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Recent evidence indicates that sex-based differences in cardiovascular disease (CVD) begin early in life, particularly when associated with risk factors such as a sedentary lifestyle. CVD is associated with elevated sympathetic nerve activity (SNA), quantified as increased SNA burst activity in humans. Whether burst characteristics are influenced by sex or sedentary conditions at younger ages is unknown. The purpose of our study is to compare SNA bursts in active and sedentary female and male rats at ages including prepuberty and young adulthood. We hypothesized that burst characteristics and blood pressure are higher under sedentary conditions and lower in female rats compared with males. We analyzed splanchnic SNA (SpSNA) recordings from Inactin-anesthetized male and female rats at 4-, 8-, and 16-wk of age. Physically active and sedentary rats were each housed in separate, environmentally controlled chambers where physically active rats had free access to an in-cage running wheel. Sympathetic bursts were obtained by rectifying and integrating the raw SpSNA signal. Burst frequency, burst height, and burst width were calculated using the Peak Parameters extension in LabChart. Our results showed that sedentary conditions produced a greater burst width in 8- and 16-wk-old rats compared with 4-wk-old rats in both males and females (P < 0.001 for both). Burst frequency and incidence were both higher in 16-wk-old males compared with 16-wk-old females (P < 0.001 for both). Our results suggest that there are sedentary lifestyle- and sex-related mechanisms that impact sympathetic regulation of blood pressure at ages that range from prepuberty into young adulthood. NEW & NOTEWORTHY: The mechanisms of decreased incidence of cardiovascular disease (CVD) in reproductive-age women compared with age-matched men are unknown. The strong association between elevated sympathetic activity and CVD led us to characterize splanchnic sympathetic bursts in female and male rats. Prepubescent males and females exhibited narrower sympathetic bursts, whereas young adult males had higher resting burst frequency compared with age-matched females. Sex-based regulation of sympathetic activity suggests a need for sex-dependent therapeutic strategies to combat CVD. [ABSTRACT FROM AUTHOR]

We explored the influence of sex and maturation on resting cervical artery hemodynamics (common carotid artery, CCA; internal carotid artery, ICA; and vertebral artery, VA), free-living physical activity, and sedentary behavior in children 6-17 yr of age. In addition, we investigated the relationship between physical activity, sedentary behavior, and cervical artery hemodynamics. Seventy-eight children and adolescents, girls (n = 42; mean age, 11.4 ± 2.5 yr) and boys (n = 36; mean age, 11.0± 2.6 yr), completed anthropometric measures, duplex ultrasound assessment of the cervical arteries, and wore an activPAL accelerometer to assess physical activity (indexed by steps/day) and sedentary behavior for 7 days. The ICA and VA diameters were similar between prepubertal and pubertal groups, as was volumetric blood flow (Q); however, the CCA diameter was significantly larger in the pubertal group (P < 0.05). Boys were found to have larger diameters in all cervical arteries than girls, as well as higher QCCA, QICA, and global cerebral blood flow (P < 0.05). The pubertal group was more sedentary (100 min/day more; P < 0.05) and took 3,500 fewer steps/day than the prepubertal group (P < 0.05). Shear rate (SR) and Q of the cervical arteries showed no relationship to physical activity or prolonged bouts of sedentary behavior; however, a significant negative relationship was apparent between total sedentary time and internal carotid artery shear rate (ICASR) after covarying for steps/day and maturation (P < 0.05). These findings provide novel insight into the potential influence sedentary behavior may have on cerebrovascular blood flow in healthy girls and boys. NEW & NOTEWORTHY Cerebral blood flow is known to change with age; however, assessing these age-related changes is complex and requires consideration of pubertal status. This, to our knowledge, is the first study to investigate the influence of sex and maturation on resting cervical artery hemodynamics and subsequently explore associations with physical activity and sedentary behavior in healthy children and adolescents. Our findings suggest that habitual sedentary behavior may influence cervical artery hemodynamics in youth, independent of physical activity, maturation, and sex. [ABSTRACT FROM AUTHOR]

Aerobic training remodels the quantity and quality (function per unit) of skeletal muscle mitochondria to promote substrate oxidation, however, there remain key gaps in understanding the underlying mechanisms during initial training adaptations. We used short-term high-intensity interval training (HIIT) to determine changes to mitochondrial respiration and regulatory pathways that occur early in remodeling. Fifteen normal-weight sedentary adults started seven sessions of HIIT over 14 days and 14 participants completed the intervention. We collected vastus lateralis biopsies before and 48 h after HIIT to determine mitochondrial respiration, RNA sequencing, and Western blotting for proteins of mitochondrial respiration and degradation via autophagy. HIIT increased respiration per mitochondrial protein for lipid (+23% P = 0.020), complex I (+18%, P = 0.0015), complex I + II (+14%, P < 0.0001), and complex II (+24% P < 0.0001). Transcripts that increased with HIIT identified several gene sets of mitochondrial respiration, particularly for complex I, whereas transcripts that decreased identified pathways of DNA and chromatin remodeling. HIIT lowered protein abundance of autophagy markers for p62 (−19%, P = 0.012) and LC3 II/I (−20%, P = 0.004) in whole tissue lysates but not isolated mitochondria. Meal tolerance testing revealed HIIT increased the change in whole body respiratory exchange ratio and lowered cumulative plasma insulin concentrations. Gene transcripts and respiratory function indicate remodeling of mitochondria within 2 wk of HIIT. Overall changes are consistent with increased protein quality driving rapid improvements in substrate oxidation. [ABSTRACT FROM AUTHOR]

The rise in oxygen consumption during the transition from rest to exercise is faster in those who are endurance-trained than those who have sedentary lifestyles, partly due to a more efficient cardiac response. However, data regarding this acute cardiac response in trained individuals are limited to heart rate (HR), stroke volume, and cardiac output. Considering this, we compared cardiac kinetics, including left ventricular (LV) strains and twist/untwist mechanics, between endurance-trained cyclists and their sedentary counterparts. Twenty young, male, trained cyclists and 23 untrained participants aged 18-25 yr performed five similar constant workload exercises on a cyclo-ergometer (target HR: 130 beats/min). During each session, LV myocardial diastolic and systolic linear strains, as well as torsional mechanics, were assessed using speckle-tracking echocardiography. Cardiac function was evaluated every 15 s during the first minute and every 30 s thereafter, until 240 s. Stroke volume increased during the first 30-45 s in both groups but to a significantly greater extent in trained cyclists (31% vs. 24%). Systolic parameters were similar in both groups. Transmitral peak filling velocity and peak filling rate responded faster to exercise and with greater amplitude in trained cyclists. Left ventricular filling pressure was lower in the former, whereas LV relaxation was greater but only at the base of the left ventricle. Basal rotation and peak untwisting rate responded faster and to a greater extent in the cyclists. This study provides new mechanical insights into the key role of LV untwisting in the more efficient acute cardiac response of endurancetrained athletes at onset of exercise. NEW & NOTEWORTHY Our study assessed for the first time, to our knowledge, the kinetics of left ventricular function during the transition from rest to constant-load exercise in endurance-trained subjects. We observed a faster cardiac response in cyclists characterized by a faster response of cardiac output, left ventricular transmitral filling, basal rotation, and untwisting. This study highlighted the key role of left ventricular twisting mechanics in the more efficient acute cardiac response of endurancetrained athletes at onset of exercise. [ABSTRACT FROM AUTHOR]

This study compared 24-h nutrient oxidation responses between a sedentary condition (SED) and a condition in which short 5-min bouts of moderate-intensity physical activity were performed hourly for nine consecutive hours over 4 days (MICRO). To determine whether any shifts in fuel use were due solely to increases in energy expenditure, we also studied a condition consisting of a single isoenergetic 45-min bout of moderate-intensity exercise (ONE). Twenty sedentary overweight or obese adults (10 men/10 women; 32.4 6.3 yr; BMI, 30.6 2.9 kg/m2 ) completed all three conditions (MICRO, SED, and ONE) in a randomized order. Each condition consisted of a 3-day free-living run-in followed by a 24-h stay in a whole-room calorimeter to measure total energy expenditure (TEE) and substrate utilization. Dietary fat oxidation was also assessed during the chamber stay by administering a [1-13C] oleic acid tracer at breakfast. Energy intake was matched across conditions. Both MICRO and ONE increased TEE relative to SED, resulting in a negative energy balance. HOMA-IR improved in both activity conditions. MICRO increased 24-h carbohydrate oxidation compared with both ONE and SED (P 0.01 for both). ONE was associated with higher 24-h total fat oxidation compared with SED, and higher 24-h dietary fat oxidation compared with both SED and MICRO. Differences in substrate oxidation remained significant after adjusting for energy balance. In overweight and obese men and women, breaking up sitting time increased reliance upon carbohydrate as fuel over 24 h, while a single energy-matched continuous bout of exercise preferentially relies upon fat over 24 h. NEW & NOTEWORTHY Insulin sensitivity, as assessed by HOMA-IR, was improved after 4 days of physical activity, independent of frequency and duration of activity bouts. Temporal patterns of activity across the day differentially affect substrate oxidation. Frequent interruptions of sedentary time with short bouts of walking primarily increase 24-h carbohydrate oxidation, whereas an energymatched single continuous bout of moderate intensity walking primarily increased 24-h fat oxidation. [ABSTRACT FROM AUTHOR]

This investigation developed models to estimate aspects of physical activity and sedentary behavior from three-axis high-frequency wrist-worn accelerometer data. The models were developed and tested on 20 participants (n = 10 males, n = 10 females, mean age = 24.1, mean body mass index = 23.9), who wore an ActiGraph GT3X+ accelerometer on their dominant wrist and an ActiGraph GT3X on the hip while performing a variety of scripted activities. Energy expenditure was concurrently measured by a portable indirect calorimetry system. Those calibration data were then used to develop and assess both machine-learning and simpler models with fewer unknown parameters (linear regression and decision trees) to estimate metabolic equivalent scores (METs) and to classify activity intensity, sedentary time, and locomotion time. The wrist models, applied to 15-s windows, estimated METs [random forest: root mean squared error (rSME) = 1.21 METs, hip: rMSE = 1.67 METs] and activity intensity (random forest: 75% correct, hip: 60% correct) better than a previously developed model that used counts per minute measured at the hip. In a separate set of comparisons, the simpler decision trees classified activity intensity (random forest: 75% correct, tree: 74% correct), sedentary time (random forest: 96% correct, decision tree: 97% correct), and locomotion time (random forest: 99% correct, decision tree: 96% correct) nearly as well or better than the machine-learning approaches. Preliminary investigation of the models' performance on two free-living people suggests that they may work well outside of controlled conditions. [ABSTRACT FROM AUTHOR]

Passive heat therapy (repeated hot tub or sauna use) reduces cardiovascular risk, but its effects on the mechanisms underlying improvements in microvascular function have yet to be studied. We investigated the effects of heat therapy on microvascular function and whether improvements were related to changes in nitric oxide (NO) bioavailability using cutaneous microdialysis. Eighteen young, sedentary, otherwise healthy subjects participated in 8 wk of heat therapy (hot water immersion to maintain rectal temperature ≥38.5°C for 60 min/session; n = 9) or thermoneutral water immersion (sham, n = 9), and participated in experiments before and after the 8-wk intervention in which forearm cutaneous hyperemia to 39°C local heating was assessed at three microdialysis sites receiving 1) Lactated Ringer's (Control), 2) Nω-nitro-l-arginine (l-NNA; nonspecific NO synthase inhibitor), and 3) 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol), a superoxide dismutase mimetic. The arm used for microdialysis experiments remained out of the water at all times. Data are means ± SE cutaneous vascular conductance (CVC = laser Doppler flux/mean arterial pressure), presented as percent maximal CVC (% CVCmax). Heat therapy increased local heating plateau from 42 ± 6 to 53 ± 6% CVCmax (P < 0.001) and increased NO-dependent dilation (difference in plateau between Control and l-NNA sites) from 26 ± 6 to 38 ± 4% CVCmax (P < 0.01), while no changes were observed in the sham group. When data were pooled across all subjects at 0 wk, Tempol had no effect on the local heating response (P = 0.53 vs. Control). There were no changes at the Tempol site across interventions (P = 0.58). Passive heat therapy improves cutaneous microvascular function by improving NO-dependent dilation, which may have clinical implications. [ABSTRACT FROM AUTHOR]

The hypothesis that the adaptive capacity is higher in human upper- than lower-body skeletal muscle was tested. Furthermore, the hypothesis that more pronounced adaptations in upper-body musculature can be achieved by "low-volume high-intensity" compared with "high-volume low-intensity" exercise training was evaluated. A group of sedentary premenopausal women aged 45 ± 6 yr (± SD) with expected high adaptive potential in both upper- and lower-extremity muscle groups participated. After random allocation to high-intensity swimming (HIS, n = 21), moderate-intensity swimming (MOS, n = 21), soccer (SOC, n = 21) or a nontraining control group (CON, n = 20), the training groups completed three workouts per week for 15 wk. Resting muscle biopsies were obtained from the vastus lateralis muscle and deltoideus muscle before and after the intervention. After the training intervention, a larger (P < 0.05) increase existed in deltoideus muscle of the HIS group compared with vastus lateralis muscle of the SOC group for citrate synthase maximal activity (95 ± 89 vs. 27 ± 34%), citrate synthase protein expression (100 ± 29 vs. 31 ± 44%), 3-hydroxyacyl-CoA dehydrogenase maximal activity (35 ± 43 vs. 3 ± 25%), muscle glycogen content (63 ± 76 vs. 20 ± 51%), and expression of mitochondrial complex II, III, and IV. Additionally, HIS caused higher (P < 0.05) increases than MOS in deltoideus muscle citrate synthase maximal activity, citrate synthase protein expression, and muscle glycogen content. In conclusion, the deltoideus muscle has a higher adaptive potential than the vastus lateralis muscle in sedentary women, and "high-intensity low-volume" training is a more efficient regime than "low-intensity high-volume" training for increasing the aerobic capacity of the deltoideus muscle. [ABSTRACT FROM AUTHOR]

Objective" methods to monitor physical activity and sedentary patterns in free-living conditions are necessary to further our understanding of their impacts on health. In recent years, many software solutions capable of automatically identifying activity types from portable accelerometry data have been developed, with promising results in controlled conditions, but virtually no reports on field tests. An automatic classification algorithm initially developed using laboratory-acquired data (59 subjects engaging in a set of 24 standardized activities) to discriminate between 8 activity classes (lying, slouching, sitting, standing, walking, running, and cycling) was applied to data collected in the field. Twenty volunteers equipped with a hip-worn triaxial accelerometer performed at their own pace an activity set that included, among others, activities such as walking the streets, running, cycling, and taking the bus. Performances of the laboratory-calibrated classification algorithm were compared with those of an alternative version of the same model including field-collected data in the learning set. Despite good results in laboratory conditions, the performances of the laboratory-calibrated algorithm (assessed by confusion matrices) decreased for several activities when applied to free-living data. Recalibrating the algorithm with data closer to real-life conditions and from an independent group of subjects proved useful, especially for the detection of sedentary behaviors while in transports, thereby improving the detection of overall sitting (sensitivity: laboratory model = 24.9%; recalibrated model = 95.7%). Automatic identification methods should be developed using data acquired in free-living conditions rather than data from standardized laboratory activity sets only, and their limits carefully tested before they are used in field studies. [ABSTRACT FROM AUTHOR]

Randomized clinical trials of exercise training regimens in sedentary individuals have provided a mechanistic understanding of the long-term health benefits and consequences of physical activity and inactivity. The sedentary control periods from these trials have provided evidence of the progressive metabolic deterioration that results from as little as 4-6 mo of continuing a physically inactive lifestyle. These clinical trials have also demonstrated that only a modest amount of physical activity is required to prevent this metabolic deterioration, and this amount of physical activity is consistent with current physical activity recommendations (150 min/wk of moderate intensity physical activity). These recommendations have been issued to the general population for a vast array of health benefits. While greater adherence to these recommendations should result in substantial improvements in the health of the population, these recommendations still remain inadequate for many individuals. An individual's physical activity requirements are influenced by such factors as an individual's diet, nonexercise physical activity patterns, genetic profile, and medications. Improving the understanding of how these factors influence an individual's physical activity requirements will help advance the field and help move the field toward the development of more personalized physical activity recommendations. [ABSTRACT FROM AUTHOR]

"Objective" methods to monitor physical activity and sedentary patterns in free-living conditions are necessary to further our understanding of their impacts on health. In recent years, many software solutions capable of automatically identifying activity types from portable accelerometry data have been developed, with promising results in controlled conditions, but virtually no reports on field tests. An automatic classification algorithm initially developed using laboratory-acquired data (59 subjects engaging in a set of 24 standardized activities) to discriminate between 8 activity classes (lying, slouching, sitting, standing, walking, running, and cycling) was applied to data collected in the field. Twenty volunteers equipped with a hip-worn triaxial accelerometer performed at their own pace an activity set that included, among others, activities such as walking the streets, running, cycling, and taking the bus. Performances of the laboratory-calibrated classification algorithm were compared with those of an alternative version of the same model including field-collected data in the learning set. Despite good results in laboratory conditions, the performances of the laboratory-calibrated algorithm (assessed by confusion matrices) decreased for several activities when applied to free-living data. Recalibrating the algorithm with data closer to real-life conditions and from an independent group of subjects proved useful, especially for the detection of sedentary behaviors while in transports, thereby improving the detection of overall sitting (sensitivity: laboratory model = 24.9%; recalibrated model = 95.7%). Automatic identification methods should be developed using data acquired in free-living conditions rather than data from standardized laboratory activity sets only, and their limits carefully tested before they are used in field studies. [ABSTRACT FROM AUTHOR]

Cardiovasomobility is a novel concept that encompasses the integration of cardiovascular and skeletal muscle function in health and disease with critical modification by physical activity, or lack thereof. Compelling evidence indicates that physical activity improves health while a sedentary, or inactive, lifestyle accelerates cardiovascular and skeletal muscle dysfunction and hastens disease progression. Identifying causative factors for vascular and skeletal muscle dysfunction, especially in humans, has proven difficult due to the limitations associated with cross-sectional investigations. Therefore, experimental models of physical inactivity and disuse, which mimic hospitalization, injury, and illness, provide important insight into the mechanisms and consequences of vascular and skeletal muscle dysfunction. This review provides an overview of the experimental models of disuse and inactivity and focuses on the integrated responses of the vasculature and skeletal muscle in response to disuse/inactivity. The time course and magnitude of dysfunction evoked by various models of disuse/inactivity are discussed in detail, and evidence in support of the critical roles of mitochondrial function and oxidative stress are presented. Lastly, strategies aimed at preserving vascular and skeletal muscle dysfunction during disuse/inactivity are reviewed. Within the context of cardiovasomobility, experimental manipulation of physical activity provides valuable insight into the mechanisms responsible for vascular and skeletal muscle dysfunction that limit mobility, degrade quality of life, and hasten the onset of disease. [ABSTRACT FROM AUTHOR]

Because elevated hemodynamic pulsatility could be mechanical stress against the brain, the dampening function of central and cerebral arteries is crucial. Regular endurance exercise training favorably restores the deteriorated dampening function of the aorta and carotid arteries in older populations, yet its effect on cerebrovascular dampening function remains unknown. To address this question, we compared cerebrovascular impedance, a frequency-domain relationship of the cerebral pressure and flow, in 21 middle-aged masters athletes who have been engaged in endurance training and races for >10 yr (MA, 53 ± 4 yr) with sedentary 21 age-matched (MS, 53 ± 5 yr) and 21 young (YS, 29 ± 6 yr) individuals. Using transfer function analysis, cerebrovascular impedance was computed from the simultaneously recorded carotid artery pressure (CAP, via applanation tonometry) and middle cerebral artery blood flow velocity (CBFV, via transcranial Doppler). In the frequency range of 0.78-3.12 Hz, coherence between pulsatile changes in CAP and CBFV was higher than 0.90 in all groups. All subjects exhibited the highest impedance modulus in the range of the first harmonic oscillations (0.78-1.56 Hz) mainly originating from cardiac ejection. Impedance modulus in this range was significantly lower in the MA than MS groups (0.88 ± 0.24 vs. 1.15 ± 0.29 mmHg·s/cm, P = 0.011) and equivalent to the YS (0.92 ± 0.30 mmHg·s/cm). Among middle-aged subjects, higher impedance modulus was correlated with lower mean CBFV (r = -0.776, P < 0.001) and cerebral cortical perfusion evaluated by MRI (r = -0.371, P = 0.015). These results suggest that middle-aged endurance athletes exhibited the significantly lower modulus of cerebrovascular impedance, which is associated with higher CBFV and cerebral cortical perfusion. NEW & NOTEWORTHY Impedance modulus in the range of first harmonic oscillations (0.78-1.56 Hz), which reflects heart rate at rest, was lower in middle-aged endurance athletes than in age-matched sedentary peers and was similar to young individuals. Prolonged endurance training is associated with the improved cerebrovascular dampening function in middle-aged adults. Lower cerebrovascular impedance modulus may contribute to maintaining brain perfusion in midlife. [ABSTRACT FROM AUTHOR]

Mitochondrial free -radical formation has been implicated as a potential mechanism underlying degenerative senescence, although human data are lacking. Therefore, the present study was designed to examine if resting and exercise-induced intramuscular free radical-mediated lipid peroxidation is indeed increased across the spectrum of sedentary aging. Biopsies were obtained from the vastus lateralis in six young (26 ± 6 yr) and six aged (71 ± 6 yr) sedentary males at rest and after maximal knee extensor exercise. Aged tissue exhibited greater (P < 0.05 vs. the young group) electron paramagnetic resonance signal intensity of the mitochondrial ubisemiquinone radical both at rest (+138 ± 62%) and during exercise (+143 ± 40%), and this was further complemented by a greater increase in α-phenyl-tert-butylnitrone adducts identified as a combination of lipid-derived alkoxyl-alkyl radicals (+295 ± 96% and +298 ± 120%). Lipid hydroperoxides were also elevated at rest (0.190 ± 0.169 vs. 0.148 ± 0.071 nmol/mg total protein) and during exercise (0.567 ± 0.259 vs. 0.320 ± 0.263 nmol/mg total protein) despite a more marked depletion of ascorbate and uptake of α/β-carotene, retinol, and lycopene (P < 0.05 vs. the young group). The impact of senescence was especially apparent when oxidative stress biomarkers were expressed relative to the age-related decline in mitochondrial volume density and absolute power output at maximal exercise. In conclusion, these findings confirm that intramuscular free radical-mediated lipid peroxidation is elevated at rest and during acute exercise in aged humans. [ABSTRACT FROM AUTHOR]

Hypertensive postmenopausal women are more likely to develop adverse cardiac remodeling and respond less effectively to drug treatment than men. High-intensity interval exercise (HIIE) is a nonpharmacological strategy for the treatment of hypertension; however, the effectiveness in women remains uncertain. This study was designed to evaluate 1) the effects of HIIE training upon morphological and functional markers of cardiovascular health in female SHR and 2) to determine whether the hormonal shift induced by ovariectomy could influence cardiovascular responses to HIIE. Thirty-six SHR were randomly assigned to four groups: ovariectomized sedentary, ovariectomized trained, sham-operated sedentary, and sham-operated trained. The trained rats performed HIIE 5 days/wk for 8 wk. Blood pressure and echocardiographic measurements were performed before and after training in animals. Cardiac response to β-adrenergic stimulation and the expression of calcium regulatory proteins and estrogen receptors in heart samples were assessed. Endothelium-dependent vasorelaxation in response to acetylcholine was evaluated in aortic rings as well as the expression of nitric oxide synthase isoforms (eNOS and P-eNOS) by Western blotting. In both groups of trained SHR, HIIE induced eccentric cardiac remodeling with greater inotropic and chronotropic effects, as well as an increase in SERCA and β1AR expression. However, although the trained rats showed improved endothelial function and expression of eNOS and P-eNOS in the aorta, there was no demonstrated effect on blood pressure. In addition, the responses to HIIE training were not affected by ovariectomy. This work highlights the importance of assessing the cardiovascular efficacy and safety of different exercise modalities in women. NEW & NOTEWORTHY: This study reports the effects of high-intensity interval exercise (HIIE) training on cardiac and endothelial function in female hypertensive rats. Despite a lack of effect on blood pressure (BP), HIIE training induces eccentric cardiac remodeling with greater functionals effects. Furthermore, training has beneficial effects on endothelial function. However, ovarian hormones do not seem to modulate cardiac and aortic adaptations to this training modality. All this underlines the need to consider training modalities on the cardiovascular system in women. [ABSTRACT FROM AUTHOR]

Lifetime physical inactivity interacts with secondary aging (i.e., aging caused by diseases and environmental factors) in three patterns of response. First, lifetime physical inactivity confers no apparent effects on a given set of physiological functions. Second, lifetime physical inactivity accelerates secondary aging (e.g., speeding the reduction in bone mineral density, maximal oxygen consumption, and skeletal muscle strength and power), but does not alter the primary aging of these systems. Third, a lifetime of physical activity to the age of ~60-70 yr old totally prevents decrements in some age-associated risk factors for major chronic diseases, such as endothelial dysfunction and insulin resistance. The present review provides ample and compelling evidence that physical inactivity has a large impact in shortening average life expectancy. In summary, physical inactivity plays a major role in the secondary aging of many essential physiological functions, and this aging can be prevented through a lifetime of physical activity. [ABSTRACT FROM AUTHOR]

We investigated the effects of early ovarian hormone deprivation on the heart and the role of physical training in this condition using different approaches: cardiac autonomic tone, contractility, morphology and function, and cardiac fibrosis. Female Wistar rats (n = 48) were assigned into two groups: ovariectomized (Ovx; 10-wk-old) and control rats (Sham; 10-wk-old). Each group was further divided into two subgroups, sedentary and trained (aerobic training by swimming for 10 wk). The sedentary groups showed similar cardiac autonomic tone values; however, only the Sham group had an increase in vagal participation for the determination of the basal heart rate after physical training. The contractile responses to cardiac β-agonists of the sedentary groups were similar, including an increased response to a β1-agonist (dobutamine) observed after physical training. The Ovx sedentary group presented changes in cardiac morphology, which resulted in decreases in the ejection fraction, fractional shortening, and cardiac index compared with the Sham sedentary group. Physical training did little to alter these findings. Moreover, histology analysis showed a significant increase in cardiac fibrosis in the sedentary Ovx group, which was not observed in the trained Ovx group. We conclude that early ovarian hormone deprivation in rats impairs autonomic control, cardiac morphology, and cardiac function and increases cardiac fibrosis; however, it does not affect the contractility induced by dobutamine and salbutamol. Furthermore, this model of physical training prevented an increase in fibrosis and promoted an increase in the cardiac contractile response but had little effect on cardiac autonomic control or morphological and functional parameters. [ABSTRACT FROM AUTHOR]

Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans. [ABSTRACT FROM AUTHOR]

Absolute total hemoglobin mass (tHbmass) and blood compartment volumes are often considered to be higher in endurance athletes compared with nonathletes, yet little data support a fitness effect in older age. Therefore, we measured tHbmass and blood compartment volumes (carbon monoxide rebreathing) in 77 healthy individuals (23% female; aged, 60–87 yr). Participants were recruited into groups based upon their lifelong (>25 yr) exercise "dose": 1) 15 sedentary individuals, <2 sessions/wk; 2) 25 casual exercisers, 2–3 sessions/wk; 3) 24 committed exercisers, 4–5 sessions/wk; and 4) 13 competitive Masters athletes, 6–7 sessions/wk, plus regular competitions. Absolute (L/min) and relative (mL/kg/min) V̇ o 2peak were higher with increasing exercise "dose" (P = 0.0005 and P < 0.0001, respectively). Hemoglobin concentration, hematocrit, and absolute tHbmass and blood compartment volumes were not significantly different between groups (all, P > 0.1328). When scaled to body mass, tHbmass (Sedentary, 9.2 ± 1.7 mL/kg; Casual, 9.2 ± 1.3; Committed, 10.2 ± 1.4; Competitive, 11.5 ± 1.4, ANOVA P < 0.0001) and blood volume were significantly different between groups [Sedentary, 63.4 (59.2–68.5) mL/kg; Casual, 67.3 (64.4–72.6); Committed, 73.5 (67.5–80.2); Competitive, 83.4 (78.9–88.6), ANOVA P < 0.0001], whereby all values were highest in Masters athletes. However, when scaled to fat-free mass (FFM), tHbmass and blood compartment volumes were greater in Competitive compared with Casual exercisers (all, P < 0.0340) and tHbmass and erythrocyte volume were also higher in Committed compared with Casual exercisers (both, P < 0.0134). In conclusion, absolute tHbmass and blood compartment volumes are not different between groups, with dose-dependent differences only among exercisers when scaled for FFM, with the highest tHbmass and blood compartment volumes in competitive Masters athletes. NEW & NOTEWORTHY: We observed that absolute oxygen carrying capacity (total hemoglobin mass, tHbmass) and blood compartment volumes were not associated with lifelong exercise dose. However, hematological adaptations associated with lifelong habitual exercise are only present among exercisers, whereby competitive Masters athletes have a greater oxygen carrying capacity (tHbmass) and expanded blood compartment volumes when scaled to fat-free mass. [ABSTRACT FROM AUTHOR]

Social jet lag (SJL) is a misalignment between sleep and wake times on workdays and free days. SJL leads to chronic circadian rhythm disruption and may affect nearly 70% of the general population, leading to increased risk for cardiometabolic diseases. This study investigated the effects of SJL on metabolic health, exercise performance, and exercise-induced skeletal muscle adaptations in mice. Ten-week-old C57BL/6J mice (n = 40) were allocated to four groups: control sedentary (CON-SED), control exercise (CON-EX), social jet lag sedentary (SJL-SED), and social jet lag exercise (SJL-EX). CON mice were housed under a 12:12-h light-dark cycle. SJL was simulated by implementing a 4-h phase delay for 3 days to simulate "weekends," followed by a 4-h phase advance back to "weekdays," for 6 wk. EX mice had free access to a running wheel. Graded exercise tests (GXTs) and glucose tolerance tests (GTTs) were performed at baseline and after intervention to monitor the effects of exercise and social jet lag on cardiorespiratory and metabolic health, respectively. SJL led to alterations in activity and running patterns and clock gene expression in skeletal muscle and decreased average running distance (P < 0.05). SJL-SED mice gained significantly more weight compared with CON-SED and SJL-EX mice (P < 0.01). SJL impaired fasting blood glucose and glucose tolerance compared with CON mice (P < 0.05), which was partially restored by exercise in SJL-EX mice. SJL also blunted improvements in exercise performance and mitochondrial content in the quadriceps. These data suggest that SJL blunted some cardiometabolic adaptations to exercise and that proper circadian hygiene is necessary for maintaining health and performance. NEW & NOTEWORTHY: In mice, disrupting circadian rhythms with social jet lag for 6 wk caused significant weight gain, higher fasting blood glucose, and impaired glucose tolerance compared with control. Voluntary exercise in mice experiencing social jet lag prevented weight gain, though the mice still experienced increased fasting blood glucose and impaired exercise performance compared with trained mice not experiencing social jet lag. Social jet lag seems to be a potent circadian rhythm disruptor that impacts exercise-induced training adaptations. [ABSTRACT FROM AUTHOR]

Our objective was to determine the influence of a high-fat diet (HFD) on fasting and postprandial skeletal muscle substrate metabolism in endurance-trained (ET) compared with sedentary (SED) humans. SED (n = 17) and ET (n = 7) males were control-fed a 10-day moderate-fat diet followed by a 5-day isocaloric HFD (55% fat, 30% carbohydrate). Skeletal muscle biopsies were taken in the fasted condition and 4 h after a high-fat meal (820 kcals; 63% fat and 25% carbohydrate). Palmitate-induced suppression of pyruvate oxidation, an indication of substrate preference, and oxidation of fat and glucose were measured in homogenized skeletal muscle in fasted and fed states. Postprandial responses were calculated as percent changes from fasting to fed states. Postprandial suppression of pyruvate oxidation was maintained after the HFD in ET, but not SED skeletal muscle, suggesting greater adaptability to dietary intake changes in the former. Fasting total fat oxidation increased due to the HFD in ET skeletal muscle (P = 0.006), which was driven by incomplete fat oxidation (P = 0.008). Fasting fat oxidation remained unchanged in skeletal muscle of SED individuals. Yet, postprandial fat oxidation was similar between groups. Fasting glucose oxidation was elevated after the HFD in ET (P = 0.036), but not SED, skeletal muscle. Postprandial glucose oxidation was reduced due to the HFD in SED (P = 0.002), but not ET, skeletal muscle. These findings provide insight into differing substrate metabolism responses between SED and ET individuals and highlight the role that the prevailing diet may play in modulating fasting and postprandial metabolic responses in skeletal muscle. NEW & NOTEWORTHY The relationship between high dietary fat intake and physical activity level and their combined effect on skeletal muscle substrate metabolism remains unclear. We assessed the influence of the prevailing diet in modulating substrate oxidation in skeletal muscle of endurance-trained compared with sedentary humans during a high-fat challenge meal. Collectively, our findings demonstrate the adaptability of skeletal muscle in endurance-trained individuals to high dietary fat intake. [ABSTRACT FROM AUTHOR]

The negative effects of sympathetic overactivity on long-term cardiovascular health are becoming increasingly clear. Moreover, recent work done in animal models of cardiovascular disease suggests that sympathetic tone to the splanchnic vasculature may play an important role in the development and maintenance of these disease states. Work from our laboratory and others led us to hypothesize that a lack of chronic physical activity increases resting and reflex-mediated splanchnic sympathetic nerve activity, possibly through changes occurring in a key brain stem center involved in sympathetic regulation, the rostral ventrolateral medulla (RVLM). To address this hypothesis, we recorded mean arterial pressure (MAP) and splanchnic sympathetic nerve activity (SSNA) in a group of active and sedentary animals that had been housed for 10-13 wk with or without running wheels, respectively. In experiments performed under Inactin anesthesia, we tested responses to RVLM microinjections of glutamate, responses to baroreceptor unloading, and vascular reactivity, the latter of which was performed under conditions of autonomic blockade. Sedentary animals exhibited enhanced resting SSNA and MAP, augmented increases in SSNA to RVLM activation and baroreceptor unloading, and enhanced vascular reactivity to α1-receptor mediated vasoconstriction. Our results suggest that a sedentary lifestyle increases the risk of cardiovascular disease by augmenting resting and reflex-mediated sympathetic output to the splanchnic circulation and also by increasing vascular sensitivity to adrenergic stimulation. We speculate that regular physical exercise offsets or reverses the progression of these disease processes via similar or disparate mechanisms and warrant further examination into physical (in)activity-induced sympathetic nervous system plasticity. [ABSTRACT FROM AUTHOR]

Sedentary aging results in a diminished rapid cutaneous vasodilator response to local heating. We investigated whether this diminished response was due to altered contributions of noradrenergic sympathetic nerves by assessing 1) the age-related decline and 2) the effect of aerobic fitness. Using laser-Doppler flowmetry, we measured skin blood flow (SkBF) in young (24 ± 1 yr) and older (64 ± 1 yr) endurance-trained and sedentary men (n = 7 per group) at baseline and during 35 min of local skin heating to 42°C at 1) untreated forearm sites, 2) forearm sites treated with bretylium tosylate (BT), which prevents neurotransmitter release from noradrenergic sympathetic nerves, and 3) forearm sites treated with yohimbine + propranolol (YP), which antagonizes or- and β-adrenergic receptors. SkBF was converted to cutaneous vascular conductance (CVC = SkBF/mean arterial pressure) and normalized to maximal CVC (%CVCmax) achieved by skin heating to 44°C. Pharmacological agents were administered using microdialysis. In the young trained group, the rapid vasodilator response was reduced at BT and YP sites (P < 0.05); by contrast, in the young sedentary and older trained groups, YP had no effect (P > 0.05), but BT did (P > 0.05). Neither BT nor YP affected the rapid vasodilator response in the older sedentary group (P > 0.05). These data suggest that the age-related reduction in the rapid vasodilator response is due to an impairment of sympathetic-dependent mechanisms, which can be partly attenuated with habitual aerobic exercise. Rapid vasodilation involves noradrenergic neurotransmitters in young trained men and nonadrenergic sympathetic cotransmitters (e.g., neuropeptide Y) in young sedentary and older trained men, possibly as a compensatory mechanism. Finally, in older sedentary men, the rapid vasodilation appears not to involve the sympathetic system. [ABSTRACT FROM AUTHOR]

Previously, it was demonstrated in exercise-trained humans that phosphocreatine (PCr) recovery is significantly altered by fraction of inspired O2 (FIO2), suggesting that in this population under normoxic conditions, O2 availability limits maximal oxidative rate. Haseler LJ, Hogan ML, and Richardson RS. J Appl Physiol 86: 2013-2018, 1999. To further elucidate these population-specific limitations to metabolic rate, we used 31P-magnetic resonance spectroscopy to study the exercising human gastrocnemius muscle under conditions of varied FIO2 in sedentary subjects. To test the hypothesis that PCr recovery from submaximal exercise in sedentary subjects is not limited by O2 availability, but rather by their mitochondrial capacity, six sedentary subjects performed three bouts of 6-min steady-state submaximal plantar flexion exercise followed by 5 min of recovery while breathing three different FIO2 (0.10, 0.21, and 1.00). PCr recovery time constants were significantly longer in hypoxia (47.0 ± 3.2 s), but there was no difference between hyperoxia (31.8 ± 1.9 s) and normoxia (30.0 ± 2.1 s) (mean ± SE). End-exemise pH was not significantly different across treatments. These results suggest that the maximal muscle oxidative rate of these sedentary subjects, unlike their exercise-trained counterparts, is limited by mitochondrial capacity and not O2 availability in normoxia. Additionally, the significant elongation of PCr recovery in these subjects in hypoxia illustrates the reliance on O2 supply at the other end of the O2 availability spectrum in both sedentary and active populations. [ABSTRACT FROM AUTHOR]

Leucine supplementation attenuates the loss of skeletal muscle mass and function in older adults during bed rest. We sought to determine whether leucine could also preserve and/or restore mitochondrial function and muscle oxidative capacity during periods of disuse and rehabilitation. Healthy, older adults (69.1 ± 1.1 yr) consumed a structured diet with supplemental leucine (LEU: 0.06 g/kg body weight/meal; n = 8) or alanine (CON: 0.06 g/kg body weight/meal; n = 8) during 7 days of bed rest and 5 days of inpatient rehabilitation. A 75-g oral glucose tolerance test (OGTT) was performed at baseline (PreBR), after bed rest (PostBR), and rehabilitation (PostRehab) and used to calculate an indicator of insulin sensitivity and metabolic clearance rate (MCR). Tissue samples from the m. vastus lateralis were collected at PreBR, PostBR, and PostRehab to assess mitochondrial respiratory capacity and protein markers of the oxidative phosphorylation and a marker of the antioxidant defense systems. During bed rest, leucine tended to preserve insulin sensitivity (change in MCR, CON vs. LEU: -3.5 ± 0.82 vs. LEU: -0.98 ± 0.88, P = 0.054), but had no effect on mitochondrial respiratory capacity (change in state 3+succinate CON vs. LEU -8.7 ± 6.1 vs. 7.3 ± 4.1 pmol O2/s/mg tissue, P = 0.10). Following rehabilitation, leucine increased ATP-linked respiration (CON vs. LEU: -8.9 ± 6.2 vs. 15.5 ± 4.4 pmol O2/s/mg tissue, P = 0.0042). Although the expression of mitochondrial respiratory and antioxidant proteins was not impacted, leucine supplementation preserved specific pathways of mitochondrial respiration, insulin sensitivity, and a marker of oxidative stress during bed rest and rehabilitation. [ABSTRACT FROM AUTHOR]

Indexes for arterial stiffness are, by their nature, influenced by the ambient blood pressure due to the curvilinear nature of arterial compliance. We developed a new concept of the "Modelflow aortic age," which is, theoretically, not influenced by the ambient blood pressure and provides an easily understood context (biological vs. chronological age) for measures of arterial stiffness. The purpose of the present study was to validate this pressure-independent index for aortic stiffness in humans. Twelve sedentary elderly (65-77 yr), 11 Masters athletes (65-73 yr), and 12 sedentary young individuals (20-42 yr) were studied. Modelflow aortic ages were comparable with chronological ages in both sedentary groups, indicating that healthy sedentary individuals have age-appropriate aortas. In contrast, Masters athletes showed younger Modelflow aortic ages than their chronological ages. The coefficient of variation of sedentary subjects was three times smaller with the Modelflow aortic age (21%) than with other indexes, such as static systemic arterial stiffness (61%), central pulse wave velocity (61%), or carotid β-stiffness index (58%). The typical error was very small and two times smaller in the Modelflow aortic age (<7%) than in static systemic arterial stiffness (>13%) during cardiac unloading by lower body negative pressure. The Modelflow aortic age can more precisely and reliably estimate aortic stiffening with aging and modifiers, such as life-long exercise training compared with the pressure-dependent index of static systemic arterial stiffness, and provides a physiologically relevant and clinically compelling context for such measurements. [ABSTRACT FROM AUTHOR]

The thermic effect of food (TEF) is an important physiological determinant of total daily energy expenditure (EE) and energy balance. TEF is believed to be mediated in part by sympathetic nervous system activation and consequent β-adrenergic receptor (β-AR) stimulation of metabolism. TEF is greater in habitually exercising than in sedentary adults, despite similar postprandial sympathetic nervous system activation. We determined whether augmented TEF in habitually exercising adults is associated with enhanced peripheral thermogenic responsiveness to β-AR stimulation. In separate experiments in 22 sedentary and 29 habitually exercising adults, we measured the increase in EE (indirect calorimetry, ventilated hood) during β-AR stimulation (intravenous isoproterenol: 6, 12, and 24 ng·kg fat-free mass-1·min-1) and EE before and after a liquid meal (40% of resting EE; 53% carbohydrate, 32% fat, 15% protein). The increase in EE during incremental isoproterenol administration was greater (P = 0.01) in habitual exercisers (0.34 ± 0.03, 0.54 ± 0.04,0.81 ± 0.05 kJ/min; means ± SE) than in sedentary adults (0.26 ± 0.03, 0.40 ± 0.03, 0.64 ± 0.04 kJ/min). The area under the TEF response curve was also greater (P = 0.04) in habitual exercisers (160 ± 9 kJ) than in sedentary adults (130 ± 11 kJ) and was positively related to β-AR thermogenic responsiveness (r = 0.32, P = 0.02). We conclude that TEF is related to β-AR thermogenic responsiveness and that the greater TEF in habitual exercisers is attributable in part to their augmented β-AR thermogenic responsiveness. Our results also suggest that peripheral thermogenic responsiveness to β-AR stimulation is a physiological determinant of TEF and hence energy balance in healthy adult humans. [ABSTRACT FROM AUTHOR]

sedentary individuals, H1 receptors mediate the early portion of postexercise skeletal muscle hyperemia, whereas H2 receptors mediate the later portion. It is not known whether postexercise hyperemia also presents in endurance-trained individuals. We hypothesized that the postexercise skeletal muscle hyperemia would also exist in endurance-trained individuals and that combined blockade of H1 and H2 receptors would abolish the long-lasting postexercise hyperemia in trained and sedentary individuals. We studied 28 sedentary and endurance trained men and women before and through 90 mm after a 60-mm bout of cycling at 60% peak O2 uptake on control and combined H1- and H2-receptor antagonist days (fexofenadine and ranitidine). We measured arterial pressure (brachial auscultation) and femoral blood flow (Doppler ultrasound). On the control day, femoral vascular conductance (calculated as flow/pressure) was elevated in all groups 60 mm after exercise (sedentary men: Δ86 ± 35%, trained men, Δ65 ± 18%; sedentary women, Δ61 ± 19%, trained women: Δ59 ± 23%, where Δ is change; all P < 0.05 vs. preexercise). In contrast, on the histamine antagonist day, femoral vascular conductance was not elevated in any of the groups after exercise (sedentary men: Δ21 ± 17%, trained men: Δ9 ± 5%, sedentary women: Δ19 ± 4%, trained women: Δ11 ± 11%; all P>0.16 vs. preexercise; P < 0.05 vs. control day). These data suggest postexercise skeletal muscle hyperemia exists in endurance trained men and women. Furthermore, histaminergic mechanisms produce the long-lasting hyperemia in sedentary and endurance-trained individuals. [ABSTRACT FROM AUTHOR]

Regular exercise-induced acute inflammatory responses are suggested to improve the inflammatory profile and insulin sensitivity. As body temperature elevations partly mediate this response, passive heating might be a viable tool to improve the inflammatory profile. This study investigated the acute and chronic effects of hot water immersion on inflammatory and metabolic markers. Ten sedentary, overweight men [body mass index (BMI): 31.0 ± 4.2 kg/m2, mean ± SD] were immersed in water set at 39°C for 1 h (HWI) or rested for 1 h at ambient temperature (AMB). Venous blood was obtained before the session, immediately postsession, and 2 h postsession for assessment of monocyte intracellular heat shock protein-72 (iHsp72) and plasma concentrations of extracellular Hsp72 (eHsp72), interleukin-6 (IL-6), fasting glucose, insulin, and nitrite. Thereafter, participants underwent a 2-wk intervention period, consisting of 10 hot water immersion sessions (INT). Eight BMI-matched participants (BMI: 30.0 ± 2.5 kg/m2) were included as control (CON). Plasma IL-6 and nitrite concentrations were higher immediately following HWI compared with AMB (IL-6 P < 0.001, HWI: 1.37 ± 0.94 to 2.51 ± 1.49 pg/ml; nitrite P = 0.04, HWI: 271 ± 52 to 391 ± 72 nM), whereas iHsp72 expression was unchanged (P = 0.57). In contrast to resting iHsp72 expression (P = 0.59), fasting glucose (P = 0.04; INT: 4.44 ± 0.93 to 3.98 ± 0.98 mmol/l), insulin (P = 0.04; INT: 68.1 ± 44.6 to 55.0 ± 29.9 pmol/l), and eHsp72 (P = 0.03; INT: 17 ± 41% reduction) concentrations were lowered after INT compared with CON. HWI induced an acute inflammatory response and increased nitric oxide bioavailability. The reductions in fasting glucose and insulin concentrations following the chronic intervention suggest that hot water immersion may serve as a tool to improve glucose metabolism. NEW & NOTEWORTHY A single hot water immersion (HWI) session induces an acute increase in plasma interleukin-6 and nitrite concentrations but does not acutely elevate heat shock protein-72 expression in monocytes [intracellular Hsp72 (iHsp72)]. A chronic HWI intervention reduces fasting glucose and insulin concentrations in the absence of changes in resting iHsp72. Therefore, HWI shows potential as a strategy to combat chronic low-grade inflammation and improve glucose metabolism in individuals without the physical capacity to do so using exercise. [ABSTRACT FROM AUTHOR]

Physical inactivity influences the development of muscle insulin resistance yet is far less understood than diet-induced muscle insulin resistance. Progress in understanding the mechanisms of physical inactivity-induced insulin resistance is limited by a lack of an appropriate preclinical model of muscle insulin resistance. Here, we discuss differences between diet and physical inactivity-induced insulin resistance, the advantages and disadvantages of the available rodent inactivity models to study insulin resistance, and our current understanding of the mechanisms of muscle insulin resistance derived from such preclinical inactivity designs. The burgeoning rise of health complications emanating from metabolic disease presents an alarming issue with mounting costs for health care and a reduced quality of life. There exists a pressing need for more complete understanding of mechanisms behind the development and progression of metabolic dysfunction. Since lifestyle modifications such as poor diet and lack of physical activity are primary catalysts of metabolic dysfunction, rodent models have been formed to explore mechanisms behind these issues. Particularly, the use of a high-fat diet has been pervasive and has been an instrumental model to gain insight into mechanisms underlying diet-induced insulin resistance (IR). However, physical inactivity (and to some extent muscle disuse) is an often overlooked and much less frequently studied lifestyle modification, which some have contended is the primary contributor in the initial development of muscle IR. In this mini-review we highlight some of the key differences between diet- and physical inactivity-induced development of muscle IR and propose reasons for the sparse volume of academic research into physical inactivity-induced IR including infrequent use of clearly translatable rodent physical inactivity models. [ABSTRACT FROM AUTHOR]

Platelet activation, including the formation of monocyte platelet aggregates (MPAs), contributes to atherosclerosis, thrombus formation, and acute coronary syndromes. Regular participation in exercise can lower cardiovascular risk, but little is known regarding the impact of exercise training on platelet function. We investigated the effect of 6 mo of walking exercise on platelet function in sedentary older adults without significant cardiovascular disease. Twenty-seven participants were randomly allocated to 6 mo of either: no-exercise (n = 13) or 3 × 50 min/wk of supervised center-based walking (n = 14). Circulating and agonist-induced MPAs were assessed using flow cytometry before [month 0(0M)] and after [month 6 (6M)] the intervention. Circulating MPAs increased from 0M (3.7 ± 1.0%) to 6M (4.7 ± 1.6%) in the no-exercise group (P = 0.009), whereas a nonsignificant decrease was observed in the walking group (0M 4.3 ± 1.7 vs. 6M 3.7 ± 1.2 %, P = 0.052). The change in MPAs between groups was significant (P = 0.001). There were no differences between groups in platelet responses to agonists across the interventions (all P > 0.05). Collectively, these data suggest that the absence of regular exercise may increase MPAs, which are cellular mediators involved in atherosclerosis, while regular walking inhibits such increases. The thrombotic function of platelets appears to be relatively unaltered by exercise training. This study provides novel data related to the cardioprotective effects associated with participation in exercise. NEW & NOTEWORTHY Monocyte-platelet aggregates contribute to atherosclerosis and exercise can lower cardiovascular risk. This is the first study to discover that a lack of regular physical activity is associated with increased monocyte-platelet aggregates over a 6-mo intervention period. In contrast, walking exercise inhibits increased monocyte-platelet aggregates in the circulation. This study highlights a novel pathway by which regular participation in exercise exerts its cardioprotective effects. [ABSTRACT FROM AUTHOR]

Moderate-intensity continuous training (MICT) improves peripheral artery function in healthy adults, a phenomenon that reverses as continued training induces structural remodeling. Sprint interval training (SIT) elicits physiological adaptations similar to MICT, despite a lower exercise volume and time commitment; however, its effect on peripheral artery function and structure is largely unexplored. We compared peripheral artery responses to 12 wk of MICT and SIT in sedentary, healthy men (age = 27 ± 8 yr). Participants performed MICT (45 min of cycling at 70% peak heart rate; n = 10) or SIT (3 × 20-s “all out” cycling sprints with 2 min of recovery; n = 9), and responses were compared with a non training control group (CTL, n = 6). Allometrically scaled brachial flow-mediated dilation (FMD) increased 2.2% after 6 wk of MICT and returned to baseline levels by 12 wk, but did not change in SIT or CTL (group × time interaction, P = 0.04). Brachial artery diameter increased after 6 and 12 wk (main effect, P = 0.03), with the largest increases observed in MICT. Neither training protocol affected popliteal relative FMD and diameter, or central and lower limb arterial stiffness (carotid distensibility, central and leg pulse wave velocity) (P > 0.05 for all). Whereas earlier and more frequent measurements are needed to establish the potential presence and time course of arterial responses to low-volume SIT, our findings suggest that MICT was superior to the intense, but brief and intermittent SIT stimulus at inducing brachial artery responses in healthy men. NEW & NOTEWORTHY We compared the effects of 12 wk of moderate-intensity continuous training (MICT) and sprint interval training (SIT) on peripheral artery endothelial function and diameter, and central and lower limb stiffness in sedentary, healthy men. Whereas neither training program affected the popliteal artery or stiffness indexes, we observed changes in brachial artery function and diameter with MICT but not SIT. Brachial artery responses to SIT may follow a different time course or may not occur at all. [ABSTRACT FROM AUTHOR]

This study assessed the mitochondrial related signaling responses to a single bout of noncontact, modified football (touch rugby), played as small-sided games (SSG), or cycling (CYC) exercise in sedentary, obese, middleaged men. In a randomized, crossover design, nine middle-aged, sedentary, obese men completed two, 40-min exercise conditions (CYC and SSG) separated by a 21-day recovery period. Heart rate (HR) and ratings of perceived exertion (RPE) were collected during each bout. Needle biopsies from the vastus lateralis muscle were collected at rest and 30 and 240 min postexercise for analysis of protein content and phosphorylation (PGC-1α, SIRT1, p53, p53Ser15, AMPK, AMPKThr172, CAMKII, CAMKIIThr286, p38MAPK, and p38MAPKThr180/Tyr182) and mRNA expression (PGC-1α, p53, NRF1, NRF2, Tfam, and cytochrome c). A main effect of time effect for both conditions was evident for HR, RPE, and blood lactate (P < 0.05), with no condition by time interaction (P > 0.05). Both conditions increased PGC1-α protein and mRNA expression at 240 min (P < 0.05). AMPKThr172 increased 30 min post CYC (P < 0.05), with no change in SSG (P > 0.05). CYC increased p53 protein content at 240 min to a greater extent than SSG (P < 0.05). mRNA expression of NRF2 decreased in both conditions (P < 0.05). No condition by time interactions were evident for mRNA expression of Tfam, NRF1, cytochrome c, and p53. The similar PGC-1α response between intensity-matched conditions suggests both conditions are of similar benefit for stimulating mitochondrial biogenesis. Differences between conditions regarding fluctuation in exercise intensity and type of muscle contraction may explain the increase of p53 and AMPK within CYC and not SSG (noncontact, modified football). [ABSTRACT FROM AUTHOR]

Physical inactivity and low aerobic capacity are primary drivers of chronic disease pathophysiology and are independently associated with all-cause mortality. Conversely, increased physical activity and exercise are central to metabolic disease prevention and longevity. Although these relationships are well characterized in the literature, what remains incompletely understood are the mechanisms by which physical activity/exercise prevents disease. Given methodological constraints of clinical research, investigators must often rely on preclinical rodent models to investigate these potential underlying mechanisms. However, there are several key barriers to applying exercise metabolism findings from rodent models to human health. These barriers include housing temperature, nutrient metabolism, exercise modality, exercise testing, and sex differences. Increased awareness and understanding of these barriers will enhance the ability to impact human health through more appropriate experimental design and interpretation of data within the context of these factors. [ABSTRACT FROM AUTHOR]

Mechanisms underlying the protective effects of both habitual endurance exercise and the female sex on vascular function are incompletely understood. Blood-borne circulating factors, such as circulating microRNAs (ci-miRs), may partially explain these effects. Blood samples were obtained from young, healthy men and women who either habitually performed endurance exercise (endurance trained) or were relatively inactive (sedentary). Women were tested during the early follicular phase of the menstrual cycle or the placebo pill phase of oral contraceptive to control for estrogen. Cultured human umbilical vein endothelial cells (HUVECs) were exposed to participants' serum in migration, proliferation, and reactive oxygen species (ROS) assays. Real-time quantitative polymerase chain reaction was used to quantify an initial array of 84 cardiovascular disease (CVD)-related ci-miRs, followed by validation of 10 ci-miRs. All participants were devoid of traditional CVD risk factors, and circulating estradiol concentration was not different between groups. Serum of endurance-trained women induced greater HUVEC migration compared with serum of sedentary women. HUVEC ROS production was greater in response to serum of sedentary men compared with serum of endurance-trained men and sedentary women. There were sex effects on the levels of nine ci-miRs, with greater levels in men, while ci-miRs-140-5p and 145-5p were also higher in sedentary compared with endurancetrained men and/or women. In a sex-specific manner, habitual endurance exercise was associated with beneficial effects of serum on HUVECs. Thus, alterations in circulating factors may contribute to the protective effects of habitual endurance exercise on vascular health. Additionally, sex had a greater impact than habitual activity level on the levels of vascular-related ci-miRs. [ABSTRACT FROM AUTHOR]

Chronic alcohol intoxication decreases muscle strength/function and causes mitochondrial dysfunction. Aerobic exercise training improves mitochondrial oxidative capacity and increases muscle mass and strength. Presently, the impact of chronic alcohol on aerobic exercise-induced adaptations was investigated. Female C57BL/6Hsd mice were randomly assigned to one of four groups: control sedentary (CON SED; n = 26), alcohol sedentary (ETOH SED; n = 27), control exercise (CON EX; n = 28), and alcohol exercise (ETOH EX; n = 25). Exercise mice had running wheel access for 2 h a day, 7 days a week. All mice were fed either control or an alcohol-containing liquid diet. Grip strength testing and EchoMRI were performed before and after the interventions. After 6 wk, hindlimb muscles were collected for molecular analyses. A subset of mice performed a treadmill run to fatigue (RTF), then abstained from alcohol for 2 wk and repeated the RTF. Alcohol decreased lean mass and forelimb grip strength compared with control-fed mice. Alcohol blunted the exercise-induced increase in muscle mass (plantaris and soleus), type IIa fiber percentage in the plantaris, and run time to fatigue. Mitochondrial markers (Citrate synthase activity and Complex I-IV, COXIV and Cytochrome C protein expression) were increased with exercise regardless of ETOH in the gastrocnemius but not tibialis anterior muscle. Two weeks of alcohol abstinence improved RTF time in ETOH EX but not in ETOH SED. These data suggest that alcohol impairs some exercise-induced adaptations in skeletal muscle, but not all were negatively affected, indicating that exercise may be a beneficial behavior even while consuming alcohol. NEW & NOTEWORTHY: Alcohol consumption during an aerobic exercise training period prevented training-induced increases in run to fatigue time and grip strength. Cessation of alcohol allowed for recovery of endurance performance within 2 wk. The worsened exercise performance after alcohol was unrelated to impairments in markers of mitochondrial health. Therefore, some adaptations to exercise training are impaired with alcohol use (endurance performance, muscle growth, and strength), while others remain mostly unaffected (mitochondrial health). [ABSTRACT FROM AUTHOR]

The impact of exercise training on sympathetic activation is not well understood, especially across untrained and trained limbs in athletes. Therefore, in eight sedentary subjects (maximal oxygen consumption = 40 ± 2 ml·kg-1·min-1) and eight competitive cyclists (maximal oxygen consumption 64 ± 2 ml·kg-1·min-1), we evaluated heart rate, blood pressure, blood flow, vascular conductance, and vascular resistance in the leg and arm during acute sympathetic stimulation [cold pressor test (CPT)]. The CPT was also performed during dynamic leg (knee extensor) or arm (handgrip) exercise at 50% of maximal work rate (WRmax) with measurements in the exercising limb. At rest, the CPT decreased vascular conductance similarly in the leg and arm of sedentary subjects (-33 ± 8% leg, -38 ± 6% arm) and cyclists (-34 ± 4% leg, -31 ± 9% arm), and during exercise CPT-induced vasoconstriction was blunted (i.e., sympatholysis) in both the leg and arm of both groups. However, the magnitude of sympatholysis was significantly different between the arm and leg of the sedentary group (-47 ± 11% arm, -25 ± 8% leg), and it was less in the arm of cyclists (-28 ± 11%) than sedentary controls. Taken together, these data provide evidence that sympathetically mediated vasoconstriction is expressed equally and globally at rest in both sedentary and trained individuals, with a differential pattern of vasoconstriction during acute exercise according to limb and exercise training status. [ABSTRACT FROM AUTHOR]

Investigates the relation between habitual endurance exercise status and the age-associated decline in maximal aerobic capacity in men. Analysis of the men's responses to graded exercise; Identification of the significant predictor variables of the age-associated changes in maximal O[sub 2] consumption.

Cardiovascular disease is an enormous public health problem, particularly in older populations. Exercise is the most potent cardioprotective intervention identified to date, with exercise in the juvenile period potentially imparting greater protection, given the plasticity of the developing heart. To test the hypothesis that voluntary wheel running early in life would be cardioprotective later in life when risk for disease is high, we provided male and female juvenile (3 wk old) mice access to a running wheel for 2 wk. Mice then returned to a home cage to age to adulthood (4--6 mo) before exposure to isoproterenol (ISO) to induce cardiac stress. Cardiac function and remodeling were compared with sedentary control mice, sedentary mice exposed to ISO, and mice that exercised in adulthood immediately before ISO. Early in life activity protected against ISO-induced stress as evidenced by attenuated cardiac mass, myocyte size, and fibrosis compared with sedentary mice exposed to ISO. ISO-induced changes in cardiac function were ameliorated in male mice that engaged in wheel running, with ejection fraction and fractional shortening reversed to control values. Adrenergic receptor expression was downregulated in juvenile male runners. This suppression persisted in adulthood following ISO, providing a putative mechanism by which exercise in the young male heart provides resilience to cardiac stress later in life. Together, we show that activity early in life induces persistent cardiac changes that attenuate ISO-induced stress in adulthood. Identification of the mechanisms by which early in life exercise is protective will yield valuable insights into how exercise is medicine across the life course. [ABSTRACT FROM AUTHOR]

Fat oxidation during exercise is increased by endurance training, and evidence suggests that fat oxidation during exercise is impaired in obesity. Thus the primary aim of this study was to compare the acute effects of exercise on 24-h fat oxidation and fat balance in lean sedentary [LS, n = 10, body mass index (BMI) = 22.5 ± 6.5 kg/m²], lean endurance-trained (LT, n = 10, BMI = 21.2 ± 1.2 kg/m²), and obese sedentary (OS, n = 7, BMI = 35.5 ± 4.4 kg/m²) men and women. Twenty-four-hour energy expenditure and substrate oxidation were measured under sedentary (control; CON) and exercise (EX) conditions while maintaining energy balance. During EX, subjects performed 1 h of stationary cycling at 55% of aerobic capacity. Twenty-four-hour fat oxidation did not differ on the CON or EX day in LS (43 ± 9 vs. 29 ± 7 g/day, respectively), LT (53 ± 8 vs. 42 ± 5 g/day), or OS (58 ± 7 vs. 80 ± 9 g/day). However, 24-h fat balance was significantly more positive on EX compared with CON (P < 0.01). Twenty-four-hour glucose, insulin, and free fatty acid (FFA) profiles were similar on the EX and CON days, but after consumption of the first meal, FFA concentrations remained below fasting levels for the remainder of the day. These data suggest that when exercise is performed with energy replacement (i.e., energy balance is maintained), 24-h fat oxidation does not increase and in fact, may be slightly decreased. It appears that the state of energy balance is an underappreciated factor determining the impact of exercise on fat oxidation. [ABSTRACT FROM AUTHOR]

The objective of this study was to evaluate the effects of exercise training on plasma removal of a cholesterol-rich nanoemulsion (LDE) that mimics low-density lipoprotein (LDL) lipid structure and binds to LDL receptors. LDE-derived cholesteryl ester plasma kinetics was studied in 24 exercise-trained and 20 sedentary male subjects. LDE labeled with [14C]cholesteryl ester was injected intravenously, and plasma samples were collected over a 24-h period to determine radioisotope decay curves. LDL cholesterol concentration was similar in both groups. Fractional clearance rate (FCR) of the nanoemulsion label was greater in the exercise-trained group compared with the sedentary group (0.138 ± 0.152 and 0.0261 ± 0.023 h-1, respectively). A positive correlation was found (r = 0.60, P < 0.01) between FCR and peak O2 consumption in trained subjects. Circulating oxidized LDL levels were lower in trained subjects compared with the sedentary group (9.0 ± 2.0 and 16.0 ± 3.0 mU/l). LDE was also injected into control and LDL receptor gene knockout mice submitted and not submitted to training. Muscle LDE uptake percentage was increased in the trained mice compared with the untrained mice (1.1 ± 0.8 and 0.2 ± 0.1, respectively, P < 0.0001) in the control group but not in the knockout animals, indicating that the LDL receptor is involved in the increased uptake elicited by exercise. These results show that exercise training increases LDE plasma removal, which in turn suggests that it also increases LDL receptors or LDL receptor activity. [ABSTRACT FROM AUTHOR]

Physical inactivity is a global health risk that can be addressed through application of exercise training suitable for an individual's health and age. People's willingness to participate in physical activity is often limited by an initially poor physical capability and early onset of fatigue. One factor associated with muscle fatigue during intense contractions is an inexcitability of skeletal muscle cells, reflecting impaired transmembrane Na+/K+ exchange and membrane depolarization, which are regulated via the transmembranous protein Na+-K+-ATPase (NKA). This short review focuses on the plasticity of NKA in skeletal muscle in humans after periods of altered usage, exploring NKA upregulation with exercise training and downregulation with physical inactivity. In human skeletal muscle, the NKA content quantified by [³H]ouabain binding site content shows robust, yet tightly constrained, upregulation of 8-22% with physical training, across a broad range of exercise training types. Muscle NKA content in humans undergoes extensive downregulation with injury that involves substantial muscular inactivity. Surprisingly, however, no reduction in NKA content was found in the single study that investigated short-term disuse. Despite clear findings that exercise training and injury modulate NKA content, the adaptability of the individual NKA isoforms in muscle (α1-3 and β1-3) and of the accessory and regulatory protein FXYD1 are surprisingly inconsistent across studies, for exercise training as well as for injury/disuse. Potential reasons for this are explored. Finally, we provide suggestions for future studies to provide greater understanding of NKA regulation during exercise training and inactivity in humans. [ABSTRACT FROM AUTHOR]

The metabolic cost of walking (MCOW), or oxygen uptake normalized to distance, provides information on the energy expended during movement. There are conflicting reports as to whether sex differences in MCOW exist, with scarce evidence investigating factors that explain potential sex differences. This study 1) tested the hypothesis that females exhibit a higher MCOW than males, 2) determined whether normalizing to stepping cadence ameliorates the hypothesized sex difference, and 3) explored whether more habitual step counts and time in intensity-related physical activity, and less sedentary time were associated with a decreased MCOW. Seventy-six participants (42 females, 24 ± 5 yr) completed a five-stage, graded treadmill protocol with speeds increasing from 0.89 to 1.79 m/s (6-min walking stage followed by 4-min passive rest). Steady-state oxygen uptake (via indirect calorimetry) and stepping cadence (via manual counts) were determined. Gross and net MCOW, normalized to distance traveled (km) and step-cadence (1,000 steps) were calculated for each stage. Thirty-nine participants (23 females) wore an activPAL on their thigh for 6.9 ± 0.4 days. Normalized to distance, females had greater gross MCOW (J/kg/km) at all speeds (P < 0.014). Normalized to stepping frequency, females exhibited greater gross and net MCOW at 1.12 and 1.79 m/s (J/kg/1,000 steps; P < 0.01) but not at any other speeds (P < 0.075). Stature was negatively associated with free-living cadence (r = −0.347, P = 0.030). Females expend more energy/kilometer traveled than males, but normalizing to stepping cadence attenuated these differences. Such observations provide an explanation for prior work documenting higher MCOW among females and highlight the importance of stepping cadence when assessing the MCOW. NEW & NOTEWORTHY: Whether there are sex differences in the metabolic cost of walking (MCOW) and the factors that may contribute to these are unclear. We demonstrate that females exhibit a larger net MCOW than males. These differences were largely attenuated when normalized to stepping cadence. Free-living activity was not associated with MCOW. We demonstrate that stepping cadence, but not free-living activity, partially explains the higher MCOW in females than males. [ABSTRACT FROM AUTHOR]

Aging is accompanied by considerable deterioration of homeostatic systems, such as autonomic imbalance characterized by heightened sympathetic activity, lower parasympathetic tone, and depressed heart rate (HR) variability, which are aggravated by hypertension. Here, we hypothesized that these age-related deficits in aged hypertensive rats can be ameliorated by exercise training, with benefits to the cardiovascular system. Therefore, male 22-mo-old spontaneously hypertensive rats (SHRs) and agematched Wistar Kyoto (WKY) submitted to moderate-intensity exercise training (T) or kept sedentary (S) for 8 wk were evaluated for hemodynamic/autonomic parameters, baroreflex sensitivity, cardiac sympathetic/parasympathetic tone and analysis of dopamine β-hydroxylase (DBH+) and oxytocin (OT+) pathways of autonomic brain nuclei. Aged SHR-S versus WKY-S exhibited elevated mean arterial pressure (MAP: +51%) and HR (+20%), augmented pressure/HR variability, no cardiac vagal tone, and depressed reflex control of the heart (HR range, -28%; gain, -49%). SHR-T exhibited a lower resting HR, a partial reduction in the MAP (-14%), in the pressure/HR variabilities, and restored parasympathetic modulation, with improvement of baroreceptor reflex control when compared with SHR-S. Exercise training increased the ascending DBH+ projections conveying peripheral information to the paraventricular nucleus of hypothalamus (PVN), augmented the expression of OT+ neurons, and reduced the density of DBH+ neurons in the rostral ventrolateral medulla (RVLM) of SHR-T. Data indicate that exercise training induces beneficial neuroplasticity in brain autonomic circuitry, and it is highly effective to restore the parasympathetic tone, and attenuation of age-related autonomic imbalance and baroreflex dysfunction, thus conferring long-term benefits for cardiovascular control in aged hypertensive individuals. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in women in developed societies. Unfavorable structural and functional adaptations within the heart and central blood vessels with sedentary aging in women can act as the substrate for the development of debilitating CVD conditions such as heart failure with preserved ejection fraction (HFpEF). The large decline in cardiorespiratory fitness, as indicated by maximal or peak oxygen uptake (V_ O2max and V_ O2peak, respectively), that occurs in women as they age significantly affects their health and chronic disease status, as well as the risk of cardiovascular and all-cause mortality. Midlife and older women who have performed structured endurance exercise training for several years or decades of their adult lives exhibit a V_ O2max and cardiac and vascular structure and function that are on par or even superior to much younger sedentary women. Therefore, regular endurance exercise training appears to be an effective preventative strategy for mitigating the adverse physiological cardiovascular adaptations associated with sedentary aging in women. Herein, we narratively describe the aging and short- and long-term endurance exercise training adaptations in V_ O2max, cardiac structure, and left ventricular systolic and diastolic function at rest and exercise in midlife and older women. The role of circulating estrogens on cardiac structure and function is described for consideration in the timing of exercise interventions to maximize beneficial adaptations. Current research gaps and potential areas for future investigation to advance our understanding in this critical knowledge area are highlighted. [ABSTRACT FROM AUTHOR]

It is still not possible to provide an evidence-based answer to the question of whether regular exercise is essential for normal growth. It is also unclear whether very low levels of exercise result in growth deficits. Regular exposure to exercise is characterized by heterogeneity in responsiveness, with most individuals experiencing improvements in fitness traits but a significant proportion showing only very minor gains. Whether a sedentary mode of life during the growing years results in a permanent deficit in cardio-respiratory fitness or a diminished ability to respond favorably to regular exercise later in life remains to be investigated. Although several genes have been associated with fitness levels or response to regular exercise, the quality of the evidence is weak mainly because studies are statistically underpowered. The special case of the obese, sedentary child is discussed, and the importance of the "energy gap" in the excess weight gain during growth is highlighted. Obese, sedentary children have high blood pressure, dyslipidemia, elevated glycemia and type 2 diabetes, hepatic steatosis, respiratory problems, orthopedic complications, and other health disorders more frequently than normal weight, physically active children. The role of genetic differences in the inclination to be sedentary or physically active is reviewed. An understanding of the true role of genetic differences and regular exercise on the growth of children will require more elaborate paradigms incorporating not only DNA sequence variants and exercise exposure but also information on nutrition, programming, and epigenetic events during fetal life and early postnatal years. [ABSTRACT FROM AUTHOR]

This investigation evaluated training responses to prolonged electrical muscle stimulation (EMS) in sedentary adults. Fifteen healthy subjects (10 men, 5 women) with a sedentary lifestyle completed a 6-wk training program during which they completed an average of 29 1-h EMS sessions, The form of EMS used by the subjects was capable of eliciting a cardiovascular exercise response without loading the limbs or joints. it achieved this by means of inducing rapid, rhythmical contractions in the large leg muscles. A crossover study design was employed with subjects undergoing their habitual activity levels during the nontraining phase of the study. The training effect was evaluated by means of a treadmill test to determine peak aerobic capacity [peak oxygen consumption (Vo2)], a 6-min walking distance test, and measurement of body mass index (BMI) and quadriceps muscle strength. At baseline, the mean values for peak Vo2, 6-min walking distance, quadriceps strength, and BMI were 2.46 ± 0.57 1/min, 493.3 ± 36.8 m, 360.8 ± 108.7 N, and 26.9 ± 3.4 kg/m², respectively. After training, subjects demonstrated statistically significant improvements in all variables except BMI. Peak Vo2 increased by an average of 0.24 ± 0.16 I/mm (P < 0.05), walking distance increased by 36.6 ± 19.7 m (P < 0.005), and quadriceps strength increased by 87.5 ± 55.9 N (P < 0.005); we did not observe a significant effect due to training on BMI (P > 0.05). These results suggest that EMS can be used in sedentary adults to improve physical fitness. It may provide a viable alternative to more conventional forms of exercise in this population. [ABSTRACT FROM AUTHOR]