Pre-Exercise Blood Glucose Levels Determine the Amount of Orally Administered Carbohydrates during Physical Exercise in Individuals with Type 1 Diabetes—A Randomized Cross-Over Trial

The aim of the study was to assess the amount of orally administered carbohydrates needed to maintain euglycemia during moderate-intensity exercise in individuals with type 1 diabetes. Nine participants with type 1 diabetes (four women, age 32.1 ± 9.0 years, BMI 25.5 ± 3.9 kg/m2, HbA1c 55 ± 7 mmol/mol (7.2 ± 0.6%)) on insulin Degludec were randomized to cycle for 55 min at moderate intensity (63 ± 7% VO2peak) for five consecutive days on either 75% or 100% of their regular basal insulin dose. The impact of pre-exercise blood glucose concentration on the carbohydrate requirement was analyzed by one-way ANOVA stratified for pre-exercise blood glucose quartiles. The effect of the basal insulin dose on the amount of orally administered carbohydrates was evaluated by Wilcoxon matched-pairs signed-rank test. The amount of orally administered carbohydrates during the continuous exercise sessions was similar for both trial arms (75% or 100% basal insulin) with median [IQR] of 36 g (9–62 g) and 36 g (9–66 g) (p = 0.78). The amount of orally administered carbohydrates was determined by pre-exercise blood glucose concentration for both trial arms (p = 0.03). Our study elucidated the importance of pre-exercise glucose concentration related orally administered carbohydrates to maintain euglycemia during exercise in individuals with type 1 diabetes

Differences in Physiological Responses to Cardiopulmonary Exercise Testing in Adults With and Without Type 1 Diabetes: A Pooled Analysis

OBJECTIVE To investigate physiological responses to cardiopulmonary exercise (CPX) testing in adults with type 1 diabetes compared with age-, sex-, and BMI-matched control participants without type 1 diabetes.RESEARCH DESIGN AND METHODS We compared results from CPX tests on a cycle ergometer in individuals with type 1 diabetes and control participants without type 1 diabetes. Parameters were peak and threshold variables of VO2, heart rate, and power output. Differences between groups were investigated through restricted maximum likelihood modeling and post hoc tests. Differences between groups were explained by stepwise linear regressions (P < 0.05).RESULTS Among 303 individuals with type 1 diabetes (age 33 [interquartile range 22; 43] years, 93 females, BMI 23.6 [22; 26] kg/m2, HbA1c 6.9% [6.2; 7.7%] [52 (44; 61) mmol/mol]), VO2peak (32.55 [26.49; 38.72] vs. 42.67 ± 10.44 mL/kg/min), peak heart rate (179 [170; 187] vs. 184 [175; 191] beats/min), and peak power (216 [171; 253] vs. 245 [200; 300] W) were lower compared with 308 control participants without type 1 diabetes (all P < 0.001). Individuals with type 1 diabetes displayed an impaired degree and direction of the heart rate-to-performance curve compared with control participants without type 1 diabetes (0.07 [−0.75; 1.09] vs. 0.66 [−0.28; 1.45]; P < 0.001). None of the exercise physiological responses were associated with HbA1c in individuals with type 1 diabetes.CONCLUSIONS Individuals with type 1 diabetes show altered responses to CPX testing, which cannot be explained by HbA1c. Intriguingly, the participants in our cohort were people with recent-onset type 1 diabetes; heart rate dynamics were altered during CPX testing

Performance Enhancing Effect of Metabolic Pre-conditioning on Upper-Body Strength-Endurance Exercise

High systemic blood lactate (La) was shown to inhibit glycolysis and to increase oxidative metabolism in subsequent anaerobic exercise. Aim of this study was to examine the effect of a metabolic pre-conditioning (MPC) on net La increase and performance in subsequent pull-up exercise (PU). Nine trained students (age: 25.1 1.9 years; BMI: 21.7 1.4) performed PU on a horizontal bar with legs placed on a box (angular hanging) either without or with MPC in a randomized order. MPC was a 26.6 2 s all out shuttle run. Each trial started with a 15-min warm-up phase. Time between MPC and PU was 8 min. Heart rate (HR) and gas exchange measures (VO2, VCO2, and VE) were monitored, La and glucose were measured at specific time points. Gas exchange measures were compared by area under the curve (AUC). In PU without MPC, La increased from 1.24 0.4 to 6.4 1.4 mmoll1, whereas with MPC, PU started at 9.28 1.98 mmoll1 La which increased to 10.89 2.13 mmoll1. With MPC, net La accumulation was significantly reduced by 75.5% but performance was significantly increased by 1 rep (4%). Likewise, net oxygen uptake VO2 (50% AUC), pulmonary ventilation (VE) (34% AUC), and carbon dioxide VCO2 production (26% AUC) were significantly increased during PU but respiratory exchange ratio (RER) was significantly blunted during work and recovery. MPC inhibited glycolysis and increased oxidative metabolism and performance in subsequent anaerobic upper-body strength-endurance exercise.(VLID)309584

The First Lactate Threshold Is a Limit for Heavy Occupational Work

Long-term heavy physical work often leads to early retirement and disability pension due to chronic overload, with a need to define upper limits. The aim of this study was to evaluate the value of the first lactate threshold (LTP1) as a physiological marker for heavy occupational work. A total of 188 male and 52 female workers performed an incremental cycle ergometer test to determine maximal exercise performance and the first and second lactate (LTP1; LTP2) and ventilatory thresholds (VT1; VT2). Heart rate (HR) recordings were obtained during one eight-hour shift (HR8h) and oxygen uptake was measured during 20 minutes of a representative work phase. Energy expenditure (EE) was calculated from gas-exchange measures. Maximal power output (Pmax), maximal oxygen consumption (VO2 max) and power output at LTP1 and LTP2 were significantly different between male and female workers. HR8h was not significantly different between male and female workers. A significant relationship was found between Pmax and power output at LTP1. HR8h as a percentage of maximum HR significantly declined with increasing performance (Pmax:r = &minus;0.56; p &lt; 0.01; PLTP1:r = &minus;0.49; p &lt; 0.01). Despite different cardio-respiratory fitness-levels; 95.4% of all workers performed their usual work below LTP1. It is therefore suggested that LTP1 represents the upper limit for sustained heavy occupational work; which supports its use to determine work capability and assessing the limits of heavy occupational work

Effects of Different Durations at Fixed Intensity Exercise on Internal Load and Recovery&mdash;A Feasibility Pilot Study on Duration as an Independent Variable for Exercise Prescription

Duration is a rarely investigated marker of exercise prescription. The aim of this study was to test the feasibility of the methodological approach, assessing effects of different duration constant-load exercise (CLE) on physiological responses (internal load) and recovery kinetics. Seven subjects performed an incremental exercise (IE) test, one maximal duration CLE at 77.6 &plusmn; 4.8% V&#729;O2max, and CLE&rsquo;s at 20%, 40%, and 70% of maximum duration. Heart rate (HR), blood lactate (La), and glucose (Glu) concentrations were measured. Before, 4, 24, and 48 h after CLE&rsquo;s, submaximal IE tests were performed. HR variability (HRV) was assessed in orthostatic tests (OT). Rating of perceived exertion (RPE) was obtained during all tests. CLE&rsquo;s were performed at 182 &plusmn; 27 W. HRpeak, Lapeak, V&#729;Epeak, and RPEpeak were significantly higher in CLE&rsquo;s with longer duration. No significant differences were found between CLE&rsquo;s for recovery kinetics for HR, La, and Glu in the submaximal IE and for HRV or OT. Despite no significant differences, recovery kinetics were found as expected, indicating the feasibility of the applied methods. Maximum tests and recovery tests closer to CLE&rsquo;s termination are suggested to better display recovery kinetics. These findings are a first step to prescription of exercise by both intensity and duration on an individual basis

Pattern of the Heart Rate Performance Curve in Subjects with Beta-Blocker Treatment and Healthy Controls

(1): Heart rate performance curve (HRPC) in incremental exercise was shown to be not uniform, causing false intensity estimation applying percentages of maximal heart rate (HRmax). HRPC variations are mediated by β-adrenergic receptor sensitivity. The aim was to study age and sex dependent differences in HRPC patterns in adults with β-blocker treatment (BB) and healthy controls (C). (2): A total of 535 (102 female) BB individuals were matched 1:1 for age and sex (male 59 ± 11 yrs, female 61 ± 11 yrs) in C. From the maximum incremental cycle ergometer exercise a first and second heart rate (HR) threshold (Th1 and Th2) was determined. Based on the degree of the deflection (kHR), HRPCs were categorized as regular (downward deflection (kHR &gt; 0.1)) and non-regular (upward deflection (kHR &lt; 0.1), linear time course). (3): Logistic regression analysis revealed a higher odds ratio to present a non-regular curve in BB compared to C (females showed three times higher odds). The odds for non-regular HRPC in BB versus C decreased with older age (OR interaction = 0.97, CI = 0.94–0.99). Maximal and submaximal performance and HR variables were significantly lower in BB (p &lt; 0.05). %HRmax was significantly lower in BB versus C at Th2 (male: 77.2 ± 7.3% vs. 80.8 ± 5.0%; female: 79.2 ± 5.1% vs. 84.0 ± 4.3%). %Pmax at Th2 was similar in BB and C. (4): The HRPC pattern in incremental cycle ergometer exercise is different in individuals receiving β-blocker treatment compared to healthy individuals. The effects were also dependent on age and sex. Relative HR values at Th2 varied substantially depending on treatment. Thus, the percentage of Pmax seems to be a stable and independent indicator for exercise intensity prescription

Molecular cloning of TRPC3a, an N-terminally extended, store-operated variant of the human C3 transient receptor potential channel

AK032317 is the GenBank accession no. of a full-length RIKEN mouse cDNA. It encodes a putative variant of the C3-type TRPC (transient receptor potential channel) that differs from the previously cloned murine TRPC3 cDNA in that it has a 5′ extension stemming from inclusion of an additional exon (exon 0). The extended cDNA adds 62 aa to the sequence of the murine TRPC3. Here, we report the cloning of a cDNA encoding the human homologue of this extended TRPC3 having a highly homologous 73-aa N-terminal extension, referred to as hTRPC3a. A query of the GenBank genomic database predicts the existence of a similar gene product also in rats. Transient expression of the longer TRPC3a in human embryonic kidney (HEK) cells showed that it mediates Ca(2+) entry in response to stimulation of the Gq–phospholipase C β pathway, which is similar to that mediated by the shorter hTRPC3. However, after isolation of HEK cells expressing hTRPC3 in stable form, TRPC3a gave rise to Ca(2+)-entry channels that are not only activated by the Gq–phospholipase C β pathway (receptor-activated Ca entry) but also by thapsigargin triggered store depletion. In conjunction with findings from our and other laboratories that TRPC1, TRPC2, TRPC4, TRPC5, and TRPC7, can each mediate store-depletion-activated Ca(2+) entry in mammalian cells, our findings with hTRC3a support our previous proposal that TRPCs form capacitative Ca-entry channels