thepresent data do not explain the mechanism for the upregulationof citrate synthase activity, and additional work is warranted inthis regard. Finally, although there are limited and equivocaldata regarding the effect of sprint interval training on resting Table 2. Muscle metabolites before and after training Fig. 4. Maximal activity of citrate synthase (CS) measured in resting muscle biopsy samples obtained before and after a 2-wk sprint training protocol.
Values are means Ϯ SE for 8 subjects, ww, Wet wt. *P Ͻ 0.05.
Values are means Ϯ SE for 8 subjects given in mmol/kg dry wt.
J Appl Physiol • VOL 98 • JUNE 2005 • ADAPTATIONS TO SHORT SPRINT INTERVAL TRAINING muscle glycogen stores (34), our results are consistent with 2 In conclusion, the results from the present study demonstrate recent studies that reported increased muscle glycogen content that six bouts of sprint interval training performed over 2 wk after 14 sessions of sprint interval training (30, 33). One (ϳ15 min total of very intense exercise) increased citrate particularly novel aspect of our data is that the magnitude of synthase maximal activity and doubled endurance capacity the increase in muscle glycogen was comparable to what has been reported after five to seven sessions of traditional endur- active subjects. The validity of this latter observation is bol- ance exercise training (average increase: ϳ20% range: 13– stered by the fact that all subjects performed extensive famil- iarization trials before testing and that a control group showedno change in cycle endurance capacity when tested 2 wk apart Effect of Short Sprint Interval Training on without any sprint training intervention. To our knowledge, this is the first study to show that sprint training dramaticallyimproves endurance capacity during a fixed-workload test in Several studies have reported increases in V which the majority of cellular energy is derived from aerobic 14 –24 sprint interval training sessions performed over 2– 8 wk metabolism. These data demonstrate that brief repeated bouts (8, 10, 25, 26). Aside from these observations, however, we are of very intense exercise can rapidly stimulate improvements in aware of no data that suggest sprint training leads to an muscle oxidative potential that are comparable to or higher increased capacity to perform exercise that is primarily aerobic than previously reported aerobic-based training studies of sim- in nature. Thus, in the present study, we decided to employ an endurance capacity test in the form of cycling at ϳ80% ofV ACKNOWLEDGMENTS
O2 peak, a task in which the vast majority of energy is supplied from oxidative metabolism. Our data show that aerobic endur- The authors thank John Moroz for technical assistance and our subjects for ance capacity was dramatically improved after only six ses- sions of sprint interval training, despite the fact that V remained unchanged. Indeed, exercise time to exhaustion more than doubled in six of eight subjects who performed the This project was supported by operating grants from the Natural Sciences training intervention (see individual data in Fig. 2) and the and Engineering Research Council of Canada (NSERC; to M. J. Gibala) andthe Canadian Institutes of Health Research (to G. J. F. Heigenhauser). K. A.
mean performance improvement was 100%. It seems unlikely Burgomaster was supported by a NSERC Canada Graduate Scholarship. S. C.
that this finding is a spurious result, given that the mean Hughes held an Ontario Graduate Scholarship and was the recipient of a improvement was substantially higher than the day-to-day Gatorade Sports Science Institute Student Research Award.
variability for this test in our laboratory (coefficient of varia-tion ϭ 12%) and that a control group showed no change in REFERENCES
cycle endurance capacity when tested ϳ2 wk apart with no 1. Barnett C, Carey M, Proietto J, Cerin E, Febbraio MA, and Jenkins
sprint training intervention. To our knowledge, this is the first D. Muscle metabolism during sprint exercise in man: influence of sprint
training. J Sci Med Sport 7: 314 –322, 2004.
study to show that short sprint interval training dramatically 2. Bergstro¨m J. Percutaneous needle biopsy of skeletal muscle in physio-
improves endurance capacity during a fixed workload test in logical and clinical research. Scand J Clin Lab Invest 35: 609 – 616, 1975.
which the majority of cellular energy is derived from aerobic 3. Bogdanis GC, Nevill ME, Boobis LH, and Lakomy HK. Contribution
of phosphocreatine and aerobic metabolism to energy supply during We can only speculate on potential mechanisms responsible repeated sprint exercise. J Appl Physiol 80: 876 – 884, 1996.
4. Bonen A, McCullagh KJ, Putman CT, Hultman E, Jones NL, and
for the dramatic improvement in cycle endurance capacity, but Heigenhauser GJ. Short-term training increases human muscle MCT1
it is plausible that a training-induced increase in mitochondrial and femoral venous lactate in relation to muscle lactate. Am J Physiol potential, as measured by citrate synthase maximal activity, Endocrinol Metab 274: E102–E107, 1998.
improved respiratory control sensitivity during exercise as 5. Bradford MM. A rapid and sensitive method for the quantitation of
microgram quantities of protein utilizing the principle of protein-dye classically proposed (18). However, the precise mechanisms binding. Anal Biochem 72: 248 –254, 1976.
that regulate endurance performance are multifactorial and 6. Carter SL, Rennie CD, Hamilton SJ, and Tarnopolsky MA. Changes
extremely complicated (9), and data from other studies suggest in skeletal muscle in males and females following endurance training. Can that sprint training can stimulate a range of adaptations that J Physiol Pharmacol 79: 386 –392, 2001.
7. Chesley A, Heigenhauser GJ, and Spriet LL. Regulation of muscle
might facilitate performance aside from changes in mitochon- glycogen phosphorylase activity following short-term endurance training.
drial potential. For example, recent investigations have shown Am J Physiol Endocrinol Metab 270: E328 –E335, 1996.
that 5– 8 wk of sprint interval training increases skeletal muscle 8. Dawson B, Fitzsimons M, Green S, Goodman C, Carey M, and Cole
blood flow and vascular conductance (21), lactate transport K. Changes in performance, muscle metabolites, enzymes and fibre types
after short sprint training. Eur J Appl Physiol 78: 163–169, 1998.
capacity and Hϩ release from active muscle (20), ionic regu- 9. Fluck M and Hoppeler H. Molecular basis of skeletal muscle plasticity-
lation (14), and sarcoplasmic reticulum function (28). Al- from gene to form and function. Rev Physiol Biochem Pharmacol 146: though the time course for these adaptations is unknown, other studies have reported similar adaptations after only 5–7 days of 10. Gorostiaga EM, Walter CB, Foster C, and Hickson RC. Uniqueness of
interval and continuous training at the same maintained exercise intensity.
aerobic-based training, including changes in blood flow kinet- Eur J Appl Physiol 63: 101–107, 1991.
ics (37), lactate extrusion from exercising muscle (4), and 11. Green HJ, Barr DJ, Fowles JR, Sandiford SD, and Ouyang J. Mal-
cation pump activity (11). We hope that the present observa- leability of human skeletal muscle Naϩ-Kϩ-ATPase pump with short-term tions will stimulate additional research to clarify the precise training. J Appl Physiol 97: 143–148, 2004.
12. Green HJ, Cadefau J, Cusso R, Ball-Burnett M, and Jamieson G.
nature, time course, and significance of the physiological Metabolic adaptations to short-term training are expressed early in sub- adaptations induced by short sprint interval training.
maximal exercise. Can J Physiol Pharmacol 73: 474 – 482, 1995.
J Appl Physiol • VOL 98 • JUNE 2005 • ADAPTATIONS TO SHORT SPRINT INTERVAL TRAINING 13. Green H, Grant S, Bombardier E, and Ranney D. Initial aerobic power
27. Nevill ME, Boobis LH, Brooks S, and Williams C. Effect of training on
does not alter muscle metabolic adaptations to short-term training. Am J muscle metabolism during treadmill sprinting. J Appl Physiol 67: 2376 – Physiol Endocrinol Metab 277: E39 –E48, 1999.
14. Harmer AR, McKenna MJ, Sutton JR, Snow RJ, Ruell PA, Booth J,
28. Ortenblad N, Lunde PK, Levin K, Andersen JL, and Pedersen PK.
Thompson MW, Mackay NA, Stathis CG, Crameri RM, Carey MF,
Enhanced sarcoplasmic reticulum Ca2ϩ release following intermittent and Eager DM. Skeletal muscle metabolic and ionic adaptations during
sprint training. Am J Physiol Regul Integr Comp Physiol 279: R152–R160, intense exercise following sprint training in humans. J Appl Physiol 89: 29. Parolin ML, Chesley A, Matsos MP, Spriet LL, Jones NL, and
15. Harris RC, Hultman E, and Nordesjo LO. Glycogen, glycolytic inter-
Heigenhauser GJ. Regulation of skeletal muscle glycogen phosphorylase
mediates and high-energy phosphates determined in biopsy samples of and PDH during maximal intermittent exercise. Am J Physiol Endocrinol musculus quadriceps femoris of man at rest: methods and variance of Metab 277: E890 –E900, 1999.
values. Scand J Clin Lab Invest 33: 109 –120, 1974.
30. Parra J, Cadefau JA, Rodas G, Amigo N, and Cusso R. The distribu-
16. Henriksson J, Chi MM, Hintz CS, Young DA, Kaiser KK, Salmons S,
tion of rest periods affects performance and adaptations of energy metab- and Lowry OH. Chronic stimulation of mammalian muscle: changes in
olism induced by high-intensity training in human muscle. Acta Physiol enzymes of six metabolic pathways. Am J Physiol Cell Physiol 251: 17. Henriksson J and Reitman JS. Quantitative measures of enzyme activ-
31. Passoneau JV and Lowry OH. Enzymatic Analysis: A Practical Guide.
ities in type I and type II muscle fibres of man after training. Acta Physiol 32. Putman CT, Jones NL, Hultman E, Hollidge-Horvat MG, Bonen A,
18. Holloszy JO and Coyle EF. Adaptations of skeletal muscle to endurance
McConachie DR, and Heigenhauser GJ. Effects of short-term submaxi-
exercise and their metabolic consequences. J Appl Physiol 56: 831– 838, mal training in humans on muscle metabolism in exercise. Am J Physiol Endocrinol Metab 275: E132–E139, 1998.
19. Jacobs I, Esbjornsson M, Sylven C, Holm I, and Jansson E. Sprint
33. Rodas G, Ventura JL, Cadefau JA, Cusso R, and Parra J. A short
training effects on muscle myoglobin, enzymes, fiber types and blood training programme for the rapid improvement of both aerobic and lactate. Med Sci Sports Exerc 19: 368 –374, 1987.
anaerobic metabolism. Eur J Appl Physiol 82: 480 – 486, 2000.
20. Juel C, Klarskov C, Nielsen JJ, Krustrup P, Mohr M, and Bangsbo J.
34. Ross A and Leveritt M. Long-term metabolic and skeletal muscle
Effect of high-intensity intermittent training on lactate and Hϩ release adaptations to short-sprint training: implications for sprint training and from human skeletal muscle. Am J Physiol Endocrinol Metab 286: tapering. Sports Med 15: 1063–1082, 2001.
35. Sale DG. Testing strength and power. In: Physiological Testing of the
21. Krustrup P, Hellsten Y, and Bangsbo J. Intense interval training
High-Performance Athlete (2nd ed.), edited by MacDougall JD, Wenger enhances human skeletal muscle oxygen uptake in the initial phase of HA, and Green HA. Champaign, IL: Human Kinetics, 1991, p. 71– 82.
dynamic exercise at high but not at low intensities. J Physiol 559: 36. Sandiford SD, Green HJ, Duhamel TA, Perco JG, Schertzer JD, and
Ouyang J. Inactivation of human muscle Naϩ-Kϩ-ATPase in vitro during
22. Leek BT, Mudaliar SR, Henry R, Mathieu-Costello O, and Richard-
prolonged exercise is increased with hypoxia. J Appl Physiol 96: 1767– son RS. Effect of acute exercise on citrate synthase activity in untrained
and trained human skeletal muscle. Am J Physiol Regul Integr Comp 37. Shoemaker JK, Phillips SM, Green HJ, and Hughson RL. Faster
Physiol 280: R441–R447, 2001.
femoral artery blood velocity kinetics at the onset of exercise following 23. Leppik JA, Aughey RJ, Medved I, Fairweather I, Carey MF, and
short-term training. Cardiovasc Res 31: 278 –286, 1996.
McKenna MJ. Prolonged exercise to fatigue in humans impairs skeletal
38. Spina RJ, Chi MM, Hopkins MG, Nemeth PM, Lowry OH, and
muscle Naϩ-Kϩ-ATPase activity, sarcoplasmic reticulum Ca2ϩ release, Holloszy JO. Mitochondrial enzymes increase in muscle in response to
and Ca2ϩ uptake. J Appl Physiol 97: 1414 –1423, 2004.
24. Linossier MT, Denis C, Dormois D, Geyssant A, and Lacour JR.
7–10 days of cycle exercise. J Appl Physiol 80: 2250 –2254, 1996.
Ergometric and metabolic adaptation to a 5-s sprint training programme.
39. Tonkonogi M, Harris B, and Sahlin K. Increased activity of citrate
Eur J Appl Physiol 67: 408 – 414, 1993.
synthase in human skeletal muscle after a single bout of prolonged 25. MacDougall JD, Hicks AL, MacDonald JR, McKelvie RS, Green HJ,
exercise. Acta Physiol Scand 161: 435– 436, 1997.
and Smith KM. Muscle performance and enzymatic adaptations to sprint
40. Trump ME, Heigenhauser GJ, Putman CT, and Spriet LL. Importance
interval training. J Appl Physiol 84: 2138 –2142, 1998.
of muscle phosphocreatine during intermittent maximal cycling. J Appl 26. McKenna MJ, Heigenhauser GJ, McKelvie RS, Obminski G, Mac-
Physiol 80: 1574 –1580, 1996.
Dougall JD, and Jones NL. Enhanced pulmonary and active skeletal
41. Tupling AR. The sarcoplasmic reticulum in muscle fatigue and disease:
muscle gas exchange during intense exercise after sprint training in men.
role of the sarco(endo)plasmic reticulum Ca2ϩ-ATPase. Can J Appl J Physiol 501: 703–716, 1997.
Physiol 29: 308 –329, 2004.
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November 2012 PRINTER-FRIENDLY VERSION AT RHEUMATOLOGYPRACTICENEWS.COM Rheumatology Practice News SPECIAL EDITION SOUMYA D. CHAKRAVARTY, MD, PHD Fellow in Rheumatology, Hospital for Special Surgery; Clinical Fellow in Medicine, Weill Cornell Medical College, New York, New York All rights r STEPHEN A. PAGET, MD, FACP, FACR Copyright © 2012 McMahon Publishing Gr Physici

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