Weight loss but not gains in cardiorespiratory fitness after exercise-training predicts improved health risk factors in metabolic syndrome.

BACKGROUND AND AIMS: To examine the relationship between changes in cardiorespiratory fitness (CRF; estimated by VO2max) and metabolic syndrome (MetS) after an exercise training intervention to confirm/contradict the high association found in cross-sectional observational studies. METHODS AND RESULTS: MetS individuals (54 ± 8 yrs old; BMI of 32 ± 5) were randomly allocated (6:1 ratio) to a group that exercised trained for 16-weeks (EXER; n = 138) or a control sedentary group (CONT; n = 22). At baseline, MetS components, body composition and exercise responses were similar between groups (all P > 0.05). After 16 weeks of intervention, only EXER reduced body weight, waist circumference (-1.21 ± 0.22 kg and -2.7 ± 0.3 cm; P < 0.001), mean arterial blood pressure and hence the composite MetS Z-score (-7.06 ± 0.77 mmHg and -0.21 ± 0.03 SD; P < 0.001). In the EXER group, CRF increased by 16% (0.302 ± 0.026, 95% CI 0.346 to 0.259 LO2·min-1; P < 0.001) but was not a significant predictor of MetS Z-score improvements (r = -0.231; ß = -0.024; P = 0.788). Instead, body weight reductions predicted 25% of MetS Z-score changes (r = 0.508; ß = 0.360; P = 0.001). CONCLUSIONS: In MetS individuals, the exercise-training increases in CRF are not predictive of the improvements in their health risk factors. Instead, body weight loss (<2%) was a significant contributor to the improved MetS Z-score and thus should be emphasized in exercise training programs. ClinicalTrials.gov identifier: NCT03019796.

Effects of intense aerobic exercise and/or antihypertensive medication in individuals with metabolic syndrome.

We studied the blood pressure lowering effects of a bout of exercise and/or antihypertensive medicine with the goal of studying if exercise could substitute or enhance pharmacologic hypertension treatment. Twenty-three hypertensive metabolic syndrome patients chronically medicated with angiotensin II receptor 1 blockade antihypertensive medicine underwent 24-hr monitoring in four separated days in a randomized order; (a) after taking their habitual dose of antihypertensive medicine (AHM trial), (b) substituting their medicine by placebo medicine (PLAC trial), (c) placebo medicine with a morning bout of intense aerobic exercise (PLAC+EXER trial) and (d) combining the exercise and antihypertensive medicine (AHM+EXER trial). We found that in trials with AHM subjects had lower plasma aldosterone/renin activity ratio evidencing treatment compliance. Before exercise, the trials with AHM displayed lower systolic (130 ± 16 vs 133 ± 15 mm Hg; P = .018) and mean blood pressures (94 ± 11 vs 96 ± 10 mm Hg; P = .036) than trials with placebo medication. Acutely (ie, 30 min after treatments) combining AHM+EXER lowered systolic blood pressure (SBP) below the effects of PLAC+EXER (-8.1 ± 1.6 vs -4.9 ± 1.5 mm Hg; P = .015). Twenty-four hour monitoring revealed no differences among trials in body motion. However, PLAC+EXER and AHM lowered SBP below PLAC during the first 10 hours, time at which PLAC+EXER effects faded out (ie, at 19 PM). Adding exercise to medication (ie, AHM+EXER) resulted in longer reductions in SBP than with exercise alone (PLAC+EXER). In summary, one bout of intense aerobic exercise in the morning cannot substitute the long-lasting effects of antihypertensive medicine in lowering blood pressure, but their combination is superior to exercise alone.

Effects of 6-month aerobic interval training on skeletal muscle metabolism in middle-aged metabolic syndrome patients.

Aerobic interval training (AIT) improves the health of metabolic syndrome patients (MetS) more than moderate intensity continuous training. However, AIT has not been shown to reverse all metabolic syndrome risk factors, possibly due to the limited duration of the training programs. Thus, we assessed the effects of 6 months of AIT on cardio-metabolic health and muscle metabolism in middle-aged MetS. Eleven MetS (54.5±0.7 years old) underwent 6 months of 3 days a week supervised AIT program on a cycle ergometer. Cardio-metabolic health was assessed, and muscle biopsies were collected from the vastus lateralis prior and at the end of the program. Body fat mass (-3.8%), waist circumference (-1.8%), systolic (-10.1%), and diastolic (-9.3%) blood pressure were reduced, whereas maximal fat oxidation rate and VO2peak were significantly increased (38.9% and 8.0%, respectively; all P<.05). The remaining components of cardio-metabolic health measured (body weight, blood cholesterol, triglycerides, and glucose) were not changed after the intervention, and likewise, insulin sensitivity (CSi) remained unchanged. Total AMPK (23.4%), GLUT4 (20.5%), endothelial lipase (33.3%) protein expression, and citrate synthase activity (26.0%) increased with training (P<.05). Six months of AIT in MetS raises capacity for fat oxidation during exercise and increases VO2peak in combination with skeletal muscle improvements in mitochondrial enzyme activity. Muscle proteins involved in glucose, fat metabolism, and energy cell balance improved, although this was not reflected by parallel improvements in insulin sensitivity or blood lipid profile.

Effects of Simultaneous or Sequential Weight Loss Diet and Aerobic Interval Training on Metabolic Syndrome.

Our purpose in this study was to investigate efficient and sustainable combinations of exercise and diet-induced weight loss (DIET), in order to combat obesity in metabolic syndrome (MetS) patients. We examined the impact of aerobic interval training (AIT), followed by or concurrent to a DIET on MetS components. 36 MetS patients (54±9 years old; 33±4 BMI; 27 males and 9 females) underwent 16 weeks of AIT followed by another 16 weeks without exercise from the fall of 2013 to the spring of 2014. Participants were randomized to AIT without DIET (E CON, n=12), AIT followed by DIET (E-then-D, n=12) or AIT concurrent with DIET (E+D, n=12) groups. Body weight decreased below E CON similarly in the E-then-D and E+D groups (~5%). Training improved blood pressure and cardiorespiratory fitness (VO2peak) in all groups with no additional effect of concurrent weight loss. However, E+D improved insulin sensitivity (HOMA) and lowered plasma triglycerides and blood cholesterol below E CON and E-then-D (all P<0.05). Weight loss in E-then-D in the 16 weeks without exercise lowered HOMA to the E+D levels and maintained blood pressure at trained levels. Our data suggest that a new lifestyle combination consisting of aerobic interval training followed by weight loss diet is similar, or even more effective on improving metabolic syndrome factors than concurrent exercise plus diet.

Hyperthermia, but not muscle water deficit, increases glycogen use during intense exercise.

We determined if dehydration alone or in combination with hyperthermia accelerates muscle glycogen use during intense exercise. Seven endurance-trained cyclists (VO2max = 54.4 ± 1.05 mL/kg/min) dehydrated 4.6% of body mass (BM) during exercise in the heat (150 min at 33 ± 1 °C, 25 ± 2% humidity). During recovery (4 h), subjects remained dehydrated (HYPO trial) or recovered all fluid losses (REH trials). Finally, subjects exercised intensely (75% VO2max ) for 40 min in a neutral (25 ± 1 °C; HYPO and REH trials) or in a hot environment (36 ± 1 °C; REHHOT ). Before the final exercise bout vastus lateralis glycogen concentration was similar in all three trials (434 ± 57 mmol/kg of dry muscle (dm)) but muscle water content was lower in the HYPO (357 ± 14 mL/100 g dm) than in REH trials (389 ± 25 and 386 ± 25 mL/100 g dm; P < 0.05). After 40 min of intense exercise, intestinal temperature was similar between the HYPO and REHHOT trials (39.2 ± 0.5 and 39.2 ± 0.4 °C, respectively) and glycogen use was similar (172 ± 86 and 185 ± 97 mmol/kg dm, respectively) despite large differences in muscle water content. In contrast, during REH, intestinal temperature (38.5 ± 0.4 °C) and glycogen use (117 ± 52 mmol/kg dm) were significantly lower than during HYPO and REHHOT . Our data suggest that hyperthermia stimulates glycogen use during intense exercise while muscle water deficit has a minor role.

Skeletal muscle water and electrolytes following prolonged dehydrating exercise.

We studied if dehydrating exercise would reduce muscle water (H2Omuscle ) and affect muscle electrolyte concentrations. Vastus lateralis muscle biopsies were collected prior, immediately after, and 1 and 4 h after prolonged dehydrating exercise (150 min at 33 ± 1 °C, 25% ± 2% humidity) on nine endurance-trained cyclists (VO2max = 54.4 ± 1.05 mL/kg/min). Plasma volume (PV) changes and fluid shifts between compartments (Cl(-) method) were measured. Exercise dehydrated subjects 4.7% ± 0.3% of body mass by losing 2.75 ± 0.15 L of water and reducing PV 18.4% ± 1% below pre-exercise values (P < 0.05). Right after exercise H2Omuscle remained at pre-exercise values (i.e., 398 ± 6 mL/100 g dw muscle(-1)) but declined 13% ± 2% (342 ± 12 mL/100 g dw muscle(-1); P < 0.05) after 1 h of supine rest. At that time, PV recovered toward pre-exercise levels. The Cl(-) method corroborated the shift of fluid between extracellular and intracellular compartments. After 4 h of recovery, PV returned to pre-exercise values; however, H2Omuscle remained reduced at the same level. Muscle Na(+) and K(+) increased (P < 0.05) in response to the H2Omuscle reductions. Our findings suggest that active skeletal muscle does not show a net loss of H2O during prolonged dehydrating exercise. However, during the first hour of recovery H2Omuscle decreases seemly to restore PV and thus cardiovascular stability.

Pseudoephedrine and circadian rhythm interaction on neuromuscular performance.

This study analyzed the effects of pseudoephedrine (PSE) provided at different time of day on neuromuscular performance, side effects, and violation of the current doping cut-off threshold [World Anti-Doping Agency (WADA)]. Nine resistance-trained males carried out bench press and full squat exercises against four incremental loads (25%, 50%, 75%, and 90% one repetition maximum [1RM]), in a randomized, double-blind, cross-over design. Participants ingested either 180 mg of PSE (supra-therapeutic dose) or placebo in the morning (7:00 h; AM(PLAC) and AM(PSE)) and in the afternoon (17:00 h; PM(PLAC) and PM(PSE)). PSE enhanced muscle contraction velocity against 25% and 50% 1RM loads, only when it was ingested in the mornings, and only in the full squat exercise (4.4-8.7%; P < 0.05). PSE ingestion raised urine and plasma PSE concentrations (P < 0.05) regardless of time of day; however, cathine only increased in the urine samples. PSE ingestion resulted in positive tests occurring in 11% of samples, and it rose some adverse side effects such us tachycardia and heart palpitations. Ingestion of a single dose of 180 mg of PSE results in enhanced lower body muscle contraction velocity against low and moderate loads only in the mornings. These mild performance improvements are accompanied by undesirable side effects and an 11% risk of surpassing the doping threshold.

Higher insulin-sensitizing response after sprint interval compared to continuous exercise.

This study investigated which exercise mode (continuous or sprint interval) is more effective for improving insulin sensitivity. Ten young, healthy men underwent a non-exercise trial (CON) and 3 exercise trials in a cross-over, randomized design that included 1 sprint interval exercise trial (SIE; 4 all-out 30-s sprints) and 2 continuous exercise trials at 46% VO2peak (CELOW) and 77% VO2peak (CEHIGH). Insulin sensitivity was assessed using intravenous glucose tolerance test (IVGTT) 30 min, 24 h and 48 h post-exercise. Energy expenditure was measured during exercise. Glycogen in vastus lateralis was measured once in a resting condition (CON) and immediately post-exercise in all trials. Plasma lipids were measured before each IVGTT. Only after CEHIGH did muscle glycogen concentration fall below CON (P<0.01). All exercise treatments improved insulin sensitivity compared with CON, and this effect persisted for 48-h. However, 30-min post-exercise, insulin sensitivity was higher in SIE than in CELOW and CEHIGH (11.5±4.6, 8.6±5.4, and 8.1±2.9 respectively; P<0.05). Insulin sensitivity did not correlate with energy expenditure, glycogen content, or plasma fatty acids concentration (P>0.05). After a single exercise bout, SIE acutely improves insulin sensitivity above continuous exercise. The higher post-exercise hyperinsulinemia and the inhibition of lipolysis could be behind the marked insulin sensitivity improvement after SIE.

Time-course effects of aerobic interval training and detraining in patients with metabolic syndrome.

BACKGROUND AND AIMS: Exercise training can improve health of patients with metabolic syndrome (MetS). However, which MetS factors are most responsive to exercise training remains unclear. We studied the time-course of changes in MetS factors in response to training and detraining. METHODS AND RESULTS: Forty eight MetS patients (52 ± 8.8 yrs old; 33 ± 4 BMI) underwent 4 months (3 days/week) of supervised aerobic interval training (AIT) program. After 1 month of training, there were progressive increases in high density lipoprotein cholesterol (HDL-c) and reductions in waist circumference and blood pressure (12 ± 3, -3.9 ± 0.4, and -12 ± 1%, respectively after 4 months; all P < 0.05). However, fasting plasma concentration of triglycerides and glucose were not reduced by training. Insulin sensitivity (HOMA), cardiorespiratory fitness (VO2peak) and exercise maximal fat oxidation (FOMAx) also progressively improved with training (-17 ± 5; 21 ± 2 and 31 ± 8%, respectively, after 4 months; all P < 0.05). Vastus lateralis samples from seven subjects revealed that mitochondrial O2 flux was markedly increased with training (71 ± 11%) due to increased mitochondrial content. After 1 month of detraining, the training-induced improvements in waist circumference and blood pressure were maintained. HDL-c and VO2peak returned to the values found after 1-2 months of training while HOMA and FOMAx returned to pre-training values. CONCLUSIONS: The health related variables most responsive to aerobic interval training in MetS patients are waist circumference, blood pressure and the muscle and systemic adaptations to consume oxygen and fat. However, the latter reverse with detraining while blood pressure and waist circumference are persistent to one month of detraining.

Ingestion of sodium plus water improves cardiovascular function and performance during dehydrating cycling in the heat.

We studied if salt and water ingestion alleviates the physiological strain caused by dehydrating exercise in the heat. Ten trained male cyclists (VO2max : 60 ± 7 mL/kg/min) completed three randomized trials in a hot-dry environment (33 °C, 30% rh, 2.5 m/s airflow). Ninety minutes before the exercise, participants ingested 10 mL of water/kg body mass either alone (CON trial) or with salt to result in concentrations of 82 or 164 mM Na(+) (ModNa(+) or HighNa(+) trial, respectively). Then, participants cycled at 63% of VO2 m ⁢ a x for 120 min immediately followed by a time-trial. After 120 min of exercise, the reduction in plasma volume was lessened with ModNa(+) and HighNa(+) trials (-11.9 ± 2.1 and -9.8 ± 4.2%) in comparison with CON (-16.4 ± 3.2%; P < 0.05). However, heat accumulation or dissipation (forearm skin blood flow and sweat rate) were not improved by salt ingestion. In contrast, both salt trials maintained cardiac output (∼ 1.3 ± 1.4 L/min; P < 0.05) and stroke volume (∼ 10 ± 11 mL/beat; P < 0.05) above CON after 120 min of exercise. Furthermore, the salt trials equally improved time-trial performance by 7.4% above CON (∼ 289 ± 42 vs 269 ± 50 W, respectively; P < 0.05). Our data suggest that pre-exercise ingestion of salt plus water maintains higher plasma volume during dehydrating exercise in the heat without thermoregulatory effects. However, it maintains cardiovascular function and improves cycling performance.

Measurement of the intensities of the long-range alpha particles from 212Po.

212Bi partially decays by ß- populating excited levels of 212Po. Some of these excited states of 212Po decay with very low probability by direct alpha-particle emissions instead of a gamma-alpha cascade. This effect was known since the earliest times after the discovery of radioactivity. Emission energies of these long-range alpha particles were measured in the past, but the activity ratios were not accurately determined. Relative intensities for these decays have now been experimentally determined. Results agree with data previously reported. It is the first time that an uncertainty estimate is provided for such experiment.

Insulin sensitivity improvement with exercise training is mediated by body weight loss in subjects with metabolic syndrome.

AIM: To determine whether exercise training improves insulin actions through concomitant body weight loss (BWL). METHODS: Subjects (aged 55±8 years) with metabolic syndrome (MetS), prediabetes (fasting blood glucose: 111±2mg·dL-1, HbA1c: 5.85±0.05%) and abdominal obesity (waist circumference: 104±7.9cm) were randomly allocated to either a group performing aerobic interval training (EXER; n=76) or a sedentary group receiving lifestyle counselling (CONT; n=20) for 16 weeks. RESULTS: At baseline, insulin sensitivity (according to HOMA2 and intravenous glucose tolerance test; CSI), body composition and VO2max were similar between the groups. After the intervention, both groups had similar BWL (1-2%), but only the EXER group showed decreased [mean (95% CI)] trunk fat mass [from 18.2 (17.4-18.9) to 17.3kg (16.6-17.9); P<0.001] and HOMA2 scores [from 1.6 (1.5-1.7) to 1.4 (1.3-1.5); P=0.001], and increased VO2max [from 2.07 (1.92-2.21) to 2.28 (2.11-2.45) LO2·min-1; P<0.001]. However, CSI did not improve in any group. Within-group subdivision by BWL (≤0%, 0-3%, ≥3%) revealed higher CSI in those with BWL≥3% in both groups. Trunk fat mass reductions were closely associated with CSI and HOMA-IR improvement (r=-0.452-0.349; P<0.001). CONCLUSION: In obese MetS subjects with prediabetes, 3% BWL is required for consistent improvement in insulin sensitivity. Thus, exercise-training programmes should be combined with calorie restriction to achieve BWL levels that prevent the development of diabetes.

Exercise improves metformin 72-h glucose control by reducing the frequency of hyperglycemic peaks.

PURPOSE: To determine the separated and combined effects of metformin and exercise on insulin sensitivity and free-living glycemic control in overweight individuals with prediabetes/type 2 diabetes (T2DM). METHODS: We recruited 16 adults with BMI of 32.7 ± 4.3 kg m-2 and insulin resistance (HOMA-IR 3.2 ± 0.4) under chronic metformin treatment (1234 ± 465 g day-1) enrolled in a high-intensity interval training (HIIT) program. Participants underwent four 72-h experimental trials in a random-counterbalanced order: (1) maintaining their habitual metformin treatment (MET); (2) replacing metformin treatment by placebo (CON); (3) placebo plus two HIIT sessions (EX + CON), and (4) metformin plus two HIIT sessions (MET + EX). We used intermittently scanned continuous glucose monitoring (isCGM) during 72 h in every trial to obtain interstitial fluid glucose area under the curve (IFGAUC) and the percentage of measurements over 180 mg dL-1 (% IFGPEAKS). Insulin sensitivity was assessed on the last day of each trial with HOMA-IR index and calculated insulin sensitivity (CSI) from intravenous glucose tolerance test. RESULTS: IFGAUC was lower in MET + EX and MET than in CON (P = 0.011 and P = 0.025, respectively). In addition, IFGAUC was lower in MET + EX than in EX + CON (P = 0.044). %IFGPEAKS were only lower in MET + EX in relation to CON (P = 0.028). HOMA-IR and CSI were higher in CON in comparison with MET + EX (P = 0.011 and P = 0.022, respectively) and MET (P = 0.006 and P < 0.001, respectively). IFGAUC showed a significant correlation with HOMA-IR. CONCLUSION: Intense aerobic exercise in patients with diabetes and prediabetes under metformin treatment reduces free-living 72-h blood hyperglycemic peaks. This may help to prevent the development of cardiovascular complications associated with diabetes.

A hybrid mathematical modeling approach of the metabolic fate of a fluorescent sphingolipid analogue to predict cancer chemosensitivity.

Sphingolipid (SL) metabolism is a complex biological system that produces and transforms ceramides and other molecules able to modulate other cellular processes, including survival or death pathways key to cell fate decisions. This signaling pathway integrates several types of stress signals, including chemotherapy, into changes in the activity of its metabolic enzymes, altering thereby the cellular composition of bioactive SLs. Therefore, the SL pathway is a promising sensor of chemosensitivity in cancer and a target hub to overcome resistance. However, there is still a gap in our understanding of how chemotherapeutic drugs can disturb the SL pathway in order to control cellular fate. We propose to bridge this gap by a systems biology approach to integrate i) a dynamic model of SL analogue (BODIPY-FL fluorescent-sphingomyelin analogue, SM-BOD) metabolism, ii) a Gaussian mixture model (GMM) of the fluorescence features to identify how the SL pathway senses the effect of chemotherapy and iii) a fuzzy logic model (FLM) to associate SL composition with cell viability by semi-quantitative rules. Altogether, this hybrid model approach was able to predict the cell viability of double experimental perturbations with chemotherapy, indicating that the SL pathway is a promising sensor to design strategies to overcome drug resistance in cancer.

Muscle contraction velocity, strength and power output changes following different degrees of hypohydration in competitive olympic combat sports.

BACKGROUND: It is habitual for combat sports athletes to lose weight rapidly to get into a lower weight class. Fluid restriction, dehydration by sweating (sauna or exercise) and the use of diuretics are among the most recurrent means of weight cutting. Although it is difficult to dissuade athletes from this practice due to the possible negative effect of severe dehydration on their health, athletes may be receptive to avoid weight cutting if there is evidence that it could affect their muscle performance. Therefore, the purpose of the present study was to investigate if hypohydration, to reach a weight category, affects neuromuscular performance and combat sports competition results. METHODS: We tested 163 (124 men and 39 woman) combat sports athletes during the 2013 senior Spanish National Championships. Body mass and urine osmolality (UOSM) were measured at the official weigh-in (PRE) and 13-18 h later, right before competing (POST). Athletes were divided according to their USOM at PRE in euhydrated (EUH; UOSM 250-700 mOsm · kgH2O(-1)), hypohydrated (HYP; UOSM 701-1080 mOsm · kgH2O(-1)) and severely hypohydrated (S-HYP; UOSM 1081-1500 mOsm · kgH2O(-1)). Athletes' muscle strength, power output and contraction velocity were measured in upper (bench press and grip) and lower body (countermovement jump - CMJ) muscle actions at PRE and POST time-points. RESULTS: At weigh-in 84 % of the participants were hypohydrated. Before competition (POST) UOSM in S-HYP and HYP decreased but did not reach euhydration levels. However, this partial rehydration increased bench press contraction velocity (2.8-7.3 %; p < 0.05) and CMJ power (2.8 %; p < 0.05) in S-HYP. Sixty-three percent of the participants competed with a body mass above their previous day's weight category and 70 of them (69 % of that sample) obtained a medal. CONCLUSIONS: Hypohydration is highly prevalent among combat sports athletes at weigh-in and not fully reversed in the 13-18 h from weigh-in to competition. Nonetheless, partial rehydration recovers upper and lower body neuromuscular performance in the severely hypohydrated participants. Our data suggest that the advantage of competing in a lower weight category could compensate the declines in neuromuscular performance at the onset of competition, since 69 % of medal winners underwent marked hypohydration.

Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise.

We identified the cardiovascular stress encountered by superimposing dehydration on hyperthermia during exercise in the heat and the mechanisms contributing to the dehydration-mediated stroke volume (SV) reduction. Fifteen endurance-trained cyclists [maximal O2 consumption (VO2max) = 4.5 l/min] exercised in the heat for 100-120 min and either became dehydrated by 4% body weight or remained euhydrated by drinking fluids. Measurements were made after they continued exercise at 71% VO2max for 30 min while 1) euhydrated with an esophageal temperature (T(es)) of 38.1-38.3 degrees C (control); 2) euhydrated and hyperthermic (39.3 degrees C); 3) dehydrated and hyperthermic with skin temperature (T(sk)) of 34 degrees C; 4) dehydrated with T(es) of 38.1 degrees C and T(sk) of 21 degrees C; and 5) condition 4 followed by restored blood volume. Compared with control, hyperthermia (1 degrees C T(es) increase) and dehydration (4% body weight loss) each separately lowered SV 7-8% (11 +/- 3 ml/beat; P < 0.05) and increased heart rate sufficiently to prevent significant declines in cardiac output. However, when dehydration was superimposed on hyperthermia, the reductions in SV were significantly (P < 0.05) greater (26 +/- 3 ml/beat), and cardiac output declined 13% (2.8 +/- 0.3 l/min). Furthermore, mean arterial pressure declined 5 +/- 2%, and systemic vascular resistance increased 10 +/- 3% (both P < 0.05). When hyperthermia was prevented, all of the decline in SV with dehydration was due to reduced blood volume (approximately 200 ml). These results demonstrate that the superimposition of dehydration on hyperthermia during exercise in the heat causes an inability to maintain cardiac output and blood pressure that makes the dehydrated athlete less able to cope with hyperthermia.

Preexercise medium-chain triglyceride ingestion does not alter muscle glycogen use during exercise.

This investigation determined whether ingestion of a tolerable amount of medium-chain triglycerides (MCT; approximately 25 g) reduces the rate of muscle glycogen use during high-intensity exercise. On two occasions, seven well-trained men cycled for 30 min at 84% maximal O(2) uptake. Exactly 1 h before exercise, they ingested either 1) carbohydrate (CHO; 0.72 g sucrose/kg) or 2) MCT+CHO [0.36 g tricaprin (C10:0)/kg plus 0.72 g sucrose/kg]. The change in glycogen concentration was measured in biopsies taken from the vastus lateralis before and after exercise. Additionally, glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the rate of glucose disappearance from plasma (R(d) glucose), as measured by stable isotope dilution techniques. The change in muscle glycogen concentration was not different during MCT+CHO and CHO (42.0 +/- 4.6 vs. 38.8 +/- 4.0 micromol glucosyl units/g wet wt). Furthermore, calculated glycogen oxidation was also similar (331 +/- 18 vs. 329 +/- 15 micromol. kg(-1). min(-1)). The coingestion of MCT+CHO did increase (P < 0.05) R(d) glucose at rest compared with CHO (26.9 +/- 1.5 vs. 20.7 +/- 0. 7 micromol.kg(-1). min(-1)), yet during exercise R(d) glucose was not different during the two trials. Therefore, the addition of a small amount of MCT to a preexercise CHO meal did not reduce muscle glycogen oxidation during high-intensity exercise, but it did increase glucose uptake at rest.

Dehydration reduces cardiac output and increases systemic and cutaneous vascular resistance during exercise.

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

Fluid and carbohydrate ingestion independently improve performance during 1 h of intense exercise.

This study determined the effects of fluid and carbohydrate ingestion on performance, core temperature, and cardiovascular responses during intense exercise lasting 1 h. On four occasions, eight men cycled at 80 +/- 1% (+/- SEM) of VO2max for 50 min followed by a performance test. During exercise, they consumed either a large volume (1330 +/- 60 ml) of a 6% carbohydrate (79 +/- 4 g) solution or water or a small volume (200 +/- 10 ml) of a 40% maltodextrin (79 +/- 4 g) solution or water. These trials were pooled so the effects of fluid replacement (Large FR vs Small FR) and carbohydrate ingestion (CHO vs NO CHO) could be determined. Performance times were 6.5% faster during Large FR than Small FR and 6.3% faster during CHO than NO CHO (P < 0.05). At 50 min, heart rate was 4 +/- 1 b.min-1 lower and esophageal temperature was 0.33 +/- 0.04 degrees C lower during Large FR than Small FR (P < 0.05) but no differences occurred between CHO and NO CHO. In summary, Large FR slightly attenuates the increase in heart rate and core temperature which occurs during Small FR. Both fluid and carbohydrate ingestion equally improve cycling performance and their effects are additive.