Single Bout Of Moderate-intensity Exercise Research Articles

A study on the influence of a single bout of moderate-intensity exercise on processing bias towards emotional information of individuals with high psychosocial stress levels

AbstractTo explore the impact of a single bout of moderate-intensity exercise on cognitive bias of individuals with high psychosocial stress levels. 42 college students with high stress levels were recruited and divided into a exercise group (N = 21) and a no-exercise group (N = 21). The psychological and behavioral characteristics were studied using word-face stroop task, memory bias task, and interpretion bias task. College students with high psychosocial stress levels have attention bias, memory bias, and Interpretion bias towards negative emotional information, and a single bout of moderate-intensity exercise can increase attention bias towards neutral and positive emotional information, and memory bias towards neutral emotional information, interpretation bias towdrds positive emotional information. A single bout of moderate-intensity exercise can increase the positive cognitive bias towards emotional information, which is beneficial for regulating psychosocial stress levels.

The Influence of Exercise-Associated Small Extracellular Vesicles on Trophoblasts In Vitro.

Exercise induces the release of small extracellular vesicles (sEVs) into circulation that are postulated to mediate tissue cross-talk during exercise. We previously reported that pregnant individuals released greater levels of sEVs into circulation after exercise compared to matched non-pregnant controls, but their biological functions remain unknown. In this study, sEVs isolated from the plasma of healthy pregnant and non-pregnant participants after a single bout of moderate-intensity exercise were evaluated for their impact on trophoblasts in vitro. Exercise-associated sEVs were found localized within the cytoplasm of BeWo choriocarcinoma cells, used to model trophoblasts in vitro. Exposure to exercise-associated sEVs did not significantly alter BeWo cell proliferation, gene expression of angiogenic growth factors VEGF and PLGF, or the release of the hormone human chorionic gonadotropin. The results from this pilot study support that exercise-associated sEVs could interact with trophoblasts in vitro, and warrant further investigation to reveal their potential role in communicating the effects of exercise to the maternal-fetal interface.

Short, frequent high-intensity physical activity breaks reduce appetite compared to a continuous moderate-intensity exercise bout.

A single exercise session can affect appetite-regulating hormones and suppress appetite. The effects of short, regular physical activity breaks across the day on appetite are unclear. This study investigated the effects of breaking up sitting with high-intensity physical activity vs a single bout of moderate-intensity exercise and prolonged sitting on appetite control. In this randomised crossover trial, 14 sedentary, inactive adults (7 women) completed 3, 8-h experimental conditions: (i) prolonged sitting (SIT); (ii) 30 min of moderate-intensity exercise followed by prolonged sitting (EX-SIT), and (iii) sitting with 2 min 32 s of high-intensity physical activity every hour (SIT-ACT). Physical activity energy expenditure was matched between EX-SIT and SIT-ACT. Subjective appetite was measured every 30 min with acylated ghrelin and total peptide-YY (PYY) measured hourly in response to two standardised test meals. An ad libitum buffet meal was provided at the end of each condition. Based on linear mixed model analysis, total area under the curve for satisfaction was 16% higher (P = 0.021) and overall appetite was 11% lower during SIT-ACT vs EX-SIT (P = 0.018), with no differences between SIT-ACT and SIT. Time series analysis indicated that SIT-ACT reduced subjective appetite during the majority of the post-lunch period compared with SIT and EX-SIT, with some of these effects reversed earlier in the afternoon (P < 0.05). Total PYY and acylated ghrelin did not differ between conditions. Relative energy intake was 760 kJ lower during SIT-ACT vs SIT (P = 0.024). High-intensity physical activity breaks may be effective in acutely suppressing appetite; yet, appetite-regulating hormones may not explain such responses.

Effects of acute endurance exercise and exhaustive exercise on innate immune signals induced by mtDNA

Objective: Numerous studies have shown that mitochondrial DNA (mtDNA) can trigger innate immune signaling, and exercise can induce mitochondrial stress. Therefore, this study is aimed at investigating the influence of different types of acute exercise on the innate immune signaling triggered by mtDNA. Methods: Male C57BL/6 mice ( n = 18) were randomly and equally divided into three groups. They were control group, acute moderate-intensity endurance exercise group (AMIE), and 3-day exhaustive exercise group (EE) respectively. Mice were sacrificed immediately after exercise. The spleen, liver, and blood were taken for analysis. Results: The amount of mtDNA in the liver cytoplasm and plasma was significantly decreased after AMIE ( p &lt; .05). However, the amount of mtDNA in plasma was increased after EE (p &lt; .05). The mRNA expression of TFAM, and most TLR9 and cGAS/STING signaling pathway-related genes in the liver and spleen was markedly elevated, whereas the expression of those genes in leukocytes was reduced after AMIE. Furthermore, AMIE significantly decreased the protein expression of NLRP3 inflammasome in the liver ( p &lt; .05) and STING in spleen ( p &lt; .01). Also, AMIE and EE caused a drop in circulating IFN-β levels ( p &lt; .05). Conclusion: A single bout of moderate-intensity exercise reduces mtDNA-induced innate immune signaling and suppresses inflammatory responses by decreasing hepatic cytoplasmic and circulating mtDNA. However, repeated bouts of exhaustive exercise stimulate innate immune signaling by increasing levels of circulating mtDNA.

Serum fetuin-A and Ser312 phosphorylated fetuin-A responses and markers of insulin sensitivity after a single bout of moderate intensity exercise.

Fetuin‐A (Fet‐A), secreted by the liver and adipose tissue, inhibits insulin receptor tyrosine kinase activity and modulates insulin action. Numerous studies have shown association of elevated serum Fet‐A concentrations with obesity, non‐alcoholic fatty liver disease, and type 2 diabetes. Both moderate body weight loss (5%–10%) and significant body weight loss have been shown to decrease serum Fet‐A and improve insulin sensitivity. Currently, there are no studies examining the effects of a single bout of exercise on serum Fet‐A or Ser312‐pFet‐A (pFet‐A) responses. We hypothesized that a single bout of moderate‐intensity exercise will lower serum Fet‐A and that these changes will be associated with an improvement in insulin sensitivity. Thirty‐one individuals with obesity and 11 individuals with normal body weight were recruited. Participants underwent a single bout of treadmill walking, expending 500 kcal at 60%–70% VO2max. Oral glucose tolerance tests (OGTT) were administered before the single bout of exercise (Pre Ex) and 24 h after exercise (24h Post Ex). In individuals with obesity, we observed a transient elevation of serum Fet‐A concentrations, but not pFet‐A, immediately after exercise (Post Ex). Further, a single bout of exercise decreased glucoseAUC, insulinAUC, and insulin resistance index in individuals with obesity. Consistent with this improvement in insulin sensitivity, we observed that Fet‐AAUC, pFet‐AAUC, 2 h pFet‐A, and 2 h pFet‐A/Fet‐A were significantly lower following a single bout of exercise. Further, reductions in serum Fet‐AAUC 24h Post Ex were correlated with a reduction in insulin resistance index. Together, this suggests that alterations in serum Fet‐A following a single bout of moderate‐intensity endurance exercise may play a role in the improvement of insulin sensitivity.Clinical Trial RegistrationNCT03478046; https://clinicaltrials.gov/ct2/show/NCT03478046.

Effects of ascorbic acid supplementation on immune status in healthy women following a single bout of exercise

This study was designed to determine the effects of ascorbic acid (AA) supplementation on immune status following a single bout of exercise. In a crossover design, 20 healthy sedentary women performed 30 min moderate-intensity cycling with (1000AA) or without (0AA) ingesting 1000 mg of AA daily for 1 week. Blood samples were taken immediately before, immediately after and 24 h post-exercise to determine the oxidative stress markers, immunophenotyping of peripheral blood lymphocytes and neutrophil phagocytic function. Moderate-intensity exercise in participants ranged in age from 21 to 23 years, showed no significant changes in oxidative stress markers in both cohorts. Plasma total creatine kinase was increased immediately after exercise and returned to baseline at 24 h post-exercise in both cohorts. Participants ingesting 1000 mg AA demonstrated significant higher level of plasma AA at pre-exercise and post-exercise as compared with the same time point in 0AA group. White blood cell and absolute neutrophil counts were increased immediately after exercise in both cohorts. Exercise resulted in increased lymphocyte count, CD4 + and CD8 + T cell counts immediately after exercise (p < 0.05) in 0AA group. AA supplement mitigated effects of exercise on CD4 + T cells. No significant change in neutrophil phagocytic function were observed when incubated with low or high concentrations of Candida albicans in both cohorts. These results suggested that a single bout of moderate-intensity exercise caused muscle injury with increased absolute CD4 + and CD8 + T cell counts, accompanied by a transient increase in neutrophil count, while their phagocytic function was not changed. However, a short-term AA supplementation does not show beneficial effects on exercise-induced changes in leukocyte subpopulations.

Reliability of arterial stiffness indices at rest and following a single bout of moderate-intensity exercise in older adults.

Short-term changes in arterial stiffness with exercise are proposed to better reflect vascular impairments than resting measures alone and are suggested as a prognostic indicator of cardiovascular risk in older adults. Arterial stiffness indices are reliable at rest, but the time-course and reliability of postexercise changes in arterial stiffness in older adults are unknown. The precision of postexercise changes in arterial stiffness should be determined prior to their use in large prospective trials. This study assessed the between-day reliability of the changes in pulse wave velocity (PWV), augmentation index (AIx75) and reflection magnitude (RM) following an exercise bout in older adults. Ten older adults (71±5years) were tested on three separate days, 7days apart. PWV, AIx75 and RM were assessed at rest, immediately post and at 20, 40 and 60min during recovery after moderate-intensity cycling. Intraclass correlation coefficient (ICC) and reliability coefficient (RC) were used to assess the relative and absolute reliability of arterial stiffness responses. PWV increased, and RM decreased immediately after exercise (P<0·05), and returned to baseline during recovery. AIx decreased during recovery (P<0·001). Resting ICC values were 0·91 (PWV), 0·72 (AIx75) and 0·40 (RM). Reliability of the immediate changes following exercise was high for PWV (ICC:0·87, RC:1·9ms-1 ) and moderate for AIx75 (ICC:0·64, RC:7%) and RM (ICC:0·59, RC:9%). Reliability of the postexercise responses was similar to that at rest for all measures of arterial stiffness. These findings indicate that postexercise changes in arterial stiffness indices are reliable in healthy older adults and supports further investigation of the prognostic value of these responses.

The immediate effects of a single bout of aerobic exercise on oral glucose tolerance across the glucose tolerance continuum

We investigated glucose tolerance and postprandial glucose fluxes immediately after a single bout of aerobic exercise in subjects representing the entire glucose tolerance continuum. Twenty‐four men with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or type 2 diabetes (T2D; age: 56 ± 1 years; body mass index: 27.8 ± 0.7 kg/m2, P > 0.05) underwent a 180‐min oral glucose tolerance test (OGTT) combined with constant intravenous infusion of [6,6‐2H2]glucose and ingestion of [U‐13C]glucose, following 1 h of exercise (50% of peak aerobic power) or rest. In both trials, plasma glucose concentrations and kinetics, insulin, C‐peptide, and glucagon were measured. Rates (mg kg−1 min−1) of glucose appearance from endogenous (RaEndo) and exogenous (oral glucose; RaOGTT) sources, and glucose disappearance (Rd) were determined. We found that exercise increased RaEndo, RaOGTT, and Rd (all P < 0.0001) in all groups with a tendency for a greater (~20%) peak RaOGTT value in NGT subjects when compared to IGT and T2D subjects. Accordingly, following exercise, the plasma glucose concentration during the OGTT was increased in NGT subjects (P < 0.05), while unchanged in subjects with IGT and T2D. In conclusion, while a single bout of moderate‐intensity exercise increased the postprandial glucose response in NGT subjects, glucose tolerance following exercise was preserved in the two hyperglycemic groups. Thus, postprandial plasma glucose responses immediately following exercise are dependent on the underlying degree of glycemic control.

Exercise and 24-h Glycemic Control

We assessed the effect of a single bout of moderate-intensity exercise on subsequent 24-h glycemic control in 60 type 2 diabetes patients. Moreover, we examined whether individual responses to exercise were related to subjects' baseline characteristics, including age, body mass index, diabetes duration, exercise performance, medication, and HbA1c content. Sixty type 2 diabetes patients (insulin-treated, n = 23) participated in a randomized crossover experiment. Patients were studied on two occasions for 3 d under strict dietary standardization but otherwise free-living conditions. Parameters of glycemic control (means [95% confidence interval]) were assessed by continuous glucose monitoring over the 24-h period after a single bout of moderate-intensity endurance-type exercise or no exercise at all (control). Type 2 diabetes patients experienced hyperglycemia (blood glucose >10 mmol·L) for as much as 8:16 h:min (6:44 to 9:48 h:min) per day. The prevalence of hyperglycemia was reduced by 31% to 5:38 h:min (3:17 to 7:00 h:min) over the 24-h period after the exercise bout (P < 0.001). Moreover, exercise lowered average blood glucose concentrations by 0.9 mmol·L (0.7 to 1.2) and reduced glycemic variability (P < 0.05). The response to exercise showed considerable variation between subjects and correlated positively with HbA1c levels (r = 0.38, P < 0.01). Nevertheless, even well-controlled patients with an HbA1c level below 7.0% (n = 28) achieved a 28% reduction in the daily prevalence hyperglycemia after exercise (P < 0.01). A single bout of moderate-intensity exercise substantially improves glycemic control throughout the subsequent day in insulin- and non-insulin-treated type 2 diabetes patients. Of all baseline characteristics, only subjects' HbA1c level is related to the magnitude of response to exercise. Nevertheless, the present study demonstrates that even well-controlled patients benefit considerably from the blood glucose-lowering properties of daily exercise.

Arterial Stiffness and Endothelial Function

Functional assessment of the blood pressure waveform helps us to obtain an estimation of the arterial stiffness or its converse, arterial elasticity.1 Several epidemiological studies have clearly demonstrated that arterial stiffness is a significant predictor of cardiovascular disease incidence in the general population.2 There is clear evidence now that decreased arterial elasticity or increased arterial stiffness in normotensive and prehypertensive subjects induces increased risk for the development of arterial hypertension. In vitro and in vivo experiments have shown that the vascular endothelium plays a crucial role in vascular tone and consequently in arterial stiffness. However, there are no data available regarding the endothelial pathways involved in the adaptation of arterial mechanics during changes in blood flow. The elegant study by Bellien et al3 in this issue of Hypertension studied the endothelial pathways involved in the adaption of arterial mechanics during changes in blood flow. Besides identifying the “endothelial-derived relaxing factor” nitric oxide (NO) as important in this biological process, a unique aspect found in their study was the “endothelial-hyperpolarizing factor” EDHF. Endothelium-dependent relaxation/vasodilation in response to neurohumoral mediators and physical forces, such as the shear stress caused by blood flow, is generally attributed to the release of NO and/or prostacyclin. However, NO and prostacyclin cannot fully explain these endothelium-mediated vasodilator responses. The relaxations observed in the presence of NO synthase and cyclooxygenase inhibitors are often associated with hyperpolarization of the vascular smooth …

Effect of a 1-hour single bout of moderate-intensity exercise on fat oxidation kinetics

The present study aimed to examine the effects of a prior 1-hour continuous exercise bout (CONT) at an intensity (Fat max) that elicits the maximal fat oxidation (MFO) on the fat oxidation kinetics during a subsequent submaximal incremental test (IncrC). Twenty moderately trained subjects (9 men and 11 women) performed a graded test on a treadmill (Incr), with 3-minute stages and 1-km·h −1 increments. Fat oxidation was measured using indirect calorimetry and plotted as a function of exercise intensity. A mathematical model (SIN) including 3 independent variables ( dilatation, symmetry, and translation) was used to characterize the shape of fat oxidation kinetics and to determine Fat max and MFO. On a second visit, the subjects performed CONT at Fat max followed by IncrC. After CONT performed at 57% ± 3% (means ± SE) maximal oxygen uptake (V̇o 2max), the respiratory exchange ratio during IncrC was lower at every stage compared with Incr ( P < .05). Fat max (56.4% ± 2.3% vs 51.5% ± 2.4% V̇o 2max, P = .013), MFO (0.50 ± 0.03 vs 0.40 ± 0.03 g·min −1, P < .001), and fat oxidation rates from 35% to 70% V̇o 2max ( P < .05) were significantly greater during IncrC compared with Incr. However, dilatation and translation were not significantly different ( P > .05), whereas symmetry tended to be greater in IncrC ( P = .096). This study showed that the prior 1-hour continuous moderate-intensity exercise bout increased Fat max, MFO, and fat oxidation rates over a wide range of intensities during the postexercise incremental test. Moreover, the shape of the postexercise fat oxidation kinetics tended to have a rightward asymmetry.

The short term effects of exercise and omega‐3 fatty acids on the plasma lipid profile in Wheaton College students

Dyslipidemia plays a major role in the development of atherosclerosis, an underlying factor in cardiovascular disease. Both exercise and dietary modifications are key to positively influence lipid profile. The purpose of this study was to examine the immediate effects of a single bout of moderate‐intensity exercise and short‐term consumption of omega‐3 fatty acids on the plasma lipid profile in men and women. Fourteen Wheaton College students (7 males and 7 females) participated in 2 single bouts of 60 minutes, moderate‐intensity exercise (55‐60% of estimated HRmax), separated by a 14 day consumption of 3 g of fish oil per day. Plasma lipid profile was measured before and after each bout of exercise; measurements were grouped as baseline (BA), post‐exercise (PE), post‐fish oil (PF), or post‐exercise and fish oil (PEF). Significant differences were found in female TRIG, male HDL, female VLDL, and male ratio TC/HDL (P &lt; 0.05). From BA to PEF, males had significantly higher HDL values by 16%, and significantly lower TC/HDL values by 13% (p &lt; 0.017). TRIG and VLDL levels in females were significantly increased by 47% and 55% (p &lt; 0.017) from BA to PEF, respectively. Separately, acute exercise and short‐term fish‐oil intake were not shown to significantly change the lipid profile; however, when combined, HDL increased in males, and TC/HDL decreased in males.

Immunological changes after a single bout of moderate-intensity exercise in a hot environment

This study was aimed to evaluate the possible changes caused by a single bout of moderate-intensity exercise in a hot environmental temperature on the immune function and on inflammatory markers. A total of 22 young male adults (VO2(max), 55.4 +/- 3.6 ml x kg(-1) x min(-1)) volunteered to participate in an exercise session of 60 minutes on a treadmill ergometer at moderate speed (60% of the maximum aerobic speed) in hot environmental conditions (35 degrees C and humidity 60%). Total leukocyte numbers, lymphocyte subsets (CD8+, CD4+, CD3+, NK and CD19+), cytokine production capacity by peripheral blood mononuclear cells (PBMCs) (IL-2, IL-4, IL-5, IL-10, IFN-gamma and TNF-alpha) as well as the concentration of several inflammation related proteins (ceruloplasmin, C-reactive protein (CRP), complement factors C3 and C4) were evaluated before and after exercise. The results show that leukocyte and neutrophil absolute values increased (P < 0.001) after the exercise period. In contrast, eosinophil values decreased (P < 0.05) after the exercise. In addition, ceruloplasmin, C3 and C4 values (P < 0.05) increased after exercise. No changes in T lymphocyte subsets, cytokine production, or CRP were observed. These data confirm previous studies suggesting that a 60 min exercise in a hot environment is enough to cause a physiologic adaptation to these special conditions leading to an increase of non-specific immune cells and promoting inflammatory processes. On the other hand, PCR values, lymphocyte subsets and the capacity of cytokine production by PBMC were not changed in a relatively short bout of exercise under these conditions in contrast with previous studies.

The impact of dietary restraint and moderate-intensity exercise on post-exercise energy intake in sedentary males

Exercise is often used for successful weight management, particularly by males. However, exercise may have the potential to promote counter-regulatory eating, because of certain cognitive and psychological factors. The purpose of this study was to investigate the unknown role of dietary restraint, BMI, and dieting status on acute and 12-hour post-exercise energy intake (PE-EI) in sedentary males following moderate-intensity exercise. The study consisted of two experimental conditions, exercise and rest, in a counterbalanced-crossover design on two days. Exercise consisted of walking on a treadmill for 60 min. Acute and 12-hour PE-EI were compared on exercise and rest days. Eighty males, mean age 30 ± 8 years, participated in the study and were categorized by dietary restraint level, BMI, and dieting status. The main effects of condition and group, and the interaction were not significant for acute or 12-hour PE-EI, suggesting that a single bout of moderate-intensity exercise did not influence PE-EI in sedentary males in reference to dietary restraint, BMI, and dieting status. Therefore, moderate-intensity exercise as a prescription for weight loss does not appear to promote counter-regulatory eating in sedentary males.

A single bout of moderate-intensity exercise increases vascular NO bioavailability and attenuates adrenergic receptor-dependent and -independent vasoconstrictor response in rat aorta

The present study investigated the effect of one bout of moderate-intensity exercise on the adrenergic receptor-dependent and -independent vasoconstrictor response in rat aortas, and the role of nitric oxide (NO) bioavailability on these vasomotor responses. One group of rats was submitted to a 60 min of exercise at approximately 60% of maximal exercise capacity on a treadmill (exercise group) and the other one was placed in the treadmill without running (control group). Immediately after this period, both groups were euthanized and the thoracic aorta was removed to evaluate the vasoconstrictor response to norepinephrine and potassium chloride, and to evaluate the vascular nitrite and nitrate concentration. One bout of exercise attenuated the maximal contractile response to both norepinephrine and potassium chloride compared to control group. These differences on vascular reactivity were not observed in endothelium-denuded aortic rings and aortic rings pre-incubated with a nitric oxide synthesis inhibitor. Additionally, exercise group increased NO bioavailability (nitrite and nitrate concentration) as compared to control group. These results demonstrate that one bout of moderate-intensity exercise is able to attenuate adrenergic receptor-dependent and -independent vasoconstrictor response in rat aorta, mainly by increasing vascular NO bioavailability.

Improved insulin sensitivity after a single bout of exercise is curvilinearly related to exercise energy expenditure

A single bout of moderate-intensity exercise increases whole-body insulin sensitivity for 12-48 h post-exercise; however, the relationship between exercise energy expenditure and the improvement in insulin sensitivity is not known. We hypothesized that the exercise-induced increase in whole-body insulin sensitivity, assessed with HOMA(IR) (homoeostasis model assessment of insulin resistance), is directly related to the energy expended during exercise. We studied 30 recreationally active non-obese men (age, 27+/-5 years; body mass index, 24+/-2 kg/m(2)) in the post-absorptive state on two separate occasions: once after exercising at 60% of VO(22peak) (peak oxygen consumption) for 30-120 min on the preceding afternoon (expending a total of 1.28-5.76 MJ) and once after an equivalent period of rest. Blood samples were obtained the following morning. Exercise-induced changes in HOMA(IR) were curvilinearly related to exercise energy expenditure (r=-0.666, P=0.001) with a threshold of approx. 3.77 MJ (900 kcal) for improvements in HOMA(IR) to be manifested. In particular, HOMA(IR) was reduced by 32+/-24% (P=0.003) in subjects who expended more than 3.77 MJ during exercise, but did not change for those who expended fewer than 3.77 MJ (-2+/-21%; P=0.301). Furthermore, the magnitude of change in HOMA(IR) after exercise was directly associated with baseline (i.e. resting) HOMA(IR) (r=-0.508, P=0.004); this relationship persisted in multivariate analysis. We conclude that improved whole-body insulin resistance after a single bout of exercise is curvilinearly related to exercise energy expenditure, and requires unfeasible amounts of exercise for most sedentary individuals.

Regulation of hexokinase II activity and expression in human muscle by moderate exercise.

A single bout of exercise increases the rate of insulin-stimulated glucose uptake and metabolism in skeletal muscle. Exercise also increases insulin-stimulated glucose 6-phosphate in skeletal muscle, suggesting that exercise increases hexokinase activity. Within 3 h, exercise increases hexokinase II (HK II) mRNA and activity in skeletal muscle from rats. It is not known, however, if a single bout of moderate-intensity exercise increases HK II expression in humans. The present study was undertaken to answer this question. Six subjects had percutaneous biopsies of the vastus lateralis muscle before and 3 h after a single 3-h session of moderate-intensity aerobic (60% of maximal oxygen consumption) exercise. Glycogen synthase, HK I, and HK II activities as well as HK I and HK II mRNA content were determined from the muscle biopsy specimens. The fractional velocity of glycogen synthase was increased by 446 +/- 84% after exercise (P < 0.005). Hexokinase II activity in the soluble fraction of the homogenates increased from 1.2 +/- 0.4 to 4.5 +/- 1.6 pmol.min-1.microgram-1 (P < 0.05) but was unchanged in the particulate fraction (4.3 +/- 1.3 vs. 5.3 +/- 1.5). HK I activity in neither the soluble nor particulate fraction changed after exercise. Relative to a 28S rRNA control signal, HK II mRNA increased from 0.091 +/- 0.02 to 0.195 +/- 0.037 (P < 0.05), whereas HK I mRNA was unchanged (0.414 +/- 0.061 vs. 0.498 +/- 0.134, P < 0.20). The increase in HK II activity after moderate exercise in healthy subjects could be one factor responsible for the enhanced rate of insulin-stimulated glucose uptake seen after exercise.