Direct Effect Of Exercise Research Articles

Mast cell degranulation is greater when exposed to dialysate collected from exercising skeletal muscle

The effect of histamine is multifaceted and potentially triggers a broad range of cellular adaptations contributing to vascular function, cellular maintenance, metabolism, and inflammation. During exercise, histamine is released from skeletal muscle. This response and the subsequent actions of histamine appear important in obtaining many of the beneficial adaptations to exercise. Increases in exercising skeletal muscle histamine release, in part, occur due to mast cell degranulation. However, the direct effect of exercise on mast cell degranulation has yet to be elucidated. To that end, this preliminary study aimed to quantify in vitro mast cell degranulation when cells are exposed to dialysate taken from exercising and non-exercising skeletal muscle. We hypothesized that greater mast cell degranulation would occur when exposed to dialysate collected from exercising skeletal muscle compared to dialysate collected from non-exercising muscle. Ten subjects (5M/5F, age 26 ± 5 years, weight 76 ± 17 kg, height 168 ± 12 cm) completed 60 minutes of single-leg dynamic knee extension exercise. Prior to exercise, a microdialysis probe was inserted into the vastus lateralis of the exercising and non-exercising legs and perfused with saline at a rate of 5 uL/min. Dialysate was collected before and every 20 minutes during exercise and the subsequent one-hour recovery period. In the exercising skeletal muscle, mast cell degranulation (quantified via b-hexosaminidase release) was greater when exposed to dialysate during exercise versus dialysate collected pre-exercise (P < 0.05). Compared to non-exercising leg dialysate, degranulation was greater for exercising leg dialysate taken between minutes 20 and 40 into exercise (20.6 ± 2.7% vs 15.8 ± 2.0%, P < 0.05) and 40 and 60 into exercise (24.0 ± 2.6 % vs 15.0 ± 2.7 %, P < 0.001) and remained greater for dialysate taken in the first 20 minutes of recovery (21.4 ± 2.8% vs 15.2 ± 3.0%, P < 0.05). These data suggest that there is a soluble factor released from exercising skeletal muscle that causes mast cell degranulation in vitro. These preliminary findings establish a bioassay for further exploration of the identity of the soluble factor released from exercising skeletal muscle, which is responsible for mast cell degranulation in vivo. This research was supported in part by National Institutes of Health Grants AG072805 and HL115027. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The direct effect of exercise on the mental health of scientific and technological professionals and the mediating effects of stress, resilience, and social support.

High working pressure is one of the main causes of occupational sub-health problems in scientific and technological professionals. With the development of exercise psychology, an increasing number of scholars have begun to focus on the influence of exercise on mental health. However, a limited number of scholars have investigated the effects of exercise on mental health and related mechanisms among scientific and technological professionals. Thus, this study aimed to investigate the relationship between exercise and the mental health of scientific and technological professionals and the mediating roles of stress, resilience, and social support. The respondents in this study were recruited using snowball sampling techniques and finally collected a total of 1,248 valid responses. Questionnaires were distributed through "www.wjx.cn (An online questionnaire website in China, which provides similar functions with Amazon MTurk)" in Henan province from November to December 2021. Participants were asked to complete the Positive Mental Health Scale, the stress subscale of the Depression Anxiety and Stress Scale (21 items), the Connor-Davidson Resilience Scale, and the Perceived Social Support Scale. A total of 1,248 valid responses were obtained. The mean exercise time of males was longer than that of females (t = 3.65, p < 0.01). Exercise and mental health were significantly associated with differences in age (F = -8.57, F = -4.66, p < 0.01) and educational background (F = 12.86, F = 7.14, p < 0.01). There were significant correlations among exercise, mental health, stress, resilience, and social support (p < 0.01). The direct effects of exercise on mental health were significant (β = 0.271, t = 9.577, p < 0.001), and the mediating effects of stress, resilience, and social support were also significant (χ2/df = 4.72, CFI = 0.940, TLI = 0.935, SRMR = 0.048, RMSEA = 0.055). This study explored the effects of exercise on mental health and related mechanisms among scientific and technological professionals, which is beneficial to providing effective suggestions for managing and preventing the mental health of scientific and technological professionals. Future research should include a wider range of participants and adopt a longitudinal follow-up design to more deeply investigate the relationship between exercise and the mental health of scientific and technological professionals.

Carbohydrate-Energy Replacement Following High-Intensity Interval Exercise Blunts Next-Day Glycemic Control in Untrained Women.

BackgroundImproved glycemic control has been reported for ∼24 h following low-volume high-intensity interval exercise (HIIE), but it is unclear if this is a direct effect of exercise or an indirect effect of the exercise-induced energy deficit. The purpose of this study was to investigate the effect of carbohydrate-energy replacement after low-volume HIIE on 24 h glycemic control in women.MethodsSeven untrained women (age: 22 ± 2 yr; BMI: 22 ± 3 kg/m2; VO2peak: 33 ± 7 ml/kg/min) completed three 2-day trials in the mid-follicular phase of the menstrual cycle. Continuous glucose monitoring was used to measure blood glucose concentrations during, and for 24 h following three conditions: (1) HIIE followed by a high-carbohydrate energy replacement drink (EX-HC); (2) HIIE followed by a non-caloric taste-matched placebo drink (EX-NC); and (3) seated control with no drink (CTL). HIIE involved an evening session (1,700 h) of 10 × 1-min cycling efforts at ∼90% maximal heart rate with 1 min recovery. Diet was standardized and identical across all three 2-day trials, apart from the post-exercise carbohydrate drink in EX-HC, which was designed to replenish the exercise-induced energy expenditure. Postprandial glycemic responses to the following days breakfast, snack, lunch, and dinner, as well as 24 h indices of glycemic control, were analyzed.ResultsThe day after HIIE, postprandial glycemia following breakfast and snack were reduced in EX-NC compared to EX-HC, as reflected by lower 3 h glucose mean (breakfast: 5.5 ± 0.5 vs. 6.7 ± 1, p = 0.01, Cohen’s d = 1.4; snack: 4.9 ± 0.3 vs. 5.7 ± 0.8 mmol/L, p = 0.02, d = 1.4) and/or area under the curve (AUC) (breakfast: 994 ± 86 vs. 1,208 ± 190 mmol/L x 3 h, p = 0.01, d = 1.5). Postprandial glycemic responses following lunch and dinner were not different across conditions (p > 0.05). The 24 h glucose mean (EX-NC: 5.2 ± 0.3 vs. EX-HC: 5.7 ± 0.7 mmol/L; p = 0.02, d = 1.1) and AUC (EX-NC: 7,448 ± 425 vs. EX-HC: 8,246 ± 957 mmol/L × 24 h; p = 0.02, d = 1.1) were reduced in EX-NC compared to EX-HC.ConclusionPost-exercise carbohydrate-energy replacement attenuates glycemic control the day following a single session of low-volume HIIE in women.

Exercise training ameliorates cognitive dysfunction in amyloid beta-injected rat model: possible mechanisms of Angiostatin/VEGF signaling.

Vascular endothelial growth factor (VEGF) regulates angio/neurogenesis and also tightly links to the pathogenesis of Alzheimer's disease (AD). Although exercise has a beneficial effect on neurovascular function and cognitive function, the direct effect of exercise on VEGF-related signaling and cognitive deficit in AD is incompletely understood. Therefore, the purpose of this study was to investigate the protective effect of exercise on angiostatin/VEGF cascade and cognitive function in AD model rats. Wistar male rats were randomly divided into five groups: control (CON), injection of DMSO (Sham-CON), CON-exercise (sham-EX), intrahippocampal injection of Aβ (Aβ), and Aβ-exercise (Aβ-EX). Rats in EX groups underwent treadmill exercise for 4weeks, then the cognitive function was measured by the Morris Water Maze (MWM) test. mRNA levels of hypoxia-induced factor-1α (HIF-1α), vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 2 (VEGFR2), and angiostatin were determined in hippocampus by RT-PCR. We found that spatial learning and memory were impaired in Aβ-injected rats, but exercise training improved it. Moreover, exercise training increased the reduced mRNA expression level of VEGF signaling, including HIF1α, VEGF, and VEGFR2 in the hippocampus from Aβ-injected rats. Also, the mRNA expression level of angiostatin was elevated in the hippocampus from Aβ-injected rats, and exercise training abrogated its expression. Our findings suggest that exercise training improves cognitive function in Aβ-injected rats, possibly through enhancing VEGF signaling and reducing angiostatin.

High-intensity exercise and cognitive function in cognitively normal older adults: a pilot randomised clinical trial

BackgroundPhysical inactivity has been consistently linked to increased risk of cognitive decline; however, studies examining the impact of exercise interventions on cognition have produced inconsistent findings. Some observational studies suggest exercise intensity may be important for inducing cognitive improvements; however, this has yet to be thoroughly examined in older adult cohorts. The objective of the current study was to evaluate the effect of systematically manipulated high-intensity and moderate-intensity exercise interventions on cognition.MethodsThis multi-arm pilot randomised clinical trial investigated the effects of 6 months of high-intensity exercise and moderate-intensity exercise, compared with an inactive control, on cognition. Outcome measures were assessed at pre- (baseline), post- (6 months), and 12 months post-intervention. Ninety-nine cognitively normal men and women (aged 60–80 years) were enrolled from October 2016 to November 2017. Participants that were allocated to an exercise group (i.e. high-intensity or moderate-intensity) engaged in cycle-based exercise two times per week for 6 months. Cognition was assessed using a comprehensive neuropsychological test battery. Cardiorespiratory fitness was evaluated by a graded exercise test.ResultsThere was a dose-dependent effect of exercise intensity on cardiorespiratory fitness, whereby the high-intensity group experienced greater increases in fitness than the moderate-intensity and control groups. However, there was no direct effect of exercise on cognition.ConclusionsWe did not observe a direct effect of exercise on cognition. Future work in this field should be appropriately designed and powered to examine factors that may contribute to individual variability in response to intervention.Trial registrationThis study is registered with the Australian New Zealand Clinical Trials Registry (ACTRN12617000643370). Registered on 3 May 2017—retrospectively registered. https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=372780

Exercise Amounts and Short- to Long-Term Weight Loss: Psychological Implications for Behavioral Treatments of Obesity

ABSTRACT Purpose: Although exercise is typically included in behavioral weight-loss programs, the amount associated with meaningful short- to long-term weight reduction required investigation. Indirect paths between exercise-associated psychological changes and weight loss might be more relevant than the direct effect of exercise on energy expenditure-related weight loss in deconditioned/obese individuals. Method: Sedentary women with obesity (N = 97; M age = 47.2 years) participated in a year-long cognitive-behavioral weight-loss treatment that emphasized building self-regulatory skills to maintain exercise in advance of transferring those skills to controlled eating. Results: There was a significant increase in exercise (metabolic equivalents/week or leisure score index; LSI), and significant improvements in mood, self-regulation for exercise, and self-regulation for eating from baseline to Months 6, 12, and 24. There were 5.9%, 5.8%, and 5.8% reductions in weight, respectively. Completion of 15–20 LSI did not significantly differ from greater amounts on associated weight losses except for the rare occurrence of ≥ 30 LSI over the full 24-month study period. There were significant bivariate relationships between completion of ≥ 15 LSI and weight loss over 6, 12, and 24 months. Within serial mediation analyses assessing changes from baseline–Months 6 and 24, there were significant indirect paths from ≥ 15 LSI→self-regulation for exercise→self-regulation for eating→weight loss, and ≥ 15 LSI→negative mood→self-regulation for exercise→self-regulation for eating→weight loss. Those paths were not significant when baseline–Month 12 changes were entered. Conclusion: Findings suggested the value of even manageable exercise amounts because of their association with psychosocial correlates of weight loss, and informed behavioral obesity treatments.

Endurance exercise training does not limit coronary atherosclerosis in familial hypercholesterolemic swine

Prospective, cohort studies in humans demonstrate that moderate to high levels of physical activity reduce both morbidity and mortality of coronary heart disease (CHD) including a decreased progression and/or regression of CHD with life‐style modification which includes exercise. However, a thorough review of both human and animal literature reveals equivocal evidence to support an intrinsic, direct exercise effect in attenuating the development of CHD. Exercise reduces development and/or causes regression of atherosclerotic lesions in mice and rabbits, however in larger mammals including primates, the evidence is more equivocal. A major limitation has been the lack of large animal models with clinically evident CHD disease. Thus, we sought to determine the effect of endurance exercise in CHD development and compensatory remodeling in a swine model of familial hypercholesterolemia (FH) that exhibits robust, complex atherosclerosis. Castrated male Rapacz familial hypercholesterolemic (FH) swine were obtained from the University of Wisconsin Swine Research and Teaching Center. Pigs were randomly assigned to either sedentary (Sed; n=9) or exercise trained (Ex; n=8) groups. At 10 months of age, Ex pigs began a 10 month treadmill‐training intervention consisting of moderate‐intensity (70% of maximal heart rate) once per day, for 5 days each week. At 14 months, all pigs were switched to a high‐fat, high‐cholesterol diet (HF; by weight 13% protein, 21.3% fat, 41.4% carbohydrate, 2% cholesterol and 1% sodium cholate). CHD was assessed by intravascular ultrasound (IVUS) both prior to (14 months of age) and after completion of 6 months on the HF diet (20 months of age). Angiograms and IVUS were obtained using standard coronary catheterization techniques. IVUS pullbacks (0.5 mm/sec; Galaxy II, Boston Scientific, 40MHz) were obtained for the proximal anterior descending (LAD) and left circumflex (LCX) arteries. For analysis, the total segment was subdivided into 3 sections and total vessel volume, lumen volume, total plaque burden volume and percent plaque burden were determined in the proximal, mid, and distal segments from 3D reconstruction (QIVUS software; Medis). Prior to HF diet, Ex resulted in a greater coronary artery size (vessel and lumen volume) in the proximal and mid sections of the LCX compared to SED, with no effect in the LAD. Relative plaque volume was minimal (~15–20% vessel area) in both Sed and Ex groups. After 6 months on HF diet, there was a 5–6 fold increase in absolute plaque volume in all segments of the LCX and LAD in both groups. Ex had no effect on absolute plaque volume at 20 months in any segment of either LCX or LAD. In both Sed and Ex groups, vessel volume was greater at 20 months compared to 14 months such that lumen volume was maintained despite the increase in plaque volume, i.e. compensatory outward remodeling was similar in both groups. Overall at 20 months, there was no significant difference in vessel volume, lumen volume, absolute or relative plaque volume in either the LCX or LAD between Sed and Ex animals. These findings fail to support an independent, direct effect of exercise in limiting CHD progression in familial hypercholesterolemia.Support or Funding InformationNIH HL52490This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Endurance exercise training does not limit coronary atherosclerosis in familial hypercholesterolemic swine.

Human studies demonstrate that physical activity reduces both morbidity and mortality of coronary heart disease (CHD) including decreased progression and/or regression of CHD with life‐style modification which includes exercise. However, evidence supporting an intrinsic, direct effect of exercise in attenuating the development of CHD is equivocal. One limitation has been the lack of a large animal model with clinically evident CHD disease. Thus, we examined the role of endurance exercise in CHD development in a swine model of familial hypercholesterolemia (FH) that exhibits robust, complex atherosclerosis. FH swine were randomly assigned to either sedentary (Sed) or exercise trained (Ex) groups. At 10 months of age, Ex pigs began a 10 months, moderate‐intensity treadmill‐training intervention. At 14 months, all pigs were switched to a high‐fat, high‐cholesterol diet. CHD was assessed by intravascular ultrasound (IVUS) both prior to and after completion of 6 months on the HFC diet. Prior to HFC diet, Ex resulted in a greater coronary artery size in the proximal and mid sections of the LCX compared to SED, with no effect in the LAD. After 6 months on HFC diet, there was a 5–6 fold increase in absolute plaque volume in all segments of the LCX and LAD in both groups. At 20 months, there was no difference in vessel volume, lumen volume, absolute or relative plaque volume in either the LCX or LAD between Sed and Ex animals. These findings fail to support an independent, direct effect of exercise in limiting CHD progression in familial hypercholesterolemia.

Cytogenesis in the adult monkey motor cortex: Perivascular NG2 cells are the major adult born cell type

ABSTRACTWe used confocal microscopy and immunohistochemistry (IHC) to look for new cells in the motor cortex of adult macaque monkeys that might form the cellular bases of improved brain function from exercise. Twenty‐four female Macaca fascicularis monkeys divided into groups by age (10–12 years, 15–17 years), postexercise survival periods, and controls, received 10 weekly injections of the thymidine analog, bromodeoxyuridine (BrdU) to mark new cells. Sixteen monkeys survived 15 weeks (5 weeks postexercise) and 8 monkeys survived 27 weeks (12 weeks postexercise) after initial BrdU injections. Additionally, five Macaca mulatta female monkeys (∼5.5–7 years) received single injections of BrdU and survived 2 days, 2 weeks, and 6 weeks after BrdU injections. Neural and glial antibodies were used to identify new cell phenotypes and to look for changes in proportions of these cells with respect to time and experimental conditions. No BrdU+/DCx+ cells were found but about 7.5% of new cells were calretinin‐positive (Cr+). BrdU+/GABA+ (gamma‐aminobutyric acid) cells were also found but no new Cr+ or GABA+ cells colabeled with a mature neuron marker, NeuN or chondroitin sulfate antibody, NG2. The proportion of new cells that were NG2+ was about 85% for short and long survival monkeys of which two, newly described perivascular phenotypes (Pldv and Elu) and a small percentage of pericytes (2.5%) comprised 44% and 51% of the new NG2+ cells, respectively. Proportions of NG2+ phenotypes were affected by post‐BrdU survival periods, monkey age, and possibly a postexercise sedentary period but no direct effect of exercise was found. J. Comp. Neurol. 523:849–868, 2015. © 2014 Wiley Periodicals, Inc.

Cytogenesis in the adult monkey motor cortex: perivascular NG2 cells are the major adult born cell type.

We used confocal microscopy and immunohistochemistry (IHC) to look for new cells in the motor cortex of adult macaque monkeys that might form the cellular bases of improved brain function from exercise. Twenty-four female Macaca fascicularis monkeys divided into groups by age (10–12 years, 15–17 years), postexercise survival periods, and controls, received 10 weekly injections of the thymidine analog, bromodeoxyuridine (BrdU) to mark new cells. Sixteen monkeys survived 15 weeks (5 weeks postexercise) and 8 monkeys survived 27 weeks (12 weeks postexercise) after initial BrdU injections. Additionally, five Macaca mulatta female monkeys (∼5.5–7 years) received single injections of BrdU and survived 2 days, 2 weeks, and 6 weeks after BrdU injections. Neural and glial antibodies were used to identify new cell phenotypes and to look for changes in proportions of these cells with respect to time and experimental conditions. No BrdU+/DCx+ cells were found but about 7.5% of new cells were calretinin-positive (Cr+). BrdU+/GABA+ (gamma-aminobutyric acid) cells were also found but no new Cr+ or GABA+ cells colabeled with a mature neuron marker, NeuN or chondroitin sulfate antibody, NG2. The proportion of new cells that were NG2+ was about 85% for short and long survival monkeys of which two, newly described perivascular phenotypes (Pldv and Elu) and a small percentage of pericytes (2.5%) comprised 44% and 51% of the new NG2+ cells, respectively. Proportions of NG2+ phenotypes were affected by post-BrdU survival periods, monkey age, and possibly a postexercise sedentary period but no direct effect of exercise was found.

You get what you give: localized vascular changes are apparent following long‐term exercise training

You get what you give: localized vascular changes are apparent following long‐term exercise training

Combined Aspirin and Cilostazol Treatment is Associated with Reduced Platelet Aggregation and Prevention of Exercise-Induced Platelet Activation

Background: Cilostazol has proven efficacy in increasing walking distance in claudicants, but it has not been demonstrated to be more effective than placebo in secondary cardiovascular prevention. The direct effect of exercise on platelet function remains less well defined. We have investigated the effect of combination treatment with aspirin and cilostazol on platelet activity in claudicants subjected to repeated treadmill exercise. Methods: Nineteen claudicants completed a double-blind, randomised, controlled, cross-over trial. Each subject received a 2-week course of aspirin (75 mg) and placebo and aspirin and cilostazol (100 mg twice daily). Following each 2-week treatment period, patients participated in a standardised treadmill test (3.2 km h−1, 10° incline) walking to maximal claudication distance. The exercise was repeated thrice in total, and blood was sampled before and after exercise. Platelet activation was measured using free platelet counting aggregation, flow cytometry for surface markers of platelet activation and soluble P-selectin assay. Results: Compared to aspirin and placebo, combination treatment with aspirin and cilostazol was associated with reduced arachidonic-acid-induced platelet aggregation (p < 0.01, Wilcoxon signed-rank test). Aspirin and placebo treatment were associated with elevated P-selectin expression, platelet-monocyte aggregation and reduced CD42b expression (p < 0.05, Wilcoxon signed-rank test) post-exercise. No difference was seen in spontaneous platelet aggregation whilst soluble P-selectin was reduced post-exercise with combination treatment with aspirin and cilostazol (p < 0.05, Wilcoxon signed-rank test). Conclusions: Combination treatment with aspirin and cilostazol results in suppression of platelet activation and reduces the effect of exercise on platelets. The benefit seen may be a result of cilostazol enhancing the inhibitory effect of aspirin on the cyclo-oxygenase pathway.

Combined Aspirin and Cilostazol Treatment is Associated with Reduced Platelet Aggregation and Prevention of Exercise-Induced Platelet Activation

Cilostazol has proven efficacy in increasing walking distance in claudicants, but it has not been demonstrated to be more effective than placebo in secondary cardiovascular prevention. The direct effect of exercise on platelet function remains less well defined. We have investigated the effect of combination treatment with aspirin and cilostazol on platelet activity in claudicants subjected to repeated treadmill exercise. Nineteen claudicants completed a double-blind, randomised, controlled, cross-over trial. Each subject received a 2-week course of aspirin (75mg) and placebo and aspirin and cilostazol (100mg twice daily). Following each 2-week treatment period, patients participated in a standardised treadmill test (3.2kmh(-1), 10 degrees incline) walking to maximal claudication distance. The exercise was repeated thrice in total, and blood was sampled before and after exercise. Platelet activation was measured using free platelet counting aggregation, flow cytometry for surface markers of platelet activation and soluble P-selectin assay. Compared to aspirin and placebo, combination treatment with aspirin and cilostazol was associated with reduced arachidonic-acid-induced platelet aggregation (p<0.01, Wilcoxon signed-rank test). Aspirin and placebo treatment were associated with elevated P-selectin expression, platelet-monocyte aggregation and reduced CD42b expression (p<0.05, Wilcoxon signed-rank test) post-exercise. No difference was seen in spontaneous platelet aggregation whilst soluble P-selectin was reduced post-exercise with combination treatment with aspirin and cilostazol (p<0.05, Wilcoxon signed-rank test). Combination treatment with aspirin and cilostazol results in suppression of platelet activation and reduces the effect of exercise on platelets. The benefit seen may be a result of cilostazol enhancing the inhibitory effect of aspirin on the cyclo-oxygenase pathway.

Changes in plasma creatine kinase activity and urea concentration monitored daily during training of elite wrestlers

The daily work load (DWL), blood urea concentration and creatine kinase (CK) activity in plasma were monitored daily for 8 days in 6 free‐style elite wrestlers. Both of the biochemical measures were correlated with DWL of the preceding day. Examination of the partial correlation coefficients computed among the three variables studied showed that CK activity was significantly correlated with DWL (r = 0.52; p ≤ 0.001) while urea concentration was not (r = 0.08; p > 0.05). This suggests that plasma CK activity is a direct effect of exercise while plasma urea is only an indirect index of the experienced work load. Nevertheless, both variables may serve as a diagnostic tool in assessing the risk of overloading in wrestlers' training.

Diet and Exercise as Regulators of Lipid Risk Factors

Comparisons of different countries have shown that populations with a low dietary intake of saturated fat also have a low mortality from coronary heart disease. Controlled-feeding experiments have shown that the potential for altering plasma cholesterol levels and, consequently, altering the risk of coronary heart disease by dietary modification is great. However, in practice the influence of dietary advice to the general population on plasma cholesterol levels has been less pronounced. Several investigators have shown that by decreasing the intake of saturated fats and dietary cholesterol and increasing the intake of polyunsaturated fats and foods providing soluble fibre, plasma cholesterol levels can be reduced by up to 29% and low density lipoprotein (LDL)-cholesterol by over 33%. In most studies, levels of high density lipoprotein (HDL)-cholesterol are not materially altered by modern lipid-lowering diets; generally, plasma levels are maintained, or increased after correction of overweight is is achieved. It has been calculated that the risk of fatal coronary heart disease is 32% lower in subjects consuming such a diet than in those following a typical American diet, and life expectancy is 5 years greater in the former group. Life expectancy is also 2 to 3 years longer in populations habitually following low fat diets than in Western populations. Frequent exercise has been inversely related to risk of coronary heart disease. Physically active individuals have a more favourable lipoprotein profile than sedentary individuals but the extent of a direct effect of exercise on lipoprotein levels is not known.

Effect of exercise on the disposal of infused ketone bodies in humans.

We previously reported that the stimulatory effect of exercise on the metabolic clearance of ketone bodies in postabsorptive subjects is abolished when plasma ketone body concentrations are elevated above 4 mmol/L by prior fasting. In this study we determined whether this process is related to fasting or to hyperketonemia itself. Eight normal postabsorptive subjects were rendered artificially hyperketonemic (approximately 6 mmol/L) by a constant infusion of acetoacetate and exercised moderately for 2 h. The kinetics of ketone bodies were determined with [14C]acetoacetate or beta-[14C]hydroxybutyrate. The metabolic clearance was slightly increased (approximately 25%) at the beginning of exercise, but this phenomenon was subsequently amplified by the progressive fall in ketonemia, which decreased to about 4 mmol/L at the end of exercise. Taking into account the fact that the metabolic clearance of ketones is inversely related to their concentration, it could be estimated that the direct effect of exercise on the metabolic clearance is negligible. Thus, the inability of exercise to enhance the metabolic clearance of ketones at high physiological plasma ketone levels is a general phenomenon that applies to both endogenous and exogenous ketosis.