Chronic Endurance Exercise Training Research Articles

Sprint interval training in the postpartum period maintains the enhanced cardiac output of pregnancy: A case study.

During pregnancy an increased cardiac output ( ) and blood volume (BV) occur to support fetal growth. Increased and BV also occur during chronic endurance exercise training and benefit performance. We investigated if sprint interval training (SIT) undertaken early postpartum maintains the elevated and BV of pregnancy and benefits performance. The participant, a competitive field hockey player and former cyclist, visited our laboratory at 2weeks of gestation (baseline) and postpartum pre-, mid- and post-intervention (PPpre, PPmid and PPpost). Delivery was uncomplicated and she felt ready to start the SIT programme 5weeks postpartum. Inert gas rebreathing was used to measure peak exercise ( peak); was measured with a metabolic cart; and postpartum haematological values were measured with carbon monoxide rebreathing. The 18 SIT sessions progressed from four to eight sprints at 130% of peak power output. peak increased from baseline at all postpartum time points (baseline 16.2 vs. 17.5, 16.8 and 17.2L/min at PPpre, PPmid and PPpost, respectively). Relative remained below baseline values at all postpartum measurements (baseline 44.9 vs. 41.0, 42.3 and 42.5mL/kg/min at PPpre, PPmid and PPpost, respectively) whereas absolute rapidly reached baseline values postpartum (baseline 3.19 vs. 3.12, 3.23 and 3.18L/min at PPpre, PPmid and PPpost, respectively). Postpartum BV (5257, 4271 and 5214mL at PPpre, PPmid and PPpost, respectively) and Hbmass (654, 525 and 641g at PPpre, PPmid and PPpost, respectively) were similar between PPpre and PPpost but decreased alongside peak at PPmid. Peak power was returned to pre-pregnancy values by intervention end (302 vs. 303W, baseline vs. PPpost). These findings show that SIT undertaken early postpartumdefends the elevated peak of pregnancy and rapidly returns absolute and peak power to baseline levels.

Exercise: A Possibly Effective Way to Improve Vitamin D Nutritional Status.

Vitamin D deficiency has become a widespread public health problem owing to its potential adverse health effects. Generally, the nutritional status of vitamin D depends on sunlight exposure and dietary or supplementary intake. However, recent studies have found that exercise can influence circulating 25(OH)D levels; although, the results have been inconclusive. In this review, we focused on the effect of exercise on circulating vitamin D metabolites and their possible mechanisms. We found that endurance exercise can significantly increase serum 25(OH)D levels in vitamin D-deficient people but has no significant effect on vitamin D-sufficient people. This benefit has not been observed with resistance training. Only chronic endurance exercise training can significantly increase serum 1,25(OH)2D, and the effect may be sex-dependent. Exercise may influence 25(OH)D levels in the circulation by regulating either the vitamin D metabolites stored in tissues or the utilization by target tissues. The effects of exercise on 25(OH)D levels in the circulation may be dependent on many factors, such as the vitamin D nutritional status, exercise type and intensity, and sex. Therefore, further research on the effects and mechanisms of exercise on vitamin D metabolites is required.

The Impact of Fitness Status on Vascular and Baroreceptor Function in Healthy Women and Men

Background: Chronic endurance exercise training elicits desirable physiological adaptations in the cardiovascular system. The volume of exercise training required to generate healthy adaptations is unclear. This study assessed the effects of differing exercise training levels on arterial stiffness, compliance, and autonomic function. Methods: Eighty healthy adults (38.5 ± 9.7 years; 44% female) defined as endurance-trained (ET, n = 29), normally active (NA, n = 27), or inactive (IN, n = 24) participated. Cardiovascular markers, including hemodynamics, large arterial compliance and small arterial compliance (LAC and SAC), carotid-femoral pulse wave velocity (PWV), and spontaneous baroreceptor sensitivity (BRS) were assessed. Results: ET showed significantly greater LAC values (21.4 ± 6.5) than NA (16.9 ± 2.5; p = 0.002) and IN (14.7 ± 3.2 mL × mm Hg × 10; p = 0.028). Values for SAC and BRS were significantly higher in ET than IN (p < 0.001 and p = 0.028, respectively), but not NA. Compared to IN, PWV values for ET and NA were significantly lower (p < 0.003). After adjusting for covariates (age, sex, and SBP), significant associations with cardiovascular fitness status were noted for all markers but BRS. Conclusion: Endurance exercise increases LAC likely due to high-volume training; however, lower volumes of physical activity may be sufficient to positively benefit vascular health overall.

Preventive effects of low-intensity endurance exercise for severe hyperglycemia-induced capillary regression in non-obese type 2 diabetes rat skeletal muscle.

Although endurance exercise is effective for reducing diabetes‐related capillary regression, it is difficult to prescribe high‐intensity endurance exercise due to the potential worsening of complications in patients with severe hyperglycemia. Therefore, this study aimed to examine whether chronic low‐intensity exercise training may prevent severe hyperglycemia‐induced capillary regression of skeletal muscle in non‐obese type 2 diabetes. Non‐diabetic Sprague Dawley rats were assigned to a control (Con) group and an exercise (Ex) group. Likewise, spontaneously diabetic Torii rats were assigned to a diabetic sedentary (DM) group or a diabetic exercise (DMEx) group. Rats in the Ex and DMEx groups were placed on a motor‐driven treadmill running at low speed (15 m/min) for 60 min/day, 5 days/week, for 14 weeks. Serum glucose levels were significantly increased in the DM group, but not in the DMEx group. Although the capillary‐to‐fiber ratio in the plantaris muscle was significantly lower in the DM group compared to the control group, the ratio in the DMEx group was significantly higher compared to the DM group. Moreover, the succinate dehydrogenase activity and expression levels of vascular endothelial growth factor and peroxisome proliferator‐activated receptor γ coactivator‐1α (PGC‐1α) were reduced in the plantaris muscle of the DM group. However, those in the DMEx group were significantly higher than those in the DM group. These results indicate that low‐intensity chronic endurance exercise training has the potential to prevent the progression of capillary regression in the skeletal muscles of non‐obese type 2 diabetes patients with severe hyperglycemia.

Effects of electrical stimulation-induced resistance exercise training on white and brown adipose tissues and plasma meteorin-like concentration in rats.

Chronic endurance exercise training induces morphological and metabolic alterations including mitochondrial biogenesis in white adipose tissue (WAT) and brown adipose tissue (BAT) in rodents. A myokine called meteorin‐like (Metrnl) is associated with morphological and metabolic adaptation and increased in blood after acute resistance exercise. However, the effects of chronic resistance exercise training (RT), which aims to increase muscle mass and strength, on WAT and BAT are unclear. Therefore, we aimed to clarify the effects of RT on morphological and metabolic parameters in WAT and BAT and on plasma Metrnl concentrations. We applied electrical stimulation to both legs of rats as RT three times a week for 4 weeks. RT reduced adipocyte size in subcutaneous WAT but induced no changes in mitochondrial and thermogenesis proteins. In BAT, peroxisome proliferator‐activated receptor gamma coactivator‐1 alpha (PGC‐1α) protein levels and mitochondrial content markers were significantly higher in the RT group compared with the control group. A significant positive correlation was found between the expression of PGC‐1α in BAT and plasma Metrnl concentrations. These results suggest that plasma Metrnl is associated with PGC‐1α and mitochondrial biogenesis in BAT. This study describes a potential role of RT in preventing metabolic diseases via altering WAT and BAT and increasing plasma Mertnl concentrations.

Effects of Endurance Training on Lactate Uptake Capacity and Its Related Proteins in Skeletal Muscles in Mice

AimsLactate has been recognized not merely as an end product of glycolysis in skeletal muscle but also as an energy fuel. Lactate also acts as a signaling molecule for muscle mitochondrial biogenesis (Hashimoto et al., 2007; Hoshino et al., 2015; Kitaoka et al., 2016). Therefore, lactate uptake to skeletal muscles is important for using lactate as a fuel and as a signaling molecule. The lactate uptake is regulated by monocarboxylate transporter (MCT) and mitochondrial content in skeletal muscles. Muscle MCTs and mitochondrial content markers are increased after chronic endurance exercise training in humans and rodents. Therefore, we aimed □ to estimate parameters related to lactate uptake capacity using blood lactate concentrations in lactate tolerance test, and □ to examine the relationship between the parameters and the protein levels of MCTs and mitochondrial enzymes in mouse skeletal muscles after 3 weeks of endurance training.MethodsWe used C57BL/6J mice and divided them into two groups, control group (CON) and endurance training (15 ~ 25 m/min, 30 min/day, 5 days/week, 3 weeks) group (END). Lactate tolerance test was performed by lactate intraperitoneal (ip) injection (1 g/kg of body weight) 24h after the last bout of endurance training. We calculated area under the curve (AUC) and peak values of blood lactate concentration. Using the time‐series data of blood lactate concentration after ip injection, the parameter k and n in the following formula were estimated. d[lactate]/dt = k[lactate]nParameter estimation was performed using minimization of residual sum of squares between experimental and simulated data. Gastrocnemius muscles were harvested 24h after the lactate tolerance test. We measured protein levels of MCTs, mitochondrial electron transport chain protein (complex I~V), peroxisome proliferator‐activated‐receptor γ coactivator 1a (PGC‐1a), pyruvate dehydrogenase (PDH) and phospho‐fructokinase by Western blot.Results &amp; DiscussionAUC and peak values of blood lactate concentration did not significantly differ between the two groups in the lactate tolerance test. Parameter k, which represents lactate uptake capacity, did not differ between the two groups. Muscle PGC1a was tended to be higher in the END than the CON (p = 0.095), but other protein levels did not significantly differ between the two groups. These results suggest that volume and/or duration of endurance training might not be enough. There was a positive correlation between the parameter k and protein levels of mitochondrial enzymes. This result suggests that the higher protein levels of mitochondrial enzymes in tricarboxylic acid cycle and electron transport chainin gastrocnemius muscles lead to the higher lactate uptake capacity. However, the relationship was not seen in the END. It is likely that lactate uptake capacity was associated with other factors in the early stage of endurance training.ConclusionLactate uptake capacity was closely related to protein levels of mitochondrial enzymes in skeletal muscles, but the relationship disappeared in the 3‐wk endurance‐trained mice.

DOES PHYSIOLOGIC CARDIAC REMODELING IN ENDURANCE ATHLETES ALTER REPOLARIZATION OR QT DYNAMICS?

Increases in QT and QTc duration, and their alterations with changes in heart rate, are associated with dysrhythmias and increased sudden death rates in population studies. Long standing endurance sport is associated with reduced cardiac mortality. Endurance athletes are known to develop physiologic LV remodeling concomitant with increases in LV mass, which may be associated with QT prolongation. However, QT dynamics in middle-aged athletes has not been studied extensively. We sought to compare the QT interval at rest and during exercise in healthy middle-aged adults with and without a history of long-standing endurance exercise. Healthy participants on no medications, between 45-65 years old (>10 years of regular physical activity participation) were recruited, and underwent physical examination. Eligible participants, including 86 endurance athletes (EA) and 24 recreationally-active (RA) adults, had a resting baseline 12-lead ECG and a standardized graded exercise testing with a 12-lead ECG taken every 1-2 minutes during exercise until exhaustion. QT intervals were measured as the longest QT in anterior precordial lead or lead 2 by two investigators and discrepancies resolved by consensus; QT intervals were corrected for rate using Bazett’s formula (QTc=QT/√RR in sec). Seventy-five participants also had a resting cardiac magnetic resonance to evaluate cardiac structure and physiological remodeling related to exercise. Participant demographics and ECG characteristics are summarized in Table 1. The higher cardiorespiratory fitness (VO2max) and left-ventricular mass reflected normal physiological adaptation to endurance exercise training. While mean resting QT interval was longer in EA vs. RA, there was no difference when QT interval was corrected for heart rate (QTc). The QT and QTc slopes (linear relationship of QT vs. RR and QTc vs. RR during exercise) were not different between EA and RA. Among long-standing middle-aged athletes with normal physiologic remodeling, there is no difference in QT intervals in EA vs. RA when corrected for their lower resting heart rate. Despite physiologic LV remodelling, chronic endurance exercise training is associated with normal repolarization at rest and during exercise among middle-aged endurance athletes.

Effects of long-term exercise training for different durations on pancreatic amylase activity and intestinal glucose transporter content in rats.

Long‐term endurance training for a relatively short duration (~1 h) is reported to increase pancreatic amylase activity in rats, suggesting that chronic exercise training enhances carbohydrate digestive capacity. However, it remains unknown whether longer exercise training duration results in greater adaptation in the pancreas and small intestine. Thus, this study aimed to examine the effects of long‐term endurance training for a longer duration on pancreatic amylase activity and intestinal glucose transporter content in rats. Male Sprague–Dawley rats were subjected to swimming exercise training for 1 h (Ex‐1h group) or 6 h (Ex‐6h group, two 3‐h sessions separated by 1 h of rest) each day, 5 days a week, for 6 weeks. Sedentary rats were used as a control (Con group). Total pancreatic amylase activity in the Ex‐6h group was significantly lower than that in the Con and Ex‐1h groups immediately after the last training session. After 24 h of recovery, total pancreatic amylase activity was significantly higher in the Ex‐1h group (~46%) than in the Con group, and a further increase was observed in the Ex‐6h group (~98%). In addition, the Ex‐6h group, but not the Ex‐1h group, showed significantly greater intestinal sodium‐dependent glucose transporter 1 (SGLT1) content compared with the Con group after 24 h of recovery. However, no significant difference was observed in glucose transporter 2 (GLUT2) content among the three groups. In conclusion, chronic endurance exercise training for a longer duration results in larger increases in pancreatic amylase activity and intestinal SGLT1 content in rats.

Protein Supplementation Does Not Augment Adaptations to Endurance Exercise Training.

Recently, it has been speculated that protein supplementation may further augment the adaptations to chronic endurance exercise training. We assessed the effect of protein supplementation during chronic endurance exercise training on whole-body oxidative capacity (V˙O2max) and endurance exercise performance. In this double-blind, randomized, parallel placebo-controlled trial, 60 recreationally active males (age, 27 ± 6 yr; body mass index, 23.8 ± 2.6 kg·m; V˙O2max, 47 ± 6 mL·min·kg) were subjected to 12 wk of triweekly endurance exercise training. After each session and each night before sleep, participants ingested either a protein supplement (PRO; 28.7 g casein protein) or an isoenergetic carbohydrate placebo (PLA). Before and after the 12 wk of training, V˙O2max and endurance exercise performance (~10-km time trial) were assessed on a cycle ergometer. Muscular endurance (total workload achieved during 30 reciprocal isokinetic contractions) was assessed by isokinetic dynamometry and body composition by dual-energy x-ray absorptiometry. Mixed-model ANOVA was applied to assess whether training adaptations differed between groups. Endurance exercise training induced an 11% ± 6% increase in V˙O2max (time effect, P < 0.0001), with no differences between groups (PRO, 48 ± 6 to 53 ± 7 mL·min·kg; PLA, 46 ± 5 to 51 ± 6 mL·min·kg; time-treatment interaction, P = 0.50). Time to complete the time trial was reduced by 14% ± 7% (time effect, P < 0.0001), with no differences between groups (time-treatment interaction, P = 0.15). Muscular endurance increased by 6% ± 7% (time effect, P < 0.0001), with no differences between groups (time-treatment interaction, P = 0.84). Leg lean mass showed an increase after training (P < 0.0001), which tended to be greater in PRO compared with PLA (0.5 ± 0.7 vs 0.2 ± 0.6 kg, respectively; time-treatment interaction, P = 0.073). Protein supplementation after exercise and before sleep does not further augment the gains in whole-body oxidative capacity and endurance exercise performance after chronic endurance exercise training in recreationally active, healthy young males.

Effects of psychological stress during exercise on markers of oxidative stress in young healthy, trained men

PurposeThose engaged in high stress occupations such as firefighters and military personnel are exposed to a variety of psychological and physiological stressors. The combination of mental and physical stress [i.e., dual stress challenges (DSC)] results in significant increases in stress hormones, which causes oxidative stress (OS) and contributes to elevated risk for cardiovascular disease. However, data are needed to determine the impact of DSC on markers of OS in exercise-trained individuals. MethodFourteen healthy trained men aged 21–30 yrs. participated in a randomized, cross-over design to investigate the impact of DSC on blood markers of OS. The exercise alone condition (EA) consisted of 35 min of cycling at 60% V̇O2 peak. The DSC involved 20 min of mental stress challenges during exercise. Blood was sampled before exercise, as well as immediately, and 30 and 60 min after exercise and analyzed for glutathione (GSH), superoxide dismutase (SOD), hydrogen peroxide (H2O2) and advanced oxidation protein products (AOPP). ResultNo significant treatment × time interactions were found. No time effects were noted for SOD, or H2O2; however, AOPP were reduced at 30 (p = .034) and 60 min post exercise (p = .006). GSH was reduced at 30 (p = .009) and 60 min post exercise (p = .031). ConclusionThese results indicate the OS response from DSC is not greater than that produced from EA in exercise trained men. Future work should investigate the impact of chronic resistance and endurance exercise training on OS resulting from DSC.

Force properties of skinned cardiac muscle following increasing volumes of aerobic exercise in rats.

The positive effects of chronic endurance exercise training on health and performance have been well documented. These positive effects have been evaluated primarily at the structural level, and work has begun to evaluate mechanical adaptations of the myocardium. However, it remains poorly understood how the volume of exercise training affects cardiac adaptation. To gain some understanding, we subjected 3-mo-old Sprague-Dawley rats ( n = 23) to treadmill running for 11 wk at one of three exercise volumes (moderate, high, and extra high). Following training, hearts were excised and mechanical testing was completed on skinned trabecular fiber bundles. Performance on a maximal fitness test was dose dependent on training volume, where greater levels of training led to greater performance. No differences were observed between animals from any group for maximal active stress and passive stress at a sarcomere length of 2.2 µm. Heart mass and passive stress at sarcomere lengths beyond 2.4 µm increased in a dose-dependent manner for animals in the control and moderate- and high-duration groups. However, hearts from animals in the extra high-duration group presented with inhibited responses for heart mass and passive stress, despite performing greatest on a graded treadmill fitness test. These results suggest that heart mass and passive stress adapt in a dose-dependent manner, until exercise becomes excessive and adaptation is inhibited. Our findings are in agreement with the beneficial role exercise has in cardiac adaptation. However, excessive exercise comes with risks of maladaptation, which must be weighed against the desire to increase performance. NEW & NOTEWORTHY For the first time, we present findings on cardiac trabecular muscle passive stiffness and show the effect of excessive exercise on the heart. We demonstrated that heart mass increases with exercise until a maximum, after which greater exercise volume results in inhibited adaptation. At paraphysiological lengths, passive stiffness increases with exercise but to a lesser degree with excessive training. Despite greater performance on graded exercise tests, animals in the highest trained group exhibited possible maladaptation.

Effects Of Chronic Endurance Exercise Training On Serum 25(OH)D Concentrations In Elderly Japanese Men

Higher levels of physical activity and cardiorespiratory fitness are positively related to serum 25-hydroxyvitamin D [25(OH)D] concentrations; however, the response of 25(OH)D concentrations to chronic endurance exercise training is unclear. PURPOSE: To elucidate whether serum 25(OH)D concentrations were directly increased by 5 weeks of endurance exercise training and influenced by changes in body fat in elderly men. METHODS: Twenty elderly Japanese men were randomized to either the 5-week endurance exercise training group (ET group; N=10) or the sedentary control group (SC group; N=10). Fasting blood samples were collected to determine serum 25(OH)D and other blood parameters. The visceral fat area and hepatic fat content were assessed by magnetic resonance imaging and proton magnetic resonance spectroscopy, respectively. RESULTS: After 5 weeks of endurance exercise training, the levels of maximal oxygen uptake (VO2 max) were significantly increased from 23.3 at baseline to 28.1 mL/kg/min at the endpoint for the ET group; levels were unchanged for the SC group. A significant seasonal reduction in serum 25(OH)D concentrations was observed in the SC group (P<0.05), while no change was found in the ET group. The results may be partly attributed to the slight decrease in intrahepatic fat in the ET group. No changes were observed in percent body fat or visceral fat area. CONCLUSIONS: The results of our study suggest that 5 weeks of endurance training could inhibit the seasonal reduction in serum 25(OH)D concentrations without changes in body fat.

Effects of chronic endurance exercise training on serum 25(OH)D concentrations in elderly Japanese men.

Higher levels of physical activity and cardiorespiratory fitness are positively related to serum 25-hydroxyvitamin D [25(OH)D] concentrations; however, the response of 25(OH)D concentrations to chronic endurance exercise training is unclear. Therefore, the purpose of this study was to elucidate whether serum 25(OH)D concentrations were directly increased by 5 weeks of endurance exercise training and influenced by changes in body fat in elderly men. Twenty elderly Japanese men were randomized to either the 5-week endurance exercise training group (ET group; N = 10) or the sedentary control group (SC group; N = 10). Fasting blood samples were collected to determine serum 25(OH)D and other blood parameters. The visceral fat area and hepatic fat content were assessed by magnetic resonance imaging and proton magnetic resonance spectroscopy, respectively. After 5 weeks of endurance exercise training, the levels of maximal oxygen uptake (VO2 max) were significantly increased from 23.3 at baseline to 28.1 mL/kg/min at the endpoint for the ET group; levels were unchanged for the SC group. A significant seasonal reduction in serum 25(OH)D concentrations was observed in the SC group (P < 0.05), while no change was found in the ET group. The results may be partly attributed to the slight decrease in intrahepatic fat in the ET group. No changes were observed in percent body fat or visceral fat area. The results of our study suggest that 5 weeks of endurance training could inhibit the seasonal reduction in serum 25(OH)D concentrations without changes in body fat.

Influence of chronic endurance exercise training on conduit artery retrograde and oscillatory shear in older adults.

With aging, there tends to be an increase in retrograde and oscillatory shear in peripheral conduit arteries of humans. Whether the increase in shear rate is due to the aging process or an effect of a less active lifestyle that often accompanies aging is unknown. Therefore, we examined whether chronic endurance exercise training attenuates conduit artery retrograde and oscillatory shear in older adults. Brachial and common femoral artery mean blood velocities and diameter were determined via Doppler ultrasound under resting conditions, and shear rate was calculated in 13 young (24±2years), 17 older untrained (66±3years), and 16 older endurance exercise-trained adults (66±7years). Brachial artery retrograde (-9.1±6.4 vs. -12.6±9.4s(-1); P=0.35) and oscillatory (0.14±0.08 vs. 0.14±0.08 arbitrary units; P=0.99) shear were similar between the older trained and untrained groups, whereas brachial artery retrograde and oscillatory shear were greater in older untrained compared to young adults (-5.0±3.4, 0.08±0.05s(-1) arbitrary units, P=0.017 and 0.048, respectively). There was no difference between the young and older trained brachial retrograde (P=0.29) and oscillatory (P=0.07) shear. Common femoral artery retrograde (-6.3±2.9s(-1)) and oscillatory (0.21±0.08 arbitrary units) shear were reduced in older trained compared to the older untrained group (-10.4±4.1 and 0.30±0.09s(-1) arbitrary units, both P=0.005 and 0.006, respectively), yet similar to young adults (-7.1±3.5 and 0.19±0.06s(-1) arbitrary units, P=0.81 and 0.87, respectively). Our results suggest that chronic endurance exercise training in older adults ameliorates retrograde and oscillatory shear rate patterns, particularly in the common femoral artery.

Long Term Endurance Exercise Training Ameliorates Conduit Artery Retrograde and Oscillatory Shear in Older Adults

With aging, there tends to be an increase in retrograde and oscillatory shear in peripheral conduit arteries of humans. Whether the increase in shear rate is due to the aging process or an effect of a less than active lifestyle that often accompanies aging is unknown. Therefore, in a cross‐sectional study we evaluated whether chronic endurance exercise training attenuates retrograde and oscillatory shear in older adults. Brachial and common femoral artery mean blood velocities and diameter were determined via Doppler ultrasound under resting conditions in 13 young (Y = 24 ± 1 years), 17 older untrained (OU = 66 ± 1 years), and 16 older endurance exercise trained adults (OT = 66 ± 2 years). Mean shear rate (s−1) was defined as 4·Vm/D, where Vm is mean blood velocity (cm · s−1) and D is arterial diameter (cm). For calculations of antegrade and retrograde shear rate, antegrade and retrograde mean blood velocities were used, respectively. Oscillatory shear index is an indicator of the magnitude of oscillation between antegrade and retrograde shear. Vascular resistance in the forearm and leg were also calculated (mean arterial pressure/blood flow) using each respective limb blood flow and mean arterial pressure derived from beat‐to‐beat finger plethysmography measurements. Brachial artery retrograde (−9.1 ± 1.7 vs. −12.6 ± 2.3 s−1; P = 0.35) and oscillatory (0.14 ± 0.02 vs. 0.14 ± 0.02 arbitrary units; P = 0.99) shear were similar between the OT and OU groups, whereas brachial retrograde and oscillatory shear were greater in OU compared to Y adults (−5.0 ± 0.9 s−1, 0.08 ± 0.01 arbitrary units, both P &lt; 0.05; respectively). There was no difference between the Y and OT brachial artery retrograde (P = 0.29) and oscillatory (P = 0.07) shear. Common femoral artery retrograde (−6.3 ± 0.7 s−1) and oscillatory (0.21 ± 0.02 arbitrary units) shear was reduced in OT compared to the OU group (−10.4 ± 1.0 s−1 and 0.30 ± 0.02 arbitrary units, both P &lt; 0.05; respectively), yet similar to Y adults (−7.1 ± 1.0 s−1 and 0.19 ± 0.02 arbitrary units, P = 0.81 and 0.87; respectively). Vascular resistance did not differ between groups in the arm (P = 0.56) or the leg (P = 0.32). However, vascular resistance was inversely related to retrograde shear in the brachial and common femoral artery (r = −0.33 and −0.37, both P &lt; 0.05; respectively) and positively related to oscillatory shear in the brachial and common femoral artery (r = 0.46 and 0.54, both P &lt; 0.05; respectively) when all subjects were pooled together. Our results suggest that chronic endurance exercise training in older adults ameliorates retrograde and oscillatory shear rate patterns, particularly in the common femoral artery.Support or Funding InformationResearch was supported by NIH HL‐105467 (DPC)

Chronic Endurance Exercise Training Preserves Contraction‐Induced Rapid Vasodilation in Older Adults

Aging is associated with attenuated exercise hyperemia and vasodilation after a single skeletal muscle contraction, as well as during steady state exercise. Chronic exercise training preserves exercise hyperemia and vasodilation in older adults during steady‐state exercise; however, whether chronic exercise training ameliorates the attenuated rapid vasodilator response to a single skeletal muscle contraction in older adults is currently unknown. Therefore, the purpose of this study was to examine the impact of chronic exercise training on rapid vasodilator responses in older adults, as well as investigate the relationship between exercise capacity (VO2peak) and peak vasodilator responses (ΔVCpeak). Young (n = 14; 23±1yr; 9M/5F), older untrained (n = 16; 66±1yr; 10M/6F) and trained older adults (n = 16; 66±2yr; 9M/7F) performed single muscle contractions in the forearm (10%, 20%, and 40% MVC) and leg (20%, 40%, 60% WRmax). Blood flow (ml·min−1) was measured using Doppler ultrasound and vascular conductance was calculated from blood flow and mean arterial pressure (mmHg) and normalized for muscle mass (kg). The peak and total hyperemic and vasodilator responses were greater in trained older adults across leg exercise intensities compared to untrained older adults (P &lt; 0.05), while there were no differences in responses between trained older and young adults (P &gt; 0.05). Within arm intensities, trained older adults exhibited higher ΔVCtotal at 10%, and ΔVCpeak at 40% compared to untrained older adults (P &lt; 0.05).There were no differences for rapid hyperemic and vasodilator responses between trained older adults and young adults at any arm exercise intensity (P &gt; 0.05). VO2peak was moderately associated with ΔVCpeak at moderate and higher leg exercise intensities in older adults (r = 0.46 and 0.55 respectively; P &lt; 0.01) but only at higher exercise intensities in young adults (r = 0.60; P &lt; 0.05). Within the arm, VO2peak was moderately associated with ΔVCpeak across exercise intensities in older adults (10% r = 0.37, 20% r = 0.36, 40% r = 0.36; P &lt; 0.05 for all), but not in young adults (r = −0.062–0.10; P &gt; 0.05). When separated by training status, there were no associations between VO2peak and ΔVCpeak in the arm or leg (P &gt; 0.05). Our data demonstrate that 1) chronic endurance exercise training preserves rapid hyperemic and vasodilator responses within both the arm and leg of trained older adults, such that age related differences in the rapid vasodilator response are abolished; and 2) VO2peak is moderately associated with peak vasodilator responses in the arm and leg of older, but not young adults.Support or Funding InformationFunded by NIH HL‐105467 (DPC) and NIH CTSA U54TR001356

Chronic endurance exercise training offsets the age-related attenuation in contraction-induced rapid vasodilation.

Aging is associated with attenuated contraction-induced rapid onset vasodilation (ROV). We sought to examine whether chronic exercise training would improve ROV in older adults. Additionally, we examined whether a relationship between cardiorespiratory fitness and ROV exists in young and older adults. Chronically exercise-trained older adults (n = 16; 66 ± 2 yr, mean ± SE) performed single muscle contractions in the forearm and leg at various intensities. Brachial and femoral artery diameter and blood velocity were measured using Doppler ultrasound. Vascular conductance (VC) was calculated as the quotient of blood flow (ml/min) and mean arterial pressure (mmHg). These data were compared with our previously published work from an identical protocol in 16 older untrained (66 ± 1 yr, mean ± SE) and 14 young (23 ± 1 yr) adults. Peak (ΔVCpeak) and total vasodilator (VCtotal) responses were greater in trained compared with untrained older adults across leg exercise intensities (P < 0.05). There were no differences in responses between trained older and young adults in the arm or leg at any exercise intensity (P > 0.05). Comparison of ΔVCpeak in a subset of subjects at an absolute workload in the leg revealed that trained older adults exhibited augmented responses relative to untrained older adults. Exercise capacity (V̇o2 peak) was associated with ΔVCpeak and VCtotal across arm (r = 0.59-0.64) and leg exercise intensities (r = 0.55-0.68, P < 0.05) in older adults. Our data demonstrate that 1) chronic exercise training improves ROV in the arm and leg of trained older adults, such that age-related differences in ROV are abolished, and 2) VO2peak is associated with ΔVCpeak responses in both limbs of older adults.

Slower V̇O₂ Kinetics in Older Individuals: Is It Inevitable?

The mechanisms controlling the rate of adjustment of oxidative phosphorylation have been debated for several years. Although disagreement exists as to what the prevailing mechanisms controlling the speed of the oxygen uptake (V̇O₂) kinetics are in both young and older individuals, it seems tenable that the slower V̇O₂ kinetics response typically observed in older adults is at least partly imposed by an O2 delivery limitation. Several studies have demonstrated that different interventions can speed V̇O₂ kinetics in older individuals so that this response can become similar to that observed in their young counterparts. These findings have opened the debate as to whether aging per se, or other factors that accompany aging, is responsible for the slower adjustment of oxidative metabolism in the elderly. This review focuses on the slower V̇O₂ kinetics often observed in older populations and discusses potential mechanisms that might mediate the slower adjustment in oxidative phosphorylation. Furthermore, interventions that have been successful in speeding V̇O₂ kinetics in the elderly are described to discriminate how the controlling factors determining the adjustment of V̇O₂ might be regulated by specific perturbations. Importantly, this review shows that the slower adjustment of oxidative phosphorylation typically seen in older compared with young individuals can be completely abolished in some exceptional situations such as chronic endurance-exercise training, despite the age-related decrease in maximal V̇O₂ still being present. Thus, this review focuses on the concept that although V̇O₂ kinetics is often slower in the elderly, this slower increase in the rise of oxygen uptake during the exercise on-transient does not need to be considered an inevitable response.

Reproductive Dysfunction from the Stress of Exercise Training is not Gender Specific: The "Exercise-Hypogonadal Male Condition".

Investigative studies point to participation in exercise training as having significant detrimental effects upon reproductive hormonal profiles in men. Specifically, men chronically exposed to training for endurance sports exhibit persistently reduced basal (resting-state) free and total testosterone concentrations without concurrent LH elevations. Men displaying these symptoms have been deemed to exhibit the "Exercise-Hypogonadal Male Condition" (EHMC). The exact physiological mechanism inducing the reduction of testosterone in these men is currently unclear, but is postulated to be a dysfunction within the hypothalamic-pituitary-gonadal regulatory axis. The potential exists for the reduced testosterone concentrations within EHMC men to be disruptive and detrimental to some anabolic-androgenic testosterone-dependent physiological processes. Findings, while limited, suggest spermatogenesis problems may exist in some cases; thus, infertility risk in such men is a critical concern. Present evidence suggests the EHMC condition is limited to men who have been persistently involved in chronic endurance exercise training for an extended period of time, and thus is not a highly prevalent occurrence. Nevertheless, it is critical that endocrinologist and fertility clinicians become more aware of the existence of EHMC as a potential problem-diagnosis in their male patients who exercise.

The endurance athletes heart: acute stress and chronic adaptation

The impact of endurance exercise training on the heart has received significant research and clinical attention for well over a century. Despite this, many issues remain controversial and clinical interpretation...