Prolonged Moderate-intensity Exercise Research Articles

Stroke volume response during prolonged exercise depends on left ventricular filling: Evidence from a beta-blockade study.

Prolonged moderate intensity exercise leads to a progressive upward drift in heart rate (HR) that may compromise stroke volume (SV). Alternatively, the HR drift may be related to abated SV due to impaired ventricular function. The aim of this study was to examine the effects of cardiovascular drift on left ventricular volumes and in turn SV. Thirteen healthy young males completed two 60-minute cycling bouts on a semi-recumbent cycle ergometer at 57%VO2max either under placebo condition (CON) or after ingesting a small dose of β1-blockers (BB). Measurements of HR, end-diastolic volume (EDV), and end-systolic volume were obtained by echocardiography and used to calculate SV. Other variables such as ear temperature, skin temperature, blood pressure, and blood volume were measured to assess potential changes in thermoregulatory needs and loading conditions. HR drift was successfully prevented when using BB from min10 to min60 (128±9 to 126±8bpm, p=0.29) but not in CON (134±10 to 148±10bpm, p<0.01). Conversely, during the same time, SV increased by 13% when using BB (103±9 to 116±7mL, p<0.01) while it was unchanged in CON (99±7 to 101±9mL, p=0.37). The SV behavior was mediated by a 4% increase in EDV in the BB condition (164±18 to 170±18mL, p<0.01), while no change was observed in the CON condition (162±18 to 160±18mL, p=0.23). In conclusion, blocking HR drift enhances EDV and SV during prolonged exercise. These findings suggest that SV behavior is tightly related to filling time and loading conditions of the left ventricle.

Prolonged Moderate-Intensity Exercise Does Not Increase Muscle Injury Markers in Symptomatic or Asymptomatic Statin Users

BackgroundStatin use may exacerbate exercise-induced skeletal muscle injury caused by reduced coenzyme Q10 (CoQ10) levels, which are postulated to produce mitochondrial dysfunction. ObjectivesWe determined the effect of prolonged moderate-intensity exercise on markers of muscle injury in statin users with and without statin-associated muscle symptoms. We also examined the association between leukocyte CoQ10 levels and muscle markers, muscle performance, and reported muscle symptoms. MethodsSymptomatic (n = 35; age 62 ± 7 years) and asymptomatic statin users (n = 34; age 66 ± 7 years) and control subjects (n = 31; age 66 ± 5 years) walked 30, 40, or 50 km/d for 4 consecutive days. Muscle injury markers (lactate dehydrogenase, creatine kinase, myoglobin, cardiac troponin I, and N-terminal pro-brain natriuretic peptide), muscle performance, and reported muscle symptoms were assessed at baseline and after exercise. Leukocyte CoQ10 was measured at baseline. ResultsAll muscle injury markers were comparable at baseline (P > 0.05) and increased following exercise (P < 0.001), with no differences in the magnitude of exercise-induced elevations among groups (P > 0.05). Muscle pain scores were higher at baseline in symptomatic statin users (P < 0.001) and increased similarly in all groups following exercise (P < 0.001). Muscle relaxation time increased more in symptomatic statin users than in control subjects following exercise (P = 0.035). CoQ10 levels did not differ among symptomatic (2.3 nmol/U; IQR: 1.8-2.9 nmol/U), asymptomatic statin users (2.1 nmol/U; IQR: 1.8-2.5 nmol/U), and control subjects (2.1 nmol/U; IQR: 1.8-2.3 nmol/U; P = 0.20), and did not relate to muscle injury markers, fatigue resistance, or reported muscle symptoms. ConclusionsStatin use and the presence of statin-associated muscle symptoms does not exacerbate exercise-induced muscle injury after moderate exercise. Muscle injury markers were not related to leukocyte CoQ10 levels. (Exercise-induced Muscle Damage in Statin Users; NCT05011643)

Dietary Nitrate Supplementation Enhances Performance and Speeds Muscle Deoxyhaemoglobin Kinetics during an End-Sprint after Prolonged Moderate-Intensity Exercise.

Short-term dietary nitrate (NO3-) supplementation has the potential to enhance performance during submaximal endurance, and short-duration, maximal-intensity exercise. However, it has yet to be determined whether NO3- supplementation before and during submaximal endurance exercise can improve performance during a short-duration, maximal-intensity end-sprint. In a randomised, double-blind, crossover study, 9 recreationally active men ingested NO3--rich (BR: 8 mmol NO3-/day) and NO3--depleted (PL: 0.75 mmol NO3-/day) beetroot powder for 7 days. On day 7, participants completed 2 h of moderate-intensity cycling, which immediately transitioned into a 60 s maximal-intensity end-sprint, with supplements ingested 2 h before and 1 h into the moderate-intensity exercise bout. Plasma [NO3-] and [NO2-] were higher in BR compared to PL pre- and post-exercise (p &lt; 0.05). Post-exercise plasma [NO3-] was higher than pre-exercise (562 ± 89 µM vs. 300 ± 73 µM; p &lt; 0.05) and plasma [NO2-] was not significantly different pre- (280 ± 58 nM) and post-exercise (228 ± 63 nM) in the BR condition (p &gt; 0.05). Mean power output during the final 30 s of the end-sprint was greater after BR (390 ± 38 W) compared to PL (365 ± 41 W; p &lt; 0.05). There were no differences between BR and PL in any muscle oxygenation variables during moderate-intensity cycling (p &gt; 0.05), but muscle [deoxyhaemoglobin] kinetics was faster during the end-sprint in BR (6.5 ± 1.4 s) compared to PL (7.3 ± 1.4 s; p &lt; 0.05). These findings suggest that NO3- supplementation has the potential to improve end-sprint performance in endurance events when ingested prior to and during exercise.

Effects of nasal breathing on partial pressure of carbon dioxide in arterial blood during prolonged exercise in a hot environment

Prolonged exercise in a hot environment increases the minute ventilation (VE) and respiratory rate (RR) with an increase in core temperature. This hyperthermia-induced hyperventilation decreases the partial pressure of arterial blood carbon dioxide (PaCO2). Conversely, nasal breathing during exercise has been reported to produce low VE and RR values and high PaCO2 values; however, no studies have investigated this in hot environments. Therefore, the purpose of this study was to clarify the effect of nasal breathing on estimated partial pressure of carbon dioxide in arterial blood (PaCO2,estimate) during prolonged exercise in a hot environment. Twelve university endurance athletes participated in the study and performed a 40-minutes steady-state cycling exercise at an intensity of 55% of peak oxygen uptake in a hot environment (room temperature 35℃, relative humidity 40%). Using randomized crossover design, two experiments were performed—nasal breathing condition (NB) and mouth breathing condition (MB). Moreover, physiological indices were measured during the exercise. Rectal temperature increased in both conditions, but there was no significant difference between these conditions. PaCO2,estimate values were significantly higher in NB between 10 minutes and 40 minutes of exercise (p < 0.05) compared to MB, and decreased with time in MB. Compared to MB, the VE was significantly lower in NB between 30 minutes and 40 minutes (p < 0.05), while the RR was significantly lower in NB between 25 minutes and 40 minutes of exercise (p < 0.05). Therefore, nasal breathing during a prolonged moderate-intensity exercise in a hot environment prevented the decrease in PaCO2,estimate due to hyperthermia-induced hyperventilation.

A Single Bout of Ultra-Endurance Exercise Reveals Early Signs of Muscle Aging in Master Athletes.

Middle-aged and master endurance athletes exhibit similar physical performance and long-term muscle adaptation to aerobic exercise. Nevertheless, we hypothesized that the short-term plasticity of the skeletal muscle might be distinctly altered for master athletes when they are challenged by a single bout of prolonged moderate-intensity exercise. Six middle-aged (37Y) and five older (50Y) master highly-trained athletes performed a 24-h treadmill run (24TR). Vastus lateralis muscle biopsies were collected before and after the run and assessed for proteomics, fiber morphometry, intramyocellular lipid droplets (LD), mitochondrial oxidative activity, extracellular matrix (ECM), and micro-vascularisation. Before 24TR, muscle fiber type morphometry, intramyocellular LD, oxidative activity, ECM and micro-vascularisation were similar between master and middle-aged runners. For 37Y runners, 24TR was associated with ECM thickening, increased capillary-to-fiber interface, and an 89% depletion of LD in type-I fibers. In contrast, for 50Y runners, 24TR did not alter ECM and capillarization and poorly depleted LDs. Moreover, an impaired succinate dehydrogenase activity and functional class scoring of proteomes suggested reduced oxidative phosphorylation post-24TR exclusively in 50Y muscle. Collectively, our data support that middle-aged and master endurance athletes exhibit distinct transient plasticity in response to a single bout of ultra-endurance exercise, which may constitute early signs of muscle aging for master athletes.

Effects of sex and wet-bulb globe temperature on heart rate variability during prolonged moderate-intensity exercise: a secondary analysis.

Sex differences in heart rate (HR) and heart rate variability (HRV), a surrogate of cardiac autonomic modulation, are evident during rest and exercise in young healthy individuals. However, it remains unclear whether sex impacts HRV during prolonged exercise at differing levels of environmental heat stress. Therefore, we completed a secondary analysis upon the effects of sex and wet-bulb globe temperature (WBGT) on HR and HRV during prolonged exercise. To achieve this, HR and HRV were assessed in non-endurance-trained and non-heat-acclimatised healthy men (n=19) and women (n=15) aged 18-45 years during 180min of treadmill walking at a moderate metabolic rate (200W/m2: equivalent to ∼35% peak aerobic power) in 16, 24, 28, and 32°C WBGT. In the final 5min prior to exercise termination, HR was observed to be higher in women relative to men in all but the 32 °C WBGT. Although no sex differences were observed for the HRV metric of root-mean-square of successive differences, high-frequency power was higher in women relative to men across WBGT conditions. These findings indicate that, in healthy non-heat-acclimatised individuals, women respond to prolonged exercise-heat stress with a greater increase in HR despite cardiac vagal autonomic modulation remaining equal or increasing compared to men. Novelty: Prior to exercise termination, females respond with a greater increase in HR under all WBGTs except the hottest (32 °C). Sexinfluenced HRV metrics during all WBGTs, but results were mixed. Further characterisation of HRV sex differences remains an important area of research.

Non-Invasive Monitoring of Inflammation in Inflammatory Bowel Disease Patients during Prolonged Exercise via Exhaled Breath Volatile Organic Compounds.

The aim of this study was to investigate volatile organic compounds (VOCs) in exhaled breath as possible non-invasive markers to monitor the inflammatory response in inflammatory bowel disease (IBD) patients as a result of repeated and prolonged moderate-intensity exercise. We included 18 IBD patients and 19 non-IBD individuals who each completed a 30, 40, or 50 km walking exercise over three consecutive days. Breath and blood samples were taken before the start of the exercise event and every day post-exercise to assess changes in the VOC profiles and cytokine concentrations. Proton transfer reaction time-of-flight mass spectrometry (PTR-ToF-MS) was used to measure exhaled breath VOCs. Multivariate analysis, particularly ANOVA-simultaneous component analysis (ASCA), was employed to extract relevant ions related to exercise and IBD. Prolonged exercise induces a similar response in breath butanoic acid and plasma cytokines for participants with or without IBD. Butanoic acid showed a significant correlation with the cytokine IL-6, indicating that butanoic acid could be a potential non-invasive marker for exercise-induced inflammation. The findings are relevant in monitoring personalized IBD management.

Repeated prolonged moderate-intensity walking exercise does not appear to have harmful effects on inflammatory markers in patients with inflammatory bowel disease

Background and objectives The role of exercise in the management of inflammatory bowel disease (IBD) is inconclusive as most research focused on short or low-intensity exercise bouts and subjective outcomes. We assessed the effects of repeated prolonged moderate-intensity exercise on objective inflammatory markers in IBD patients. Methods In this study, IBD patients (IBD walkers, n = 18), and a control group (non-IBD walkers, n = 19), completed a 30, 40 or 50 km walking exercise on four consecutive days. Blood samples were taken at baseline and every day post-exercise to test for the effect of disease on exercise-induced changes in cytokine concentrations. A second control group of IBD patients who did not take part in the exercise, IBD non-walkers (n = 19), was used to test for the effect of exercise on faecal calprotectin. Both IBD groups also completed a clinical disease activity questionnaire. Results Changes in cytokine concentrations were similar for IBD walkers and non-IBD walkers (IL-6 p = .95; IL-8 p = .07; IL-10 p = .40; IL-1β p = .28; TNF-α p = .45), with a temporary significant increase in IL-6 (p < .001) and IL-10 (p = .006) from baseline to post-exercise day 1. Faecal calprotectin was not affected by exercise (p = .48). Clinical disease activity did not change in the IBD walkers with ulcerative colitis (p = .92), but did increase in the IBD walkers with Crohn’s disease (p = .024). Conclusion Repeated prolonged moderate-intensity walking exercise led to similar cytokine responses in participants with or without IBD, and it did not affect faecal calprotectin concentrations, suggesting that IBD patients can safely perform this type of exercise.

Contrasting effects of heat stress on neuromuscular performance.

What is the central question of this review? Is exposure to a hot environment detrimental to neuromuscular performance? What is the main finding and what is its importance? Elevating body temperature improves peak power during short-duration, high-intensity exercise but trades off with an accelerated rate of decay. Higher muscle temperatures and cross-bridge cycling rate resemble a shift in contractile characteristic to a faster phenotype. Prolonged moderate-intensity exercise capacity is impaired in a hot environment. Fatigue appears to combine a reduced drive from the CNS and increased cardiovascular strain to maintain skeletal muscle perfusion and thermoregulation. The effect of thermal stress on human work capacity and neuromuscular function has been of interest to physiologists since the 19th century. The aim of the present review is to examine the impact of exposure to heat stress on neuromuscular performance. Exposure to heat stress during exercise is known to increase strain on the cardiovascular system owing to the competing demands of skeletal muscle perfusion and homeostatic thermoregulation. The effects of exposure to heat stress on the neuromuscular system are more complex, because in some circumstances an elevation in muscle temperature leads to an improvement in function, whereas in other circumstances an increase in temperature leads to a decrement in function that is a consequence of the mode, metabolic demand and duration of the exercise. The ability to sustain isometric tension is impaired with an elevated muscle temperature and so too is locomotor capacity over prolonged periods of time. In contrast, peak power production is enhanced by increasing muscle temperature but is achieved at the expense of maintaining power output, owing to a higher rate of decay in power production. The different effects on neuromuscular function at an elevated muscle temperature are explained, in part, by a higher rate of energy turnover. In addition, the effect of an elevated core temperature also appears to impair neuromuscular performance either owing to a reduced voluntary drive in motor unit recruitment or to a failure in muscle afferent feedback, or a combination of the two.

The Impact of Protein Supplementation on Exercise-Induced Muscle Damage, Soreness and Fatigue Following Prolonged Walking Exercise in Vital Older Adults: A Randomized Double-Blind Placebo-Controlled Trial.

Background: It is unknown whether protein supplementation can enhance recovery of exercise-induced muscle damage in older adults who have a disturbed muscle protein synthetic response. We assessed whether protein supplementation could attenuate exercise-induced muscle damage and soreness after prolonged moderate-intensity walking exercise in older adults. Methods: In a double-blind, placebo-controlled intervention study, 104 subjects (81% male, ≥65 years) used either a protein (n = 50) or placebo supplement (n = 54) during breakfast and directly after exercise. Within a walking event, study subjects walked 30/40/50 km per day on three consecutive days. Muscle soreness and fatigue were determined with a numeric rating scale, and creatine kinase (CK) concentrations and serum inflammation markers were obtained. Results: Habitual protein intake was comparable between the protein (0.92 ± 0.27 g/kg/d) and placebo group (0.97 ± 0.23 g/kg/d, p = 0.31). At baseline, comparable CK concentrations were found between the protein and the placebo group (110 (IQR: 84–160 U/L) and 115 (IQR: 91–186 U/L), respectively, p = 0.84). Prolonged walking (protein: 32 ± 9 km/d, placebo: 33 ± 6 km/d) resulted in a cumulative increase of CK in both the protein (∆283 (IQR: 182–662 U/L)) and placebo group (∆456 (IQR: 209–885 U/L)) after three days. CK elevations were not significantly different between groups (p = 0.43). Similarly, no differences in inflammation markers, muscle soreness and fatigue were found between groups. Conclusions: Protein supplementation does not attenuate exercise-induced muscle damage, muscle soreness or fatigue in older adults performing prolonged moderate-intensity walking exercise.

A short bout of high-intensity intermittent exercise before moderate-intensity prolonged exercise as a mean to potentiate fat oxidation ?

ABSTRACTModerate-intensity continuous exercise (MICE) improves fat oxidation. High-intensity intermittent exercise (HIIE) is thought to have a greater potential for fat oxidation but it might be too demanding in the long term for patients. We hypothesized that an initial bout of HIIE could maximize fat oxidation during MICE and the following passive recovery. Eighteen healthy participants performed two acute isocaloric exercise sessions at random. MICE consisted of 45-min cycling at 50% of maximal aerobic power (Pmax). COMB began with five 1-min bouts of HIIE at Pmax (interspaced with 1-min recovery periods) followed by 35-min MICE. Gas exchange allowed substrate oxidation rate assessment.Expressed as a % of energy expenditure, fat oxidation (%) increased during in the passive recovery following COMB (Recovery: 36.0 ± 19.4 vs 23.0 ± 20.3%; ES: 0.66; p < 0.0001). An initial bout of HIIE preceding a prolonged moderate-intensity exercise may potentiate fat oxidation during the following recovery. This might be relevant for health management of overweight/obese persons.

Impact of skeletal muscle IL-6 on subcutaneous and visceral adipose tissue metabolism immediately after high- and moderate-intensity exercises.

White adipose tissue is a major energy reserve for the body and is essential for providing fatty acids for other tissues when needed. Skeletal muscle interleukin-6 (IL-6) has been shown to be secreted from the working muscle and has been suggested to signal to adipose tissue and enhance lipolysis. The aim of the present study was to investigate the role of skeletal muscle IL-6 in visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) lipolysis and glyceroneogenesis with prolonged moderate-intensity exercise and high-intensity exercise in mice. Female inducible muscle-specific IL-6 knockout (IL-6 iMKO) mice and littermate control (Floxed) mice performed a single exercise bout for either 120 min at 16 m/min and 10° slope (moderate intensity) or 30 min at 20 m/min and 10° slope (high intensity), or they remained rested (rest). Visceral and subcutaneous adipose tissues, quadriceps muscles, and blood were quickly obtained. Plasma IL-6 increased in Floxed mice but not in IL-6 iMKO mice with high-intensity exercise. VAT signal transducer and activator of transcription (STAT)3Tyr705 phosphorylation was lower, and VAT hormone-sensitive lipase (HSL)Ser563 phosphorylation was higher in IL-6 iMKO mice than in Floxed mice at rest. Furthermore, HSLSer563 and HSLSer660 phosphorylation increased in VAT and phosphoenolpyruvate carboxykinase protein decreased in SAT with moderate-intensity exercise in both genotypes. On the other hand, both exercise protocols increased pyruvate dehydrogenaseSer232 phosphorylation in VAT only in IL-6 iMKO mice and decreased tumor necrosis factor-α messenger RNA in SAT and VAT only in Floxed mice. In conclusion, the present findings suggest that skeletal muscle IL-6 regulates markers of lipolysis in VAT in the basal state and pyruvate availability for glyceroneogenesis in VAT with exercise. Moreover, skeletal muscle IL-6 may contribute to exercise-induced anti-inflammatory effects in SAT and VAT.

Ionized and Total Magnesium Levels Change during Repeated Exercise in Older Adults.

Magnesium is essential for health and performance. Sub-optimal levels have been reported for older persons. In addition, physical exercise is known to temporally decrease magnesium blood concentrations. To investigate these observations in conjunction we assessed total (tMg) and ionized magnesium (iMg) concentrations in plasma and whole blood, respectively, during 4 consecutive days of exercise in very old vital adults. 68 participants (age 83.7±1.9 years) were monitored on 4 consecutive days at which they walked 30-40km (average ~8 hours) per day at a self-determined pace. Blood samples were collected one or two days prior to the start of exercise (baseline) and every walking day immediately post-exercise. Samples were analysed for tMg and iMg levels. Baseline tMg and iMg levels were 0.85±0.07 and 0.47±0.07 mmol/L, respectively. iMg decreased after the first walking day (-0.10±0.09 mmol/L, p<.001), increased after the second (+0.11±0.07 mmol/L, p<.001), was unchanged after the third and decreased on the final walking day, all compared to the previous day. tMg was only higher after the third walking day compared to the second walking day (p=.012). In 88% of the participants, iMg levels reached values considered to be sub-optimal at day 1, in 16% of the participants values were sub-optimal for tMg at day 2. Prolonged moderate intensity exercise caused acute effects on iMg levels in a degree comparable to that after a bout of intensive exercise. These effects were not associated with drop-out or health problems. After the second consecutive day of exercise, levels were returned to baseline values, suggesting rapid adaptation/resilience in this population.

Individual glucose responses to prolonged moderate intensity aerobic exercise in adolescents with type 1 diabetes: The higher they start, the harder they fall.

To evaluate the pattern of change in blood glucose concentrations and hypoglycemia risk in response to prolonged aerobic exercise in adolescents with type 1 diabetes (T1D) that had a wide range in pre-exercise blood glucose concentrations. Individual blood glucose responses to prolonged (~60 minutes) moderate-intensity exercise were profiled in 120 youth with T1D. The mean pre-exercise blood glucose concentration was 178 ± 66 mg/dL, ranging from 69 to 396 mg/dL, while the mean change in glucose during exercise was -76 ± 55 mg/dL (mean ± SD), ranging from +83 to -257 mg/dL. Only 4 of 120 youth (3%) had stable glucose levels during exercise (ie, ± ≤10 mg/dL), while 4 (3%) had a rise in glucose >10 mg/dL, and the remaining (93%) had a clinically significant drop (ie, >10 mg/dL). A total of 53 youth (44%) developed hypoglycemia (≤70 mg/dL) during exercise. The change in glucose was negatively correlated with the pre-exercise glucose concentration (R2 = 0.44, P < 0.001), and tended to be greater in those on multiple daily insulin injections (MDI) vs continuous subcutaneous insulin infusion (CSII) (-98 ± 15 vs -65 ± 7 mg/dL, P = 0.05). No other collected variables appeared to predict the change in glucose including age, weight, height, body mass index, disease duration, daily insulin dose, HbA1c , or sex. Youth with T1D have variable glycemic responses to prolonged aerobic exercise, but this variability is partially explained by their pre-exercise blood glucose levels. When no implementation strategies are in place to limit the drop in glycemia, the incidence of exercise-associated hypoglycemia is ~44% and having a high pre-exercise blood glucose concentration is only marginally protective.

Beetroot juice ingestion during prolonged moderate-intensity exercise attenuates progressive rise in O2 uptake.

Nitrate-rich beetroot juice (BR) supplementation has been shown to increase biomarkers of nitric oxide availability with implications for the physiological responses to exercise. We hypothesized that BR supplementation before and during prolonged moderate-intensity exercise would maintain an elevated plasma nitrite concentration ([[Formula: see text]]), attenuate the expected progressive increase in V̇o2 over time, and improve performance in a subsequent time trial (TT). In a double-blind, randomized, crossover design, 12 men completed 2 h of moderate-intensity cycle exercise followed by a 100-kJ TT in three conditions: 1) BR before and 1 h into exercise (BR + BR); 2) BR before and placebo (PL) 1 h into exercise (BR + PL); and 3) PL before and 1 h into exercise (PL + PL). During the 2-h moderate-intensity exercise bout, plasma [[Formula: see text]] declined by ~17% in BR + PL but increased by ~8% in BR + BR such that, at 2 h, plasma [[Formula: see text]] was greater in BR + BR than both BR + PL and PL + PL ( P < 0.05). V̇o2 was not different among conditions over the first 90 min of exercise but was lower at 120 min in BR + BR (1.73 ± 0.24 l/min) compared with BR + PL (1.80 ± 0.21 l/min; P = 0.08) and PL + PL (1.83 ± 0.27 l/min; P < 0.01). The decline in muscle glycogen concentration over the 2-h exercise bout was attenuated in BR + BR (~28% decline) compared with BR + PL (~44% decline) and PL + PL (~44% decline; n = 9, P < 0.05). TT performance was not different among conditions ( P > 0.05). BR supplementation before and during prolonged moderate-intensity exercise attenuated the progressive rise in V̇o2 over time and appeared to reduce muscle glycogen depletion but did not enhance subsequent TT performance. NEW & NOTEWORTHY We show for the first time that ingestion of nitrate during exercise preserves elevated plasma [nitrite] and negates the progressive rise in O2 uptake during prolonged moderate-intensity exercise.

Glycemic control during consecutive days with prolonged walking exercise in individuals with type 1 diabetes mellitus

AimsDespite its general benefits for health, exercise complicates the maintenance of stable blood glucose concentrations in individuals with type 1 diabetes. The aim of the current study was to examine changes in food intake, insulin administration, and 24-h glycemic control in response to consecutive days with prolonged walking exercise (∼8h daily) in individuals with type 1 diabetes. MethodsTen individuals with type 1 diabetes participating in the worlds’ largest walking event were recruited for this observational study. Simultaneous measurements of 24-h glycemic control (continuous glucose monitoring), insulin administration and food intake were performed during a non-walking day (control) and during three subsequent days with prolonged walking exercise (daily distance 40 or 50km). ResultsDespite an increase in daily energy (31±18%; p<0.01) and carbohydrate (82±71g; p<0.01) intake during walking days, subjects lowered their insulin administration by 26±16% relative to the control day (p<0.01). Average 24-h blood glucose concentrations, the prevalence of hyperglycemia (blood glucose >10 mmol/L) and hypoglycemia (blood glucose <3.9mmol/L) did not differ between the control day and walking days (p>0.05 for all variables). The prolonged walking exercise was associated with a modest increase in glycemic variability compared with the control day (p<0.05). ConclusionProlonged walking exercise allows for profound reductions in daily insulin administration in persons with type 1 diabetes, despite large increments in energy and carbohydrate intake. When taking such adjustments into account, prolonged moderate-intensity exercise does not necessarily impair 24-h glycemic control.

Increases in core temperature counterbalance effects of haemoconcentration on blood viscosity during prolonged exercise in the heat.

What is the central question of this study? The purpose of the present study was to determine the effects of exercise-induced haemoconcentration and hyperthermia on blood viscosity. What is the main finding and its importance? Exercise-induced haemoconcentration, increased plasma viscosity and increased blood aggregation, all of which increased blood viscosity, were counterbalanced by increased red blood cell (RBC) deformability (e.g. RBC membrane shear elastic modulus and elongation index) caused by the hyperthermia. Thus, blood viscosity remained unchanged following prolonged moderate-intensity exercise in the heat. Previous studies have reported that blood viscosity is significantly increased following exercise. However, these studies measured both pre- and postexercise blood viscosity at 37 °C even though core and blood temperatures would be expected to have increased during the exercise. Consequently, the effect of exercise-induced hyperthermia on mitigating change in blood viscosity may have been missed. The purpose of this study was to isolate the effects of exercise-induced haemoconcentration and hyperthermia and to determine their combined effects on blood viscosity. Nine subjects performed 2 h of moderate-intensity exercise in the heat (37 °C, 40% relative humidity), which resulted in significant increases from pre-exercise values for rectal temperature (from 37.11 ± 0.35 to 38.76 ± 0.13 °C), haemoconcentration (haematocrit increased from 43.6 ± 3.6 to 45.6 ± 3.5%) and dehydration (change in body weight = -3.6 ± 0.7%). Exercise-induced haemoconcentration significantly (P < 0.05) increased blood viscosity by 9% (from 3.97 to 4.33 cP at 300 s(-1)), whereas exercise-induced hyperthermia significantly decreased blood viscosity by 7% (from 3.97 to 3.69 cP at 300 s(-1)). When both factors were considered together, there was no overall change in blood viscosity (from 3.97 to 4.03 cP at 300 s(-1)). The effects of exercise-induced haemoconcentration, increased plasma viscosity and increased red blood cell aggregation, all of which increased blood viscosity, were counterbalanced by increased red blood cell deformability (e.g. red blood cell membrane shear elastic modulus and elongation index) caused by the hyperthermia. Thus, blood viscosity remained unchanged following prolonged moderate-intensity exercise in the heat.

Exercise and Sport Participation for Individuals with Type 1 Diabetes

Exercise and Sport Participation for Individuals with Type 1 Diabetes

The Physiological Regulation of Skeletal Muscle Fatty Acid Supply and Oxidation During Moderate-Intensity Exercise.

Energy substrates that are important to the working muscle at moderate intensities are the non-esterified fatty acids (NEFAs) taken up from the circulation and NEFAs originating from lipolysis of the intramuscular triacylglycerol (IMTAG). Moreover, NEFA from lipolysis via lipoprotein lipase (LPL) in the muscle of the very-low-density lipoproteins and in the (semi) post-prandial state chylomicrons may also contribute. In this review, the NEFA fluxes and oxidation by skeletal muscle during prolonged moderate-intensity exercise are described in terms of the integration of physiological systems. Steps involved in the regulation of the active muscle NEFA uptake include (1) increased energy demand; (2) delivery of NEFA to the muscle; (3) transport of NEFA into the muscle by NEFA transporters; and (4) activation of the NEFAs and either oxidation or re-esterification into IMTAG. The increased metabolic demand of the exercising muscle is the main driving force for all physiological regulatory processes. It elicits functional hyperemia, increasing the recruitment of capillaries and muscle blood flow resulting in increased NEFA delivery and accessibility to NEFA transporters and LPL. It also releases epinephrine that augments adipose tissue NEFA release and thereby NEFA delivery to the active muscle. Moreover, NEFA transporters translocate to the plasma membrane, further increasing the NEFA uptake. The majority of the NEFAs taken up by the active muscle is oxidized and a minor portion is re-esterified to IMTAG. Net IMTAG lipolysis occurs; however, the IMTAG contribution to total fat oxidation is rather limited compared to plasma-derived NEFA oxidation, suggesting a complex role and regulation of IMTAG utilization.

Analysis of the Effectiveness of Proper Nutritious Diet in Prevention of Exercise-induced Fatigue

This current study focused on the potency of proper nutritious diet to alleviate and eliminate prolonged moderate-intensity Exercise Induced-Fatigue (EIF) for exercisers who vary in nutritional metabolism and supplement since they are engaged in different exercises. We performed a systematic literature review and logic analysis to investigate the effectiveness of proper nutritious diet in prevention of EIF, aiming at finding more evidence that may help exercisers recover from EIF.