Tracy Baynard

Moderate exercise training provides modest protection against adipose tissue inflammatory gene expression in response to high‐fat feeding

As white adipose tissue (WAT) expands under obesogenic conditions, local WAT hypoxia may contribute to the chronic low‐grade inflammation observed in obesity. Aerobic exercise training is beneficial in treating WAT inflammation after obesity is established, but it remains unknown whether exercise training, while on a concomitant high‐fat (HF) diet, influences WAT inflammation during the development of obesity. We sought to determine the effects of 4, 8, and 12 weeks of HF feeding and/or moderate intensity treadmill exercise training (EX) on the relationship between inflammatory and hypoxic gene expression within mouse WAT. Male C57Bl6/J mice (n = 113) were randomized into low‐fat (LF)/sedentary (SED), LF/EX, HF/SED, or HF/EX groups. The low‐fat and high‐fat diets contained 10% and 60% energy from fat, respectively. Exercise training consisted of treadmill running 5 days/week at 12 m/min, 8% incline, 40 min/day. Quantitative real‐time PCR was used to assess gene expression. HF diet impaired glucose regulation, and upregulated WAT gene expression of inflammation (IL‐1β, IL‐1ra, TNFα), macrophage recruitment and infiltration (F4/80 and monocyte chemoattractant protein), and M1 (CD11c) and M2 (CD206 and Arginase‐1) macrophage polarization markers. Treadmill training resulted in a modest reduction of WAT macrophage and inflammatory gene expression. HF diet had little effect on hypoxia‐inducible factor‐1α and vascular endothelial growth factor, suggesting that WAT inflammatory gene expression may not be driven by hypoxia within the adipocytes. Treadmill training may provide protection by preventing WAT expansion and macrophage recruitment.

Exercise Training Effects on Inflammatory Gene Expression in White Adipose Tissue of Young Mice

We aimed to determine the effects of 6 wks of exercise on inflammatory markers in mice concomitantly fed either high-fat (HF) or normal chow (NC) diets in young mice. C57BL/6 mice were randomized into (n = 10/group) an NC/sedentary (NC/SED), NC/exercise (NC/EX), HF/SED, and HF/EX groups. Treadmill exercise was performed 5 d/wk at 12 m/min, with 12% grade for 40 min/d. Liver triglycerides and gene expression of F4/80, MCP-1, TNF-α, leptin, and VEGF in visceral white adipose were determined. NC groups had lower body weights after 6 wks versus the HF groups (22.8 ± 0.2 versus 25.7 ± 0.4 g) (P < 0.0001). F4/80 gene expression (indicator of macrophage infiltration) and liver triglycerides were greatest amongst the HF/SED group, with no differences between the remaining groups. VEGF (indicator of angiogenesis) was greatest in the HF/EX versus the other 3 groups (P < 0.05). Exposure of an HF diet in sedentary young mice increased visceral adipose depots and liver triglycerides versus an NC diet. Exercise training while on the HF diet protected against hepatic steatosis and possibly macrophage infiltration within white adipose tissue. This suggests that moderate exercise while on an HF diet can offer some level of protection early on in the development of obesity.

Effects of aerobic, resistance and balance training in adults with intellectual disabilities

Adults with intellectual disability (ID) have decreased cardiovascular fitness and strength present with lower rates of physical activity (PA), and often have balance and functional impairments. The purpose of this study was to investigate the effect of a combined PA program (CPAP) utilizing aerobic, strength and balance training on cardiovascular fitness, strength, balance and functional measures in a controlled clinical trial. Adults with mild to moderate ID were assigned into either the intervention group (IG; n=37) or the control group (CG; n=29). The IG trained 3 day/week, 1 h/day over 14 weeks, while the CG did not participate in any exercise program. Cardiovascular fitness, strength, balance, flexibility and functional ability were assessed pre-post training. The IG increased cardiovascular fitness (26.8 vs. 29.3 ml kg(-1) min(-1)), handgrip strength (19.2 vs. 21.9 kg), leg strength, and balance following the training period (p<.05). Body weight (70.1 vs. 68.1 kg) and body mass index (27.4 vs. 26.6 kg m(-2)) decreased (p<.05) in the IG group. The CG showed no changes in any parameter. These data suggest a combined aerobic, strength and balance exercise training program is beneficial among individuals with ID.

Caffeine delays autonomic recovery following acute exercise

Background Impaired autonomic recovery of heart rate (HR) following exercise is associated with an increased risk of sudden death. Caffeine, a potent stimulator of catecholamine release, has been shown to augment blood pressure (BP) and sympathetic nerve activity; however, whether caffeine alters autonomic function after a bout of exercise bout remains unclear. Methods In a randomized, crossover study, 18 healthy individuals (26 ± 1 years; 23.9 ± 0.8 kg·m−2) ingested caffeine (400 mg) or placebo pills, followed by a maximal treadmill test to exhaustion. Autonomic function and ventricular depolarization/repolarization were determined using heart rate variability (HRV) and corrected QT interval (QTc), respectively, at baseline, 5, 15, and 30 minutes post-exercise. Results Maximal HR (HRmax) was greater with caffeine (192 ± 2 vs. 190 ± 2 beat·min−1, p < 0.05). During recovery, HR, mean arterial pressure (MAP), and diastolic blood pressure (DBP) remained elevated with caffeine (p < 0.05). Natural log transformation of low-to-high frequency ratio (LnLF/LnHF) of HRV was increased compared with baseline at all time points in both trials (p < 0.05), with less of an increase during 5 and 15 minutes post-exercise in the caffeine trial (p < 0.05). QTc increased from baseline at all time points in both trials, with greater increases in the caffeine trial (p < 0.05). Conclusions Caffeine ingestion disrupts post-exercise autonomic recovery because of increased sympathetic nerve activity. The prolonged sympathetic recovery time could subsequently hinder baroreflex function during recovery and disrupt the stability of autonomic function, potentiating a pro-arrhythmogenic state in young adults.

Heart rate complexity in response to upright tilt in persons with Down syndrome.

People with Down syndrome (DS) show altered autonomic response to sympatho-excitation. Cardiac autonomic modulation may be examined with heart rate (HR) complexity which is associated uniquely with cardiovascular risk. This study examined whether the response of HR complexity to passive upright tilt differs between persons with and without DS and whether potential between-group differences in this response are accounted for by differences in body mass index (BMI). The electrocardiogram of 16 persons with DS (8 women, 8 men) and 16 persons without DS (8 women, 8 men) was recorded during 10 min of supine rest and 10 min of upright tilt. For each participant, 550 continuous, steady state, and ectopy-free R-R intervals under each condition were analyzed. Dependent variables were approximate entropy, correlation dimension, StatAv, and the mean R-R interval. In response to tilt, changes in approximate entropy and correlation dimension were reduced in participants with DS (p<0.05). These differences were explained by higher BMI in participants with DS. StatAv increased in persons with DS (p < 0.05) and stayed the same in those without DS even when controlling for BMI. The response of R-R interval did not differ between groups. None of the variables differed between groups at rest. Therefore, people with DS show smaller decrease in HR complexity in response to upright tilt than people without DS partially due to their higher BMI. Resting HR complexity does not differ between persons with and without DS. These results may have implications for cardiovascular risk in people with DS.

Defining the System: Contributors to Exercise Limitations in Heart Failure

One of the primary hallmarks of patients diagnosed with heart failure (HF) is a reduced tolerance to exercise and compromised functional capacity. This limitation stems from poor pumping capacity but also major changes in functioning of the vasculature, skeletal muscle, and respiratory systems. Advances in the understanding of the central and peripheral mechanisms of exercise intolerance during HF are critical for the future design of therapeutic modalities devised to improve outcomes. The interrelatedness between systems cannot be discounted. This review summarizes the current literature related to the pathophysiology of HF contributing to poor exercise tolerance, and potential mechanisms involved.

The effects of high fat diet and moderate exercise on TGFβ1 and collagen deposition in mouse skeletal muscle

Obesity is a primary cause of muscle insulin resistance and is also associated with morphological and functional changes in the skeletal muscle including fibrosis. Studies suggest that macrophages in obese skeletal muscle may be primed to secrete transforming growth factor β1 (TGFβ1), a factor that can stimulate type I collagen gene expression via Smad3 activation but the extent to which exercise could modulate high fat (HF) diet-induced inflammation and fibrosis in skeletal muscle remains to be determined. The purpose of this study was to determine the extent to which moderate intensity exercise training can attenuate pro-inflammatory cytokine gene expression and markers of fibrosis in skeletal muscle in response to concomitant HF diet. Male C57BL/6J mice (6 wk old) were randomly assigned to one of four treatment groups: (1) Control diet-No Exercise (CON-No Ex), (2) CON-Ex, (3) HF-No Ex, or (4) HF-Ex. Mice were exercised on a motorized treadmill 40min/day at 12m/min, 5% grade, 5days/wk, for 12weeks. Macrophage (F4/80, CD11c, CD206), inflammatory cytokine (TNFα, IL-6, IL-10), TGFβ1, and collagen (Col1α) gene expression were evaluated in skeletal muscle by qPCR. Frozen muscle sections were stained to assess collagen content and fiber cross sectional area (CSA). F4/80, CD206 and IL-6 gene expression were increased by HF diet, and exercise only attenuated the increase in F4/80 and IL-6 (p<0.05). No differences in CD11c, TNFα and IL-10 gene expression were found between the groups. HF diet increased TGFβ1 protein expression, Smad3 activation, and collagen deposition in skeletal muscle, and exercise attenuated TGFβ1 protein expression and collagen deposition in skeletal muscle (p<0.05). Muscle fiber CSA was not different between the groups. The results from this study suggest that HF diet can increase skeletal muscle macrophage gene expression and fibrosis and that exercise can attenuate these changes.

Resting and post exercise arterial-ventricular coupling in endurance-trained men and women.

The relationship between effective arterial elastance (EA) and left ventricular end-systolic elastance (ELV) is a determinant of cardiac performance, known as arterial–ventricular coupling (AVC). The purpose of this study was to examine the acute effects of high-intensity interval (HI) and low-intensity steady state (SS) exercise on AVC. Twenty-three (13 men, 10 women) young (26 years), endurance-trained individuals completed a VO2 peak test followed by an acute SS and HI exercise bout on separate visits. Before (Pre) and 30- and 60-min after each bout, measures of aortic end-systolic pressure (ESP), left ventricular end-systolic volume and stroke volume were obtained. Across both conditions (HI and SS) and both sexes, at 30 and 60 min post exercise, ESP and ELV were reduced from Pre 30 and 60-min exercise (ESP: 86±7, 77±8 and 73±8 mm Hg; ELV: 4.93±1.53, 4.19±1.38 and 4.10±1.53 mm Hg ml−1 m−2). EA was only reduced at 60 min post exercise (1.90±0.36, 1.78±0.50 and 1.57±0.36). Both EA and ELV were reduced following acute SS and HI exercise. This is likely because of similar reductions in total peripheral resistance following both exercise bouts. These results suggest that endurance-trained individuals are able to match peripheral vascular changes with changes in left ventricular function following dynamic exercise of different intensities.

Exercise training improves hemodynamic recovery to isometric exercise in obese men with type 2 diabetes but not in obese women

OBJECTIVES Women with type 2 diabetes (T2D) show greater rates of mortality due to ischemic heart disease than men with T2D. We aimed to examine cardiovascular and autonomic function responses to isometric handgrip (IHG) exercise between men and women with T2D, before and after an exercise training program. MATERIALS/METHODS Hemodynamic responses were measured in 22 men and women with T2D during and following a 3-min IHG test, and before and after 16 wks of aerobic exercise training. RESULTS Women had a smaller decrease in mean arterial pressure (MAP) and systolic blood pressure (BP) during recovery from IHG (ΔMAP(REC)) than men pre- and post-training (P<0.05). Men showed a greater reduction in diastolic BP during recovery from IHG (P<0.05), and exercise training improved this response in men but not in women (men, pre-training: -13.9±1.8, post-training: -20.5±5.3 mmHg vs. women, pre-training: -10.7±1.7, post-training: -4.1±4.9 mmHg; P<0.05). Men had a greater reduction in sympathetic modulation of vasomotor tone (P<0.05), as estimated by blood pressure variability, following IHG. This response was accentuated after training, while this training effect was not seen in women. Post-training ΔMAP(REC) was correlated with recovery of low frequency component of the BP spectrum (ΔLF(SBPrec), r=0.52, P<0.05). CONCLUSIONS Differences in BP recovery immediately following IHG may be attributed to gender differences in cardiovascular autonomic modulation. An improvement in these responses occurs following aerobic exercise training in obese men, but not in obese women with T2D which reflects a better adaptive autonomic response to exercise training.

The effect of acute maximal exercise on postexercise hemodynamics and central arterial stiffness in obese and normal‐weight individuals

Central arterial stiffness is associated with incident hypertension and negative cardiovascular outcomes. Obese individuals have higher central blood pressure (BP) and central arterial stiffness than their normal‐weight counterparts, but it is unclear whether obesity also affects hemodynamics and central arterial stiffness after maximal exercise. We evaluated central hemodynamics and arterial stiffness during recovery from acute maximal aerobic exercise in obese and normal‐weight individuals. Forty‐six normal‐weight and twenty‐one obese individuals underwent measurements of central BP and central arterial stiffness at rest and 15 and 30 min following acute maximal exercise. Central BP and normalized augmentation index (AIx@75) were derived from radial artery applanation tonometry, and central arterial stiffness was obtained via carotid‐femoral pulse wave velocity (cPWV) and corrected for central mean arterial pressure (cPWV/cMAP). Central arterial stiffness increased in obese individuals but decreased in normal‐weight individuals following acute maximal exercise, after adjusting for fitness. Obese individuals also exhibited an overall higher central BP (P < 0.05), with no exercise effect. The increase in heart rate was greater in obese versus normal‐weight individuals following exercise (P < 0.05), but there was no group differences or exercise effect for AIx@75. In conclusion, obese (but not normal‐weight) individuals increased central arterial stiffness following acute maximal exercise. An assessment of arterial stiffness response to acute exercise may serve a useful detection tool for subclinical vascular dysfunction.