Jurnal 5 Diabetes English

Hindawi Publishing Corporation Journal of Diabetes Research Volume 2013, Article ID 591574, 6 pages Clinical Study Exploring the Variability in Acute Glycemic Responses to Exercise in Type 2 Diabetes Tasuku Terada,1 Alanna Friesen,1 Baljot S. Chahal,1 Gordon J. Bell,1 Linda J. McCargar,2 and Normand G. Boulé1 1 2 Faculty of Physical Education & Recreation, University of AB, 1-059 Li Ka Shing Center, Edmonton, AB, Canada T6G 2H9 Department of Agricultural,
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  Hindawi Publishing CorporationJournal o Diabetes ResearchVolume 󰀲󰀰󰀱󰀳, Article ID 󰀵󰀹󰀱󰀵󰀷󰀴, 󰀶 pages󰀱󰀰.󰀱󰀱󰀵󰀵/󰀲󰀰󰀱󰀳/󰀵󰀹󰀱󰀵󰀷󰀴 Clinical Study  Exploring the Variability in Acute Glycemic Responses toExercise in Type 2 Diabetes Tasuku Terada, 1  Alanna Friesen, 1 Baljot S. Chahal, 1 Gordon J. Bell, 1 Linda J. McCargar, 2 and Normand G. Boulé 1 󰀱 Faculty of Physical Education & Recreation, University of AB, 󰀱-󰀰󰀵󰀹 Li Ka Shing Center, Edmonton, AB, Canada 󰀶G 󰀲H󰀹 󰀲 Department of Agricultural, Food and Nutritional Science, University of AB, 󰀲-󰀰󰀱󰀲D Li Ka Shing Center, Health Research Innovation,Edmonton, AB, Canada 󰀶G 󰀲H󰀹 Correspondence should be addressed to Normand G. Boul´e; nboule@ualberta.caReceived 󰀲 March 󰀲󰀰󰀱󰀳; Revised 󰀳󰀰 May 󰀲󰀰󰀱󰀳; Accepted 󰀱󰀰 June 󰀲󰀰󰀱󰀳Academic Editor: Francesco ChiarelliCopyright © 󰀲󰀰󰀱󰀳 asuku erada et al. Tis is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the srcinal work is properly cited.  Aim . o explore the actors associated with exercise-induced acute capillary glucose (CapBG) changes in individuals with type 󰀲diabetes (󰀲D).  Methods . Fifeen individuals with 󰀲D were randomly assigned to energy-matched high intensity interval exercise(HI-IE)andmoderateintensitycontinuousexercise(MI-CE)interventionsandperormedadesignatedexerciseprotocol󰀵daysperweek or 󰀱󰀲 weeks. Te duration o exercise progressed rom 󰀳󰀰 to 󰀶󰀰 minutes. CapBG was measured immediately beore and afereachexercisesession.imingooodandantihyperglycemicmedicationintakepriortoexercisewasrecorded. Results .Overall,themeanCapBGwasloweredby󰀱.󰀹mmol/L(  < 0.001 )withthechangerangingrom − 󰀸.󰀹to+󰀲.󰀷mmol/L.PreexerciseCapBG(󰀴󰀴%;  < 0.001 ), medication (󰀵%;   < 0.001 ), ood intake (󰀴%;   = 0.043 ), exercise duration (󰀵%;   < 0.001 ), and exercise intensity (󰀱%;   = 0.007 ) were all associated with CapBG changes, explaining 󰀵󰀹% o the variability.  Conclusion . Te greater reduction inCapBG seen in individuals with higher preexercise CapBG may suggest the importance o exercise in the population with elevatedglycemia.Lowerbloodglucosecanbeachievedwithmoderateintensityexercise,butprolongingexercisedurationand/orincludingbrie bouts o intense exercise accentuate the reduction, which can urther be magni󿬁ed by perorming exercise afer meals andantihyperglycemic medication. Tis trial is registered with Clinical  NC󰀰󰀱󰀱󰀴󰀴󰀰󰀷󰀸. 1. Introduction One o the major goals o prescribing exercise or individualswith type 󰀲 diabetes (󰀲D) is to reduce hyperglycemia, a risk actor or long-term complications. Tere have been severalmeta-analyses demonstrating that, on average, exercise hasa clinically meaningul impact on glycemic control in indi- viduals with 󰀲D [󰀱–󰀳]. However, while the overall glucose- lowering effect o exercise is well recognized, large glycemicheterogeneity among studies and within individuals is ofenunder appreciated. Indeed, there are divergent 󿬁ndings as towhich characteristics best predict long-term improvementsinglycemiccontrol.Onesystematicreviewshowedthatexer-cise volume was the major determinant o glycemic changesin response to exercise training [󰀴], while another showedexercise intensity is more closely associated [󰀵]. Te long-term glycemic bene󿬁t o exercise training isconsidered as the sum o the effects o each successive bouto exercise [󰀶]. Accordingly, an enhanced understanding o  the heterogeneous acute responses to exercise may elucidatethe varied degree o training effects. o date, a number o studies have examined the acute effects o different exerciseinterventions on blood glucose and, on the basis o theseresults, it is generally agreed that moderate intensity exercisereduces blood glucose [󰀷, 󰀸]. Glycemic responses to high intensity exercise, on the other hand, are inconsistent withsome studies showing a greater reduction than moderateintensity exercise [󰀸, 󰀹] while another showing markedly  increased glucose concentration [󰀱󰀰]. Some researchers alsoargued that total exercise volume independent o exerciseintensitydeterminesthedegreeoglycemicreduction[󰀱󰀱,󰀱󰀲]. Consequently, although exercise is an important actor or  󰀲 Journal o Diabetes Researchbetter glucoregulation, it is not clear how different exerciseinterventions acutely in󿬂uence blood glucose.Whilethecontributionodifferentexerciseinterventionsto the heterogeneity o glycemic responses remains to beclari󿬁ed, available evidence suggests that the timing o exer-cise in relation to meals and medications also need to beconsidered. For example, Poirier et al. showed that moderateintensity exercise perormed afer a meal elicits a meaninguldecrease in blood glucose but results in little change i perormedundertheastingcondition[󰀱󰀳].Furthermore,theinteractive effects o oral antihyperglycemic medication andexerciseonbloodglucosereductionhavebeensuggested[󰀱󰀴]. Collectively, it can be speculated that glycemic responses toexercisearetheresultoacomplexinterplaybetweenexternalactors that in󿬂uence blood glucose concentrations and theeffects o different exercise interventions.Giventhatexerciseisofenperormedatdifferenttimeso thedaywhenthein󿬂uenceomedicationandoodintakecan vary,itisoimportancetoinvestigatetheeffectotheexerciseinterventioninconjunctionwiththetimingoexercise.Eluci-dating the actors associated with varied glycemic responsesmay help explain heterogeneity in effect sizes and, thereby,lead to the development o more effective implementationo exercise interventions. Te purpose o this study wasto simultaneously investigate the effects o different exer-cise interventions and external actors known to in󿬂uenceexercise-induced changes in glucose concentration. 2. Methods 󰀲.󰀱. Participants.  Post hoc analysis o a study examining theeffects o high intensity interval exercise (HI-IE) and mod-erate intensity continuous exercise (MI-CE) on glycosylatedhemoglobin (A󰀱c) and abdominal at [󰀱󰀵] was conducted. Inbrie, participants were required to be diagnosed with 󰀲D,󰀵󰀵–󰀷󰀵 years o age, nonsmokers, relatively sedentary ( < 󰀱󰀵󰀰minutesostructuredexerciseperweek),andabletoexercise󰀵 days per week (see [󰀱󰀵] or complete details). Participantsmeeting the criteria had their blood pressure (BP) measured,and those with BP  <  󰀱󰀴󰀰/󰀹󰀰mmHg perormed a gradedexercise stress test under the supervision o a physician tocon󿬁rm the absence o any underlying contraindications toperorming high intensity exercise. All participants providedwritten inormed consent. Ethical approval was obtainedromtheUniversityoAlbertaHealthResearchEthicsBoard. 󰀲.󰀲. Baseline Measurement.  Detailed baseline assessmentwas described elsewhere [󰀱󰀵]. Brie󿬂y, eligible participants reported to laboratories at the University o Alberta to assessbaseline anthropometric characteristics and peak oxygenconsumption (VO 2 peak  ). VO 2 peak   was determined using acycle ergometer (Monark 󰀸󰀱󰀸; Monark, Varberg, Sweden)and a rueMax (ParvoMedics, Sandy, U) metabolic mea-surement system that was calibrated or air volume and gasconcentration according to the manuacturer’s instruction. 󰀲.󰀳. Study Protocol.  Te exercise intervention was comprisedo a 󰀲-week run-in period ollowed by a 󰀱󰀲-week trainingperiod. Te run-in period was to habituate the participantsto the exercise intervention protocols and to assess theircompliance. A total o 󰀶 exercise sessions (󰀳 sessions perweek) were held during the run-in period, and participantswere instructed to complete a minimum o 󰀵 sessions to beeligible or the study. Te sessions alternated daily betweenstationary cycling and treadmill walking or 󰀳󰀰 minutesat an exercise intensity corresponding to 󰀴󰀰% o individu-ally determined oxygen consumption reserve (VO 2 R) [󰀱󰀶]. Appropriate intensity was prescribed by adjusting the speedandslopeonthetreadmill,orpoweroutputonthestationary cycle.Afer the 󰀲-week run-in period, the participants wererandomly assigned (strati󿬁ed by sex) to the HI-IE and MI-CE training interventions, which were matched or exerciseduration,requency,andaveragerelativeintensity.Stationary cycling and treadmill walking were alternated daily orexercise variety. Participants were required to complete anentire exercise session on either bike or treadmill and couldnot alternate on a given day. Te MI-CE group perormedcontinuous exercise at 󰀴󰀰% VO 2 R, whereas the HI-IE grouprepetitively perormed a 󰀱 minute interval at 󰀱󰀰󰀰% VO 2 R ol-lowed by 󰀳 minutesat 󰀲󰀰% VO 2 R on Monday throughFriday with the exception o Wednesday, when they perormed MI-CE protocol. Te duration o exercise was 󰀳󰀰, 󰀴󰀵, and 󰀶󰀰minutespersessionorweeks󰀱–󰀴,weeks󰀵–󰀸,andweeks󰀹–󰀱󰀲,respectively.Bothgroupsexercisedatthetimeoparticipants’convenience 󰀵 days per week or 󰀱󰀲 consecutive weeks. Alltraining sessions were supervised. 󰀲.󰀴. Daily Measurement.  Upon arrival to the 󿬁tness centeror their exercise session, participants reported the timingo their most recent ood intake and oral anti-hyperglycemicmedication intake. Te timing o events was chosen by theparticipants and not in󿬂uenced by the investigators. A singleCapBG was measured immediately ( < 󰀱󰀰 minutes) beore andafereachexerciseboutwithavalidated[󰀱󰀷]OneouchUltra󰀲 (LieScan Milpitas, CA USA) handheld glucose monitor.Brie󿬂y, a 󿬁nger was cleaned with an alcohol pad, allowed todry, and then was pricked with a disposable lancet. Te 󿬁rstdrop o blood was wiped off with gauze, and the second dropwas applied to the strip. 󰀲.󰀵. Data Analyses.  Due to interdependent nature o thedata, raw CapBG data rom each participant were strati󿬁edaccording to exercise modality (bike versus treadmill), exer-ciseintensity,exerciseduration,medication,andoodintake.Mean blood glucose concentrations rom each stratum wereused or analysis.Teintervalbetweentheindividualexerciseboutandthemost recent meal intake was strati󿬁ed into  < 󰀲 hours, 󰀲–󰀶hours, and  > 󰀶 hours prior to exercise, while the time intervalromthemostrecentoralanti-hyperglycemicmedicationwasstrati󿬁ed into  ≤ 󰀶 hours and  > 󰀶 hours. Te cutoffs or oodintake and medication were determined, respectively, rompreviousobservationswhichrevealedthathyperglycemiawasmost prominent or the 󿬁rst 󰀲 hours subsequent to mealintakeandremainedelevatedorthenext󰀴hours[󰀱󰀸,󰀱󰀹]and rom the plasma elimination hal-lie o metormin [󰀲󰀰], themost commonly used medication in these participants.  Journal o Diabetes Research 󰀳 󰁡󰁢󰁬󰁥 󰀱: Baseline characteristics.MI-CE HI-IE otal    value 󽠵  (M/F) 󰀴/󰀴 󰀴/󰀳 󰀸/󰀷󰀲D duration (yr)  8 ± 4 6 ± 4 7 ± 5  󰀰.󰀴󰀱Body weight (Kg)  93.9 ± 18.3 80.5 ± 9.9 87.7 ± 16.0  󰀰.󰀱󰀰BMI (Kg/m 󰀲 )  33.1 ± 4.5 28.4 ± 4.1 30.9 ± 4.8  󰀰.󰀰󰀶Hypoglycemic medicationMetormin alone,  󽠵  󰀴 󰀴 󰀸Metormin and sitagliptin,  󽠵  󰀱 󰀱 󰀲Sulonylurea and metormin,  󽠵  󰀲 󰀰 󰀲Sulonylurea and sitagliptin,  󽠵  󰀱 󰀰 󰀱Fasting blood glucose (mmol/L)  7.3 ± 1.7 6.8 ± 0.8 7.1 ± 1.3  󰀰.󰀴󰀸A󰀱c (%)  6.7 ± 0.9 6.6 ± 0.6 6.7 ± 0.7  󰀰.󰀷󰀶VO 󰀲peak   (mL/kg/min)  18.1 ± 2.7 22.8 ± 5.4 a 20.1 ± 4.5  󰀰.󰀱󰀰 MI-CE: moderate intensity continuous exercise; HI-IE: high intensity interval exercise; VO 󰀲peak  : peak oxygen consumption; A󰀱c: glycated hemoglobin.   value reers to comparisons between HI-IE and MI-CE by independent  󽠵 -test.Values are presented as mean  ±  standard deviation. Tere was no signi󿬁cant difference between HI-IE and MI-CE. a 􍠵 = 6 , VO 󰀲peak   was not available or one participant. reatment group differences in baseline characteristicswere tested using independent  􍠵 -test. Dependent  􍠵 -test wasused to compare pre- and postexercise CapBG concentra-tions. o determine the independent association o exer-cise modality, exercise intensity, exercise duration, oodintake, medication, and preexercise CapBG concentrationson exercise-induced CapBG changes, multiple regressionanalysiswasperormed.Categoricaldataweredummycodedor the analysis. Analysis o covariance (ANCOVA) withpreexercise CapBG used as a covariate was also perormedtoassess i there were any interaction effects between externalactors and exercise interventions.Data are presented as mean  ±  standard deviation unlessotherwise stated. All statistical tests were two-tailed and    values o   < 󰀰.󰀰󰀵 were considered signi󿬁cant. Normality o thedata and lack o multicollinearity were examined by investi-gating the distributions o residuals and by variance in󿬂ationactor, respectively. Statistical analyses were perormed withMinitab 󰀱󰀵 statistical sofware (Minitab Inc., State College,PA, USA). 3. Results 󰀳.󰀱. Participants.  Seven participants in HI-IE group and 󰀸 inMI-CE completed all phases o the study. No severe adverseeffect o exercise was observed, and no participants droppedout rom the training program once they were randomized.Adherence rates or the group mean attendance were 󰀶󰀱sessions or HI-IE and 󰀶󰀲 or MI-CE, respectively, ( > 󰀹󰀷%o eligible exercise sessions or both groups). Descriptivecharacteristics o the 󰀱󰀵 participants (󰀸 males and 󰀷 emales)are summarized in able 󰀱. 󰀳.󰀲. Glycemic Responses to Acute Exercise.  In total, 󰀷󰀳󰀰pre- and 󰀷󰀳󰀰 postexercise CapBG measures were obtained.Preexercise CapBG did not change over the course o eithertraining intervention and was consistently higher in MI-CE(  < 0.001 ). Overall changes in CapBG induced by exercise − 3 − 2.5 − 2 − 1.5 − 1 − 0.50    H   I  -   I   E   M   I  -   C   E   3   0  m   i  n   4   5  m   i  n   6   0  m   i  n   T  r  e  a    d  m   i    l    l   B   i    k  e ExerciseinterventionExercisedurationExercisemodality Foodintake Medicationψ       Δ    C  a   p   B   G    (  m  m  o    l   /   L    )  <    2    h  r      >    6    h  r      >    6    h  r   2  –   6    h  r      ≤    6    h  r †‡∗  § F󰁩󰁧󰁵󰁲󰁥󰀱:Effectsoexerciseintervention,exerciseduration,exercisemodality, ood intake, and medication on exercise-induced CapBGreduction. Values are least square mean  ±  SE. ∗ HI-IE (  = 0.007 ), † 󰀴󰀵min exercise (  = 0.015 ),  ‡ 󰀶󰀰min exercise (  < 0.001 ),  § oodintake  < 󰀲 hours (  = 0.043 ), and  󝠵 medication  ≤ 󰀶 hours o exercise(  < 0.001 ) were all associated with greater CapBG reduction. HI-IE: high intensity interval exercise; MI-CE: moderate intensity continuous exercise; CapBG: capillary blood glucose. were signi󿬁cant ( −1.9 ± 1.7 mmol;   < 0.001 ). However,despite the overall glucose-lowering effect o exercise, thedegree o changes was highly heterogeneous, ranging roman 󰀸.󰀹mmol/L reduction to a 󰀲.󰀷mmol/L increase. Multipleregression analysis revealed that higher preexercise CapBG(󰀴󰀴%;   < 0.001 ), anti-hyperglycemic medication within󰀶 hours o exercise (󰀵%;   < 0.001 ), ood intake within 󰀲hours o exercise (󰀴%,   = 0.043 ), longer exercise duration(󰀵%;   = 0.010 ), and high exercise intensity (󰀱%;   =0.007 ) were all associated with greater CapBG reduction,explaining 󰀵󰀹% o the total variability (  < 0.001 ; Figure 󰀱).Mean preexercise CapBG and changes in CapBG obtainedor each participant under different conditions were plottedto schematically present the effects o preexercise CapBG onglucose concentration changes (Figure 󰀲). Variance in󿬂ation actors among the independent variables were low ( < 󰀲.󰀳),  󰀴 Journal o Diabetes Research − 8 − 6 − 4 − 2020 2 4 6 8 10 12 14 16Preexercise CapBG (mmol/L)       Δ    C  a   p   B   G    (  m  m  o    l   /   L    ) F󰁩󰁧󰁵󰁲󰁥 󰀲: Correlations between preexercise CapBG and exercise-induced CapBG changes or both HI-IE and MI-CE. Filled andopen squares represent MI-CE and HI-IE, respectively. Dotted andstraight lines are regression lines o MI-CE and HI-IE, respectively.Glucose data obtained rom each participant are categorized basedon exercise intensity, duration, and modality, as well as ood andmedication status. Each box in the 󿬁gure represents the meanglucose value obtained rom each participant under different con-ditions. HI-IE: high intensity interval exercise; MI-CE: moderateintensity continuous exercise; CapBG: capillary blood glucose. indicating small degree o multicollinearity among the vari-ables. Repeated ANCOVA consistently indicated signi󿬁canteffects o above variables on CapBG changes induced by exercise; however, no signi󿬁cant interaction effects existedbetween exercise and ood or medication. 4. Discussion Tis study examined the actors associated with heteroge-neous CapBG responses to exercise and their individualcontribution to the exercise-induced CapBG reduction inindividuals with 󰀲D. Te primary 󿬁nding o this study isthat variability in the acute glycemic response to exercise canin large part be explained by easily acquired variables such aspreexercise glucose concentrations. In addition, while higherpreexerciseCapBGwasthestrongestdeterminantoexercise-induced CapBG changes, our results also showed that longerexercisedurationandhigherexerciseintensity,aswellasanti-hyperglycemic medication and ood intake prior to exercise,magniy the reduction in CapBG.Te correlation between preexercise CapBG and CapBGchange observed in the present study is in line with the󿬁nding o Jeng et al. in which higher preexercise CapBG wasmost strongly associated with a greater reduction in CapBGafer exercise ollowed by exercise duration and intensity,explaining 󰀳󰀷% o the variance [󰀸]. By including the external actors such as timing o medication and ood intake, how-ever,weshowedthatourmodelexplainsmorevariance(󰀵󰀹%)associated with exercise. Furthermore, because the previousstudy[󰀸]didnottakeexercisevolumeintoaccount,itwasnotclear whether the effect was due to exercise intensity   per se  ordue to greater total exercise volume that accompanies higherexercise intensity. Te setting in our study where the exercise volume was equated between 󰀲 exercise intervention groupsallowed us to investigate the effect o exercise intensity independent o exercise volume.Our results demonstrated that, although its contributionto overall change in CapBG is small, higher exercise inten-sity results in greater reduction in CapBG than moderateintensity exercise matched or exercise volume. Te MI-CEgroup had higher BMI at baseline, which may explain higherastingbloodglucoseandpreexerciseCapBG.AferadjustingorthepreexerciseCapBG,however,ourstudydemonstratedthat high intensity exercise lowers CapBG signi󿬁cantly morethan MI-CE. Tis 󿬁nding contradicts with previous studiesshowingthattheeffectoexerciseonbloodglucosereductionis related to exercise volume but not to exercise intensity [󰀱󰀱, 󰀱󰀲]. Because, unlike these previous studies where energy  demand was matched by altering exercise duration, wematched exercise volume and also exercise duration betweenthe two interventions, different exercise interventions may explain the divergent glycemic responses reported. Our 󿬁nd-ing builds on previous studies indicating potential superiorbene󿬁ts o HI-IE on body composition [󰀲󰀱] and insulin sensitivity  [󰀲󰀲] to isocaloric moderate intensity exercise and suggests that HI-IE may also coner an additional bene󿬁t interms o acute glycemic regulation.Te association between longer exercise duration and agreaterCapBGdeclineobservedinthisstudyisinaccordancewith previous studies [󰀷, 󰀸]. Enhanced direct oxidation o  excessive blood glucose associated with greater exercise vol-ume is likely to be responsible or greater reduction inCapBG. Likewise, small difference in calculated exercise volume (󰀰.󰀷 KJ ⋅ min −1 difference) may explain the lack o difference in CapBG responses between bike and treadmill.Collectively, our results suggest that both greater exerciseintensity and volume may contribute to greater reduction inCapBG.Another important 󿬁nding rom the present study wasthatthetimingoexercisecanin󿬂uencetheexercise-inducedCapBG reduction. Multiple regression analysis revealed thatin addition to preexercise CapBG and exercise intervention,medication within 󰀶 hours and ood intake within 󰀲 hourso exercise signi󿬁cantly increased the glucose-lowering effecto exercise. ANCOVA with preexercise CapBG as a covariatealso con󿬁rmed signi󿬁cant effects o ood intake and medica-tion afer accounting or preexercise CapBG differences (  <0.05 ). Tese results suggest that exercise afer meal intakecan enhance the glucose-lowering effect o exercise and thatmedication and exercise have an additive effect on CapBGreduction.Te󿬁ndingthatoodintakeaccentuatesexercise-inducedCapBG reduction seen in our study was similar to that o Poirier et al., who reported little changes in plasma glucosewhen individuals with 󰀲D perormed moderate intensity aerobic exercise under asting conditions while reportedsigni󿬁cant decreases in plasma glucose under ed conditions[󰀱󰀳]. In addition to these 󿬁ndings, however, we propose thatthe effect o prior meal intake persists during HI-IE. Whenmeals are consumed beore exercise, meal-induced hyper-glycemia and hyperinsulinemia blunt hepatic glucose output[󰀲󰀳], which may have led to a greater imbalance betweenglucose production and utilization and thereby accentuatedthe reduction in CapBG. It is also possible that exercise wasperormed during the period when postprandial glucose was


Jul 23, 2017
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