Consecutive days of exercise decrease insulin response more than a single exercise session in healthy, inactive men.

PURPOSE: It is reported that a single bout of exercise can lower insulin responses 12-24 h post-exercise; however, the insulin responses to alternate or consecutive bouts of exercise is unknown. Thus, the purpose of this study was to examine the effect of exercise pattern on post-exercise insulin and glucose responses following a glucose challenge. METHODS: Ten male participants (n = 10, mean ± SD, Age 29.5 ± 7.7 years; BMI 25.7 ± 3.0 kg/m2) completed three exercise trials of walking for 60 min at ~ 70% of VO2max. The trials consisted of: three consecutive exercise days (3CON), three alternate exercise days (3ALT), a single bout of exercise (SB), and a no exercise control (R). Twelve to fourteen hours after the last bout of exercise or R, participants completed a 75 g oral glucose tolerance test (OGTT) and blood was collected at 30 min intervals for the measurement of glucose, insulin, and C-peptide. RESULT: Calculated incremental area under the curve (iAUC) for glucose and C-peptide was not different between the four trials. Insulin iAUC decreased 34.9% for 3CON compared to R (p < 0.01). CONCLUSION: Three consecutive days of walking at ~ 70% VO2max improved insulin response following an OGTT compared to no exercise. It is possible, that for healthy males, the effect of a single bout of exercise or exercise bouts separated by more than 24 h may not be enough stimulus to lower insulin responses to a glucose challenge.

Exercise heat acclimation causes post-exercise hypotension and favorable improvements in lipid and immune profiles: A crossover randomized controlled trial.

BACKGROUND: Passive hyperthermic exposure causes an acute hypotensive response following the cessation of heat stress. Chronic heat stress is well documented in animal studies to instigate metabolic and lipid alterations. However, it is unknown if exercise-heat acclimation also causes favorable chronic blood pressure, lipid, and immune responses in humans. PURPOSE: This project tested the hypothesis that 10-day exercise-heat acclimation (HA) would cause greater post-exercise reductions in arterial blood pressure and favorable metabolic, lipid, and immune responses compared to 10-day exercise under neutral conditions (CON). METHODS: Thirteen healthy sedentary participants (8M/5F, 28 ±â€¯6y, 78 ±â€¯17 kg), completed a 10-day (90 min/day exercise bout) clamped hyperthermia HA (increase internal temperature 1.5 °C, in 42 °C, 28% Rh) and control (CON: 23 °C, 42% Rh) protocols in a counterbalanced design with a 2 month washout. Pre- and post-exercise HA/CON blood pressures were taken 1-h post-exercise on exercise days 1 and 10. Metabolic, lipid and immune panels were taken pre-post HA/CON. RESULTS: Exercise under heat stress had greater post-exercise hypotension (systolic; -6 mmHg, diastolic; -8 mmHg; and mean arterial pressure; -7 mmHg) on both days 1 and 10 compared to exercise under neutral conditions (main effect for condition, P ≤ 0.004). Only from pre-to-post HA, total cholesterol (168 ±â€¯19 to 157 ±â€¯15; P < 0.03) and triglycerides (137 ±â€¯45 to 111 ±â€¯30; P < 0.03) were reduced, while absolute lymphocytes (-26%), monocytes (-22%), and basophils (-49%) significantly decreased (each P ≤ 0.04). Relative values of neutrophils increased (18%) and lymphocytes decreased (-20%) only after HA (P ≤ 0.04). CONCLUSION: These data indicate that exercise in the heat (regardless of acclimation status) causes a profound post-exercise hypotensive response, while HA causes favorable lipid, and immune profile changes. Further examination of exercise-heat acclimation on vascular, metabolic, and immune responses will offer insight for benefits in other clinical populations with vascular, metabolic and immune dysfunction.

The change in metabolic heat production is a primary mediator of heat acclimation in adults.

PURPOSE: This study examined whether heat acclimation (HA) results in either predominate improvements in heat dissipation or reduced endogenous heat production via individual components of the human heat balance equation. METHODS: Twelve healthy inactive subjects (5 females, mean ± SD): age 28 ± 6y, 77.9 ± 2kg), completed a 10-day HA (42°C, 28% RH) hyperthermia clamp (90min/day exercise, ∆1.5°C in rectal temperature (Tre)) and control workload matched (CON: 23°C, 42% RH) protocols in a counterbalanced design separated by at least 2 mo. Pre-and post-HA were matched for external work rate (EXWR; day 1 and day 10 first 30min at 118 ± 29W, last 60min at 11 ± 5W); and metabolic heat production (Hprod; day 1 and day 9, first 30min at 296 ± 26Wm-2, last 60min 187 ± 33Wm-2). RESULTS: When Pre- and post- HA was matched for Hprod, there was no difference during the first 30 or last 60min of exercise for metabolic energy expenditure (MEE 363 ± 70/ 195 ± 32Wm-2), Hprod (296 ± 67/ 187 ± 33Wm-2) or Tre (∆2.1 ± 0.5°C). When pre- and post-HA was EXWR equivalent, HA significantly attenuated MEE during the first 30 and last 60min (303 ± 49/ 174 ± 35Wm-2), Hprod (241 ± 44/ 168 ± 33, W·m-2), and ∆Tre (∆1.3 ± 0.4°C) (each P < 0.0001). When ∆Tre, ∆Tsk, ∆Tb were each normalized per 100W Hprod, no differences were found for any pre-to post-HA comparison. Heat loss required (Ereq) to maintain steady state internal temperature (Ereq = 220 ± 32Wm-2), maximal capacity of the climate for evaporative heat loss (Emax = 266 ± 56Wm-2), evaporative heat loss from skin (Esk = 207 ± 38Wm-2) or skin wettedness (Ereq/Emax = 0.88 ± 0.23Wm-2) were not different among each condition during the last 60min. CONCLUSION: The mechanisms that underlie heat acclimation are not wholly attributed to heat dissipation enhancements per se, but are significantly influenced by metabolic heat production alterations under uncompensable heat stress environments.

Omega-3 fatty acid supplementation combined with acute aerobic exercise does not alter the improved post-exercise insulin response in normoglycemic, inactive and overweight men.

PURPOSE: The aim of this study was to determine if omega-3 (n-3) supplementation combined with acute aerobic exercise would improve glucose and insulin responses in normoglycemic, inactive, overweight men. METHODS: In a random order, ten inactive and normoglycemic men (30.6 ± 10 years, 85.4 ± 11 kg, 26.7 ± 4 BMI) completed a rest (R) and exercise trial (EX) without n-3 supplementation. Following 42 days of n-3 supplementation, participants again completed a rest (R + n-3) and exercise trial (EX + n-3) with continued n-3 supplementation. The exercise trial consisted of 3 days of ~70 % VO2peak for 60 min/session. N-3 supplementation entailed 4.55 g/day of n-3 (EPA 2.45 g, DHA 1.61 g). A 75 g oral glucose tolerance (OGTT) test was administered 14-16 h after each trial. RESULTS: Relative to R (35,278 ± 9169 pmol/L), EX without n-3 reduced the incremental area under the curve for insulin (iAUCinsulin) during an OGTT by 21.3 % (27765 ± 4925 pmol/L, p = 0.018) and 20.6 % after the EX + n-3 trial (27,999 ± 8370 pmol/L; p = 0.007). In addition, EX (96 ± 21 pmol/L; p = 0.006) reduced C-peptide by 13.5 % when compared to R (111 ± 26 pmol/L). No difference was observed between R and n-3 trials for iAUCinsulin and iAUCC-peptide. Only EX improved insulin sensitivity index by 5.6 % (p = 0.02) when compared to R. CONCLUSIONS: These data suggest that n-3 supplementation does not add any additional benefit beyond the exercise induced insulin responses in inactive men. Furthermore, n-3 supplementation alone does not appear to impair insulin action in normoglycemic, inactive, overweight men.

Prior Exercise Does Not Reduce Postprandial Lipemia Following a Mixed Glucose Meal When Compared with a Mixed Fructose Meal.

This study examined the effect of prior exercise on postprandial lipemia (PPL) concentration following a mixed meal (MM) made with either glucose or fructose. Sedentary women completed four trials in random order: 1) Rest-Fructose: RF, 2) Rest-Glucose: RG, 3) Exercise-Fructose: EF, 4) Exercise-Glucose: EG. Exercise expended 500 kcal while walking at 70%VO2max. Rest was 60 min of sitting. The morning after each trial, a fasting (12 hr) blood sample was collected followed by consumption of the MM. The MM was blended with whole milk and ice cream plus a glucose or fructose powder. Glucose and fructose powder accounted for 30% of the total kcal within the MM. Blood was collected periodically for 6 hr post-MM and analyzed for PPL. Magnitude of PPL over the 6 hr postmeal was quantified using the triglyceride incremental area under the curve (TG AUCI). Significant differences (p < .05) between trials were determined using repeated-measures ANOVA and Bonferroni post hoc test. There was no significant difference in the TG AUCI between the four trials (p > .05). A significant trial by time interaction for TG concentration was reported (p < .05). Despite lack of change in the AUCI with prior exercise, the lower TG concentration at multiple time points in the EG trial does indicate that prior exercise has some desirable effect on PPL. This study suggests that replacing fructose with glucose sugars and incorporating exercise may minimize PPL following a mixed meal but exercise will need to elicit greater energy expenditure.

An acute bout of whole body passive hyperthermia increases plasma leptin, but does not alter glucose or insulin responses in obese type 2 diabetics and healthy adults.

Acute and chronic hyperthermic treatments in diabetic animal models repeatedly improve insulin sensitivity and glycemic control. Therefore, the purpose of this study was to test the hypothesis that an acute 1h bout of hyperthermic treatment improves glucose, insulin, and leptin responses to an oral glucose challenge (OGTT) in obese type 2 diabetics and healthy humans. Nine obese (45±7.1% fat mass) type 2 diabetics (T2DM: 50.1±12y, 7.5±1.8% HbA1c) absent of insulin therapy and nine similar aged (41.1±13.7y) healthy non-obese controls (HC: 33.4±7.8% fat mass, P<0.01; 5.3±0.4% HbA1c, P<0.01) participated. Using a randomized design, subjects underwent either a whole body passive hyperthermia treatment via head-out hot water immersion (1h resting in 39.4±0.4°C water) that increased internal temperature above baseline by ∆1.6±0.4°C or a control resting condition. Twenty-four hours post treatments, a 75g OGTT was administered to evaluate changes in plasma glucose, insulin, C-peptide, and leptin concentrations. Hyperthermia itself did not alter area under the curve for plasma glucose, insulin, or C-peptide during the OGTT in either group. Fasting absolute and normalized (kg·fat mass) plasma leptin was significantly increased (P<0.01) only after the hyperthermic exposure by 17% in T2DM and 24% in HC groups (P<0.001) when compared to the control condition. These data indicate that an acute hyperthermic treatment does not improve glucose tolerance 24h post treatment in moderate metabolic controlled obese T2DM or HC individuals.

The effects of two bouts of high- and low-volume resistance exercise on glucose tolerance in normoglycemic women.

The purpose of the study was to determine the efficacy of a low-volume, moderate-intensity bout of resistance exercise (RE) on glucose, insulin, and C-peptide responses during an oral glucose tolerance test (OGTT) in untrained women compared with a bout of high-volume RE of the same intensity. Ten women (age 30.1 ± 9.0 years) were assessed for body composition, maximal oxygen uptake, and 1-repetition maximum (1RM) before completing 3 treatments administered in random order: 1 set of 10 REs (RE1), 3 sets of 10 REs (RE3), and no exercise (C). Twenty-four hours after completing each treatment, an OGTT was performed after an overnight fast. Glucose area under the curve response to an OGTT was reduced after both RE1 (900 ± 113 mmol·L(-1)·min(-1), p = 0.056) and RE3 (827.9 ± 116.3, p = 0.01) compared with C (960.8 ± 152.7 mmol·L(-1)·min(-1)). Additionally, fasting glucose was significantly reduced after RE3 (4.48 ± 0.45 vs. 4.90 ± 0.44 mmol·L(-1), p = 0.01). Insulin sensitivity (IS), as determined from the Cederholm IS index, was improved after RE1 (10.8%) and after RE3 (26.1%). The reductions in insulin and C-peptide areas after RE1 and RE3 were not significantly different from those in the C treatment. In conclusion, greater benefits in glucose regulation appear to occur after higher volumes of RE. However, observed reductions in glucose, insulin, C-peptide areas after RE1 suggest that individuals who may not well tolerate high-volume RE protocols may still benefit from low-volume RE at moderate intensity (65% 1RM).

Whey protein improves glycemia during an oral glucose tolerance test compared to vigorous-intensity aerobic exercise in young adult men.

BACKGROUND: Both aerobic exercise and whey protein can improve glucose regulation. The purpose of this study was to investigate how a single bout of vigorous-intensity aerobic exercise and whey protein, independently, as well as when combined, influence glycemia during an oral glucose tolerance test in sedentary, young men. METHODS: Healthy males (n = 11) completed four randomized trials: no exercise/no whey protein (R); exercise (EX; walking at 70% VO2max for 60 min); 50 g of whey protein (W); and exercise combined with 50 g of whey protein (EXW). Each trial included a 75 g oral glucose tolerance test (OGTT) that was completed after an overnight fast. Blood samples were collected over a two-hour period during the OGTT. For EX and EXW, the exercise was performed the evening before the OGTT and the 50 g of whey protein was dissolved in 250 mL of water and was consumed as a preload 30 min prior to the OGTT. For R and EX, participants consumed 250 mL of water prior to the OGTT. Plasma samples were analyzed for glucose, insulin, C-peptide, glucagon, gastric inhibitory peptide (GIP) and glucagon like peptide 1 (GLP-1), and postprandial incremental area under the curve (iAUC) was calculated for each. RESULTS: Glucose iAUC was reduced during W (- 32.9 ± 22.3 mmol/L) compared to R (122.7 ± 29.8 mmol/L; p < 0.01) and EX (154.3 ± 29.2 mmol/L; p < 0.01). Similarly, glucose iAUC was reduced for EXW (17.4 ± 28.9 mmol/L) compared to R and EX (p < 0.01 for both). There were no differences in iAUC for insulin, C-peptide, GIP, GLP-1, and glucagon between the four trials. Insulin, C-peptide, glucagon, GIP, and GLP-1 were elevated during the whey protein preload period for W and EXW compared to EX and R (p < 0.01). There were no differences for insulin, C-peptide, glucagon, GIP, or GLP-1 between trials for the remaining duration of the OGTT. CONCLUSIONS: Glucose responses during an oral glucose tolerance test were improved for W compared to EX. There were no additional improvements in glucose responses when vigorous-intensity aerobic exercise was combined with whey protein (EXW).

Responses of LDL and HDL particle size and distribution to omega-3 fatty acid supplementation and aerobic exercise.

The purpose of this investigation was to determine the independent and combined effects of aerobic exercise and omega-3 fatty acid (n-3fa) supplementation on lipid and lipoproteins. Sedentary, normoglycemic, nonsmoking men (n = 11) were assigned to perform rest and exercise before and during n-3fa supplementation. Exercise consisted of 3 consecutive days of treadmill walking at 65% maximum O(2) consumption for 60 min. Supplementation consisted of 42 days of 4.55 g/day of n-3fa. A two-way factorial ANOVA with repeated measures revealed significant reductions in total cholesterol (P = 0.001, -9.2%) and triglyceride (P = 0.007, -32.4%) concentrations postexercise. In addition, exercise increased LDL peak particle size (P = 0.001) from 26.2 to 26.4 nm, but not HDL size. The n-3fa supplementation resulted in a significant shift in the distribution of HDL-cholesterol (HDL-C) carried by HDL(2b+2a) (P = 0.001, 14.2%) and HDL(3a+3b) (P = 0.001, -22.8%), despite no significant changes in lipid and lipoprotein-cholesterol concentrations. The majority of the shift in HDL-C was noted in HDL(2b) (P = 0.001, 20.9%) and HDL(3a) (P < 0.001, -31.0%) particles. There were no combined effects of exercise and n-3fa supplementation on lipids and lipoproteins. Three consecutive days of aerobic exercise reduced triglyceride and total cholesterol concentrations with a concomitant increase in LDL peak particle size. In contrast, n-3fa supplementation shifted HDL-C from HDL(3) particles to HDL(2) particles, despite no significant changes in HDL(2)-C and HDL(3)-C concentrations. Exercise and n-3fa supplementation do not synergistically improve serum lipids and lipoproteins, but rather independently affect the metabolism of lipids and lipoproteins.

Pilot study: an acute bout of high intensity interval exercise increases 12.5 h GH secretion.

The purpose of this study was to test the hypothesis that high-intensity interval exercise (HIE) significantly increases growth hormone (GH) secretion to a greater extent than moderate-intensity continuous exercise (MOD) in young women. Five young, sedentary women (mean ± SD; age: 22.6±1.3 years; BMI: 27.4±3.1 kg/m2 ) were tested during the early follicular phase of their menstrual cycle on three occasions. For each visit, participants reported to the laboratory at 1700 h, exercised from 1730-1800 h, and remained in the laboratory until 0700 h the following morning. The exercise component consisted of either 30-min of moderate-intensity continuous cycling at 50% of measured peak power (MOD), four 30-s "all-out" sprints with 4.5 min of active recovery (HIE), or a time-matched sedentary control using a randomized, cross-over design. The overnight GH secretory profile of each trial was determined from 10-min sampling of venous blood from 1730-0600 h, using deconvolution analysis. Deconvolution GH parameters were log transformed prior to statistical analyses. Calculated GH AUC (0-120 min) was significantly greater in HIE than CON (P = 0.04), but HIE was not different from MOD. Total GH secretory rate (ng/mL/12.5 h) was significantly greater in the HIE than the CON (P = 0.05), but MOD was not different from CON or HIE. Nocturnal GH secretion (ng/mL/7.5 h) was not different between the three trials. For these women, in this pilot study, a single bout of HIE was sufficient to increase 12.5 h pulsatile GH secretion. It remains to be determined if regular HIE may contribute to increased daily GH secretion.

Obese type 2 diabetics have a blunted hypotensive response to acute hyperthermia therapy that does not affect the perception of thermal stress or physiological strain compared to healthy adults.

PURPOSE: The objective of this study was to test the hypothesis that a hyperthermia-hypotensive challenge via whole body hot water immersion would alter the perception of hyperthermia and physiological strain in obese type 2 diabetics (T2DM) compared to healthy non-obese (HC) individuals. Additionally, we hypothesize that the mechanisms would be attributed to impaired blood pressure adjustments and afferent signals (via changes in internal and mean skin temperatures). METHODS: In random order, eleven obese T2DM (50±12y, 45±7% fat mass, 7.5±1.8% HbA1c) and nine similar aged (41±14y, P>0.05) HC non-obese (33±8% fat mass, P<0.01) non-diabetic (5.3±0.4% HbA1c, P<0.01) underwent a 60min bout of whole body passive hyperthermia followed by 60min of recovery or a 2h resting control condition. The perception of thermal sensation (TS, scale range: 1-13), calculated physiological strain (PSI), internal (Tre, rectal) and mean skin (Tsk) temperatures, heart rate (HR) and blood pressures (BP) were the primary dependent variables. RESULTS: Hyperthermia similarly increased Tre by 1.4±0.4°C, Tsk by 6.5±0.8°C and HR by 34±8bpm in both groups (P>0.5). Hyperthermia reduced diastolic BP (27% in T2DM and 33% in HC, P<0.05) and mean arterial BP (reduced by 15% in T2DM and by 19% in HC) relative to control conditions (P<0.05). The reduction of mean arterial BP area under the curve was attenuated in T2DM (12%) compared to HC (30%) (group×condition, P<0.01). TS and PSI during hyperthermia were not different between groups. Pearson product correlation reported strong correlations (r=0.69-0.89) with Tre and Tsk with TS in both populations. The linear stepwise regression analysis revealed similar relative contributions for Tre (~60%) and Tsk (~40%) on TS for both groups. CONCLUSIONS: These data indicate that obese T2DM with moderate metabolic control have an attenuated hyperthermia-hypotensive response that does not affect TS and PSI. This also may suggest behavioral thermoregulation is intact in this study group.

Effects of oral contraceptives on glucoregulatory responses to exercise.

Some of the effects of oral contraceptives (OCs) to alter glucoregulation may be ameliorated by exercise. To test this premise, the effects of acute aerobic exercise on postprandial glucose, insulin, and C-peptide responses (area under the curve [AUC]) were measured in 8 users of low-dose estrogen and progestin OCs (OC(+)) and 10 women not using OCs (OC(-)). They completed 2 randomly ordered intervention trials: (1) aerobic exercise on 3 consecutive days with a 2.5-hour, 75-g oral glucose tolerance test (OGTT) on day 4, and (2) no exercise for 3 days prior to the OGTT (control trial). The exercise was 50 minutes of treadmill walking at 70% (.-)VO(2max). The groups were similar in age (27 +/- 3 years), waist-to-hip ratio (0.74 +/- 0.01), and cardiorespiratory fitness (32.5 +/- 1.6 mL x kg body mass(-1) x min(-1)). Fasting plasma glucose, C-peptide, and insulin levels were similar (P >.05) between groups in the control trial. In both trials, glucose(AUC) was significantly greater (13%, P <.05) in OC(+). Exercise resulted in a significant (P <.05) decrease in fasting plasma glucose and insulin, insulin(AUC), glucose(AUC) x insulin(AUC), and C-peptide(AUC) in both groups, suggesting enhanced insulin action and/or reduced pancreatic insulin secretion. Hepatic insulin extraction ([C-peptide(AUC) - insulin(AUC)())]/C-peptide(AUC)) was increased following exercise only in OC(+). Thus, insulin action was enhanced in response to exercise in young sedentary women independent of OC use. The mechanisms for the acute exercise effect on insulin action may be different in OC users compared with normally menstruating women.

A single 1-h session of moderate-intensity aerobic exercise does not modify lipids and lipoproteins in normolipidemic obese women.

The purpose of this study was to quantify the effects of a single session of aerobic exercise on lipids and lipoproteins in women who were sedentary and obese. Women (n = 12) who were premenopausal, sedentary, and obese (body mass index, 30-40 kg·m(-2); waist circumference > 88 cm) completed exercise and control trials in a randomly assigned order. Exercise consisted of a single session of treadmill walking at 70% maximum oxygen uptake until 500 kcal were expended, and the control protocol consisted of 60 min of seated rest. Fasting blood samples were collected immediately prior to, 24 h, and 48 h following the exercise and control sessions and analyzed for triglyceride, total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), HDL(2)-C, and HDL(3)-C concentrations, and mean LDL, HDL(2), and HDL(3) particle size and cholesterol distributions. A 2 × 3 (trial × time) ANOVA with repeated measures revealed no significant (p > 0.05) changes in the lipid and lipoprotein variables 24 and 48 h following exercise. In contrast to previously published data in lean men and women, a single session of treadmill exercise at 70% maximum oxygen uptake that expended 500 kcal was insufficient to modify lipids and lipoproteins in women who were sedentary, normolipidemic, and obese.

Responses of blood lipids and lipoproteins to extended-release niacin and exercise in sedentary postmenopausal women.

Niacin and exercise positively alter blood lipids and lipoproteins via different mechanisms. However, the effects of niacin combined with exercise on blood lipid and lipoprotein profiles have not been investigated in sedentary postmenopausal women. The current study examined the responses of blood lipids and lipoproteins to niacin and exercise in 18 sedentary postmenopausal women, who underwent four conditions: no-niacin rest, no-niacin exercise, niacin rest, and niacin exercise. Participants ingested 1,000 mg/day of extended-release niacin for 4 weeks during the niacin condition. As an exercise treatment, participants performed a single bout of exercise on a treadmill at 60% heart rate reserve until 400 kcal were expended. Extended-release niacin without the exercise intervention significantly (p < .001) increased high-density lipoprotein cholesterol and high-density lipoprotein-2 cholesterol by 12.4% and 33.3%, respectively, and decreased the total cholesterol to high-density lipoprotein cholesterol ratio by 14.8%. Thus, 4 weeks of 1,000 mg/day of extended-release niacin can improve the blood lipid and lipoprotein profiles in sedentary postmenopausal women.