Walk training with blood flow occlusion (OCC-walk) leads to muscle hypertrophy; however, cardiorespiratory endurance in response to OCC-walk is unknown. Ischemia enhances the adaptation to endurance training such as increased maximal oxygen uptake (VO₂(max)) and muscle glycogen content. Thus, we investigated the effects of an OCC-walk on cardiorespiratory endurance, anaerobic power, and muscle strength in elite athletes. College basketball players participated in walk training with (n = 7) and without (n = 5) blood flow occlusion. Five sets of a 3-min walk (4-6 km/h at 5% grade) and a 1-min rest between the walks were performed twice a day, 6 days a week for 2 weeks. Two-way ANOVA with repeated measures (groups x time) was utilized (P < 0.05). Interactions were found in VO₂(max) (P = 0.011) and maximal minute ventilation (VE(max); P = 0.019). VO₂(max) (11.6%) and VE(max) (10.6%) were increased following the OCC-walk. For the cardiovascular adaptations of the OCC-walk, hemodynamic parameters such as stroke volume (SV) and heart rate (HR) at rest and during OCC-walk were compared between the first and the last OCC-walk sessions. Although no change in hemodynamics was found at rest, during the last OCC-walk session SV was increased in all five sets (21.4%) and HR was decreased in the third (12.3%) and fifth (15.0%) sets. With anaerobic power an interaction was found in anaerobic capacity (P = 0.038) but not in peak power. Anaerobic capacity (2.5%) was increased following the OCC-walk. No interaction was found in muscle strength. In conclusion, the 2-week OCC-walk significantly increases VO₂(max) and VE(max) in athletes. The OCC-walk training might be used in the rehabilitation for athletes who intend to maintain or improve endurance.

. Arterial baroreflex alters strength and mechanisms of muscle metaboreflex during dynamic exercise. Am J Physiol Heart Circ Physiol 288: H1374 -H1380, 2005. First published November 11, 2004; doi:10.1152/ajpheart.01040. 2004.-Previous studies showed that the arterial baroreflex opposes the pressor response mediated by muscle metaboreflex activation during mild dynamic exercise. However, no studies have investigated the mechanisms contributing to metaboreflex-mediated pressor responses during dynamic exercise after arterial baroreceptor denervation. Therefore, we investigated the contribution of cardiac output (CO) and peripheral vasoconstriction in mediating the pressor response to graded reductions in hindlimb perfusion in conscious, chronically instrumented dogs before and after sinoaortic denervation (SAD) during mild and moderate exercise. In control experiments, the metaboreflex pressor responses were mediated via increases in CO. After SAD, the metaboreflex pressor responses were significantly greater and significantly smaller increases in CO occurred. During control experiments, nonischemic vascular conductance (NIVC) did not change with muscle metaboreflex activation, whereas after SAD NIVC significantly decreased with metaboreflex activation; thus SAD shifted the mechanisms of the muscle metaboreflex from mainly increases in CO to combined cardiac and peripheral vasoconstrictor responses. We conclude that the major mechanism by which the arterial baroreflex buffers the muscle metaboreflex is inhibition of metaboreflex-mediated peripheral vasoconstriction. sinoaortic denervation; cardiac output; pressor response THE MUSCLE METABOREFLEX is activated when intramuscular metabolites accumulate because of a mismatch between blood flow and metabolism, and this accumulation stimulates group III and IV afferent neurons within the active muscle. Activation of these nerves transmits signals to the brain stem, which elicits a reflex increase in sympathetic nerve activity and systemic arterial blood pressure (10,11,27). The reflex acts to partially restore blood flow to the hypoperfused muscle (22). This muscle metaboreflex mediated-pressor response is attributable to increases in cardiac output (CO) and peripheral vasoconstriction (12,18,39).Previous studies showed that during mild to moderate exercise the pressor response primarily depends on increased CO to improve the ischemic condition in active skeletal muscles (16,18,39). If a reduction in blood flow to active skeletal muscle occurs when there is sufficient cardiac reserve during mild to moderate exercise, the metaboreflex will increase CO and thus the total amount of blood flow available to active skeletal muscle. O'Leary and Augustyniak (18) demonstrated that activation of the muscle metaboreflex in conscious dogs during dynamic exercise produced significant increases in CO via the reflex tachycardia with constant stroke volume (SV), and this was the major mechanism causing the reflex increase in arterial pressure. However, when CO is at or near maximal l...

When oxygen delivery to active skeletal muscle is insufficient for the metabolic demands, afferent nerves within muscles are activated, which elicit reflex increases in heart rate (HR), cardiac output (CO), and arterial pressure (AP), termed the muscle metaboreflex (MMR). To what extent the increases in CO are the result of increased ventricular contractility is unclear. A widely accepted index of contractility is maximal left ventricular elastance (Emax), the slope of the end-systolic pressure-volume relationship, such as during rapidly imposed reductions in preload. The objective of the present study was to determine whether MMR activation elicits increases in Emax. Experiments were performed using conscious dogs chronically instrumented to measure left ventricular pressure and volume at rest and during mild or moderate treadmill exercise with and without partial hindlimb ischemia to elicit MMR responses. At both workloads, MMR activation significantly increased CO, HR, AP, and maximum rate of change of left ventricular pressure. During both mild and moderate exercise, MMR activation increased Emax to 159.6 Ϯ 8.83 and 155.8 Ϯ 6.32% of the exercise value under free-flow conditions, respectively. We conclude that the increase of ventricular elastance associated with MMR activation indicates that a substantial increase in ventricular contractility contributes to the rise in CO during dynamic exercise. elastance; pressor response; cardiac function DURING DYNAMIC EXERCISE, when oxygen delivery to active skeletal muscle is insufficient to meet the metabolic demands, metabolites (e.g., lactic acid, adenosine, potassium, diprotonated phosphate, H ϩ , arachidonic acid products, and others) accumulate within the active muscle and stimulate group III and IV afferent neurons. These sensory neurons project to the central nervous system, eliciting a reflex pressor response consisting of increases in efferent sympathetic nerve activity (SNA), mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), plasma levels of vasoactive hormones, and peripheral vasoconstriction termed the muscle metaboreflex (MMR) (1, 2, 8, 12, 14, 19, 21, 25-28, 30, 32, 33, 35-38, 42, 44). These mechanisms act in concert to partially restore blood flow and arterial oxygen delivery to the hypoperfused muscles (27,31). Previous studies have shown that in normal dogs exercising at mild and moderate workloads, the increases in MAP elicited by this MMR activation are mainly due to increases in CO. The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (26, 35). In this way the MMR-induced increases in ventricular performance act to sustain or slightly increase stroke volume (SV) despite decreases in ventricular filling time due to the reflex tachycardia (2, 26, 44). Furthermore, O'Leary an Augustyniak (26) showed that in normal dogs in which HR was fixed at 225 beats/min during mild exercise, MMR activation caused such a rise in SV that the increases in CO were approximately equal to t...

. Attenuated arterial baroreflex buffering of muscle metaboreflex in heart failure. Am J Physiol Heart Circ Physiol 289: H2416 -H2423, 2005. First published July 29, 2005; doi:10.1152/ajpheart.00654.2005.-Previous studies have shown that heart failure (HF) or sinoaortic denervation (SAD) alters the strength and mechanisms of the muscle metaboreflex during dynamic exercise. However, it is still unknown to what extent SAD may modify the muscle metaboreflex in HF. Therefore, we quantified the contribution of cardiac output (CO) and peripheral vasoconstriction to metaboreflex-mediated increases in mean arterial blood pressure (MAP) in conscious, chronically instrumented dogs before and after induction of HF in both barointact and SAD conditions during mild and moderate exercise. The muscle metaboreflex was activated via partial reductions in hindlimb blood flow. After SAD, the metaboreflex pressor responses were significantly higher with respect to the barointact condition despite lower CO responses. The pressor response was significantly lower in HF after SAD but still higher than that of HF in the barointact condition. During control experiments in the barointact condition, total vascular conductance summed from all beds except the hindlimbs did not change with muscle metaboreflex activation, whereas in the SAD condition both before and after induction of HF significant vasoconstriction occurred. We conclude that SAD substantially increased the contribution of peripheral vasoconstriction to metaboreflex-induced increases in MAP, whereas in HF SAD did not markedly alter the patterns of the reflex responses, likely reflecting that in HF the ability of the arterial baroreflex to buffer metaboreflex responses is impaired. sinoaortic denervation; exercise; cardiac output; arterial baroreflex; exercise pressor response DURING DYNAMIC EXERCISE, group III and IV afferent neurons within the active skeletal muscle are stimulated when metabolites accumulate because of a decrease in the ratio of oxygen supply to oxygen demand. These sensory neurons relay information to the central nervous system and elicit a powerful pressor response termed the muscle metaboreflex (8,12,21,27). Activation of the muscle metaboreflex during mild to moderate exercise elicits increases in heart rate (HR), cardiac output (CO), mean arterial blood pressure (MAP), ventricular performance, central blood volume mobilization, and vasoconstriction in the renal and nonischemic skeletal muscle vasculature (6, 13, 18 -21, 28, 34). The major mechanism mediating the rise in MAP during submaximal dynamic exercise in normal dogs is the large increase in CO, which thereby partially restores blood flow and O 2 delivery to the ischemic active skeletal muscle (6,18,20,25,28,34). The large pressor response arising from stimulation of skeletal muscle afferents is opposed by the arterial baroreflex (11, 29, 33). Our laboratory recently demonstrated (11) that the restraint of the muscle metaboreflex pressor response by the arterial baroreflex occurs mainly via baroref...

DS. Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise. Am J Physiol Heart Circ Physiol 292: H2159 -H2166, 2007. First published December 22, 2006; doi:10.1152/ajpheart.01240.2006.-Underperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex (MMR). In normal dogs during mild exercise, MMR activation causes large increases in cardiac output (CO) and mean arterial pressure (MAP); however, in heart failure (HF) although MAP increases, the rise in CO is virtually abolished, which may be due to an impaired ability to increase left ventricular contractility (LVC). The objective of the present study was to determine whether the increases in LVC seen with MMR activation during dynamic exercise in normal animals are abolished in HF. Conscious dogs were chronically instrumented to measure CO, MAP, and left ventricular (LV) pressure and volume. LVC was calculated from pressure-volume loop analysis [LV maximal elastance (E max) and preload-recruitable stroke work (PRSW)] at rest and during mild and moderate exercise under free-flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) before and after rapid ventricular pacing-induced HF. In control experiments, MMR activation at both workloads [mild exercise (3.2 km/h) and moderate exercise (6.4 km/h at 10% grade)] significantly increased CO, E max, and PRSW. In contrast, after HF was induced, CO, Emax, and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, E max and PRSW did not change. In addition, MMR activation caused no significant change in CO, E max, or PRSW at either workload. We conclude that MMR causes large increases in LVC in normal animals but that this ability is abolished in HF. pressor response; elastance; preload recruitable stroke work WHEN EXERCISING SKELETAL MUSCLE does not receive sufficient blood flow to meet the ongoing metabolic demands, by-products of metabolism such as lactic acid, H ϩ , adenosine, potassium, diprotonated phosphate, and arachidonic acid products, among others, accumulate within the muscle and stimulate group III and IV afferent neurons, which evokes a reflex response known as the muscle metaboreflex (MMR). This reflex response consists of increases in efferent sympathetic nerve activity (SNA) and mean arterial pressure (MAP) (1, 3, 11, 17, 18, 24, 31-35, 39, 40, 43, 46, 47, 52, 53). In addition, MMR activation causes increases in cardiac output (CO), heart rate (HR), and plasma levels of vasoactive hormones and produces vasoconstriction in the renal and the nonischemic active skeletal muscle vasculature to partially restore arterial O 2 delivery and blood flow to the hypoperfused muscles (25,33,36). The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (32,42,43). By this means the MMR-induced increases in ventricular performance act to slightly increase or sustain stroke volume (SV) despite decreas...

BackgroundRecently, breast cancer incidence and prevalence has been increasing. Patients' health related quality of life is important considerations in the treatment of breast cancer. The EQ-5D-3L is one of most popular instruments to measure health related quality of life. This study was aimed to evaluate the validity and reliability of EQ-5D-3L in post-operative breast cancer patients from Korea.MethodsA total of 827 patients visiting the ambulatory cancer center of 1 tertiary hospital after breast cancer surgery self-administered the EQ-5D-3L and Functional Assessment of Cancer Therapy-Breast Cancer (FACT-B). We evaluated known-group validity using differences in the EQ-5D-3L index and EQ-VAS score according to demographic and clinical data. The discriminatory ability of the EQ-5D-3L was determined by comparing the mean FACT-B subscale scores between subjects with no problems and subjects with moderate or severe problems in each EQ-5D-3L dimension. Construct validity was evaluated by Pearson correlation coefficients among the EQ-5D-3L index and FACT-B subscales, respectively. Reliability was assessed in terms of test-retest reliability using Cohen’s kappa value and intra-class correlation coefficient (ICC).ResultsThe EQ-5D-3L index and EQ-VAS score were higher in the educated, current radiotherapy and unmarried groups. The correlation of EQ-5D-3L index and subscales for the FACT-B was highest in physical well-being (r = 0.553) and lowest in social well-being (r = 0.199). For reliability, the Kappa values’ range was from 0.32 to 0.70, and ICCs of the EQ-5D-3L index and EQ-VAS scores were 0.70 and 0.48, respectively.ConclusionsThis study indicated that the EQ-5D-3L could be a valid health related quality of life instrument for postoperative breast cancer patients.

This study determined whether an elevated muscle metaboreflex contributes to the excessive blood pressure response to exercise in postmenopausal women. Thirty healthy female volunteers were studied (15 postmenopausal and 15 premenopausal). Stroke volume, heart rate, cardiac output (CO), systolic blood pressure, diastolic blood pressure, and total vascular conductance (TVC) were continuously assessed throughout the experiment. To activate the muscle metaboreflex, occlusion of the vasculature was induced via inflation of a blood pressure cuff (2 min) on the upper arm following static handgrip exercise. Muscle metaboreflex activation increased mean arterial pressure (MAP) in both groups. However, this pressor response was greater in the postmenopausal women (ΔMAP: 21.4 ± 3 vs. 14.5 ± 2 mmHg) (P < 0.05) even though the corresponding increase in CO was less (ΔCO: 0.0 ± 0.2 vs. 0.3 ± 0.2 l/min) (P < 0.05). TVC decreased in both the groups but was more pronounced in the postmenopausal group (ΔTVC: -10.7 ± 2.6 vs. -17.1 ± 3.6 ml/min/mmHg) (P < 0.05). In conclusion, the exaggerated blood pressure response to exercise in postmenopausal women is mediated, in part, by an overactive metaboreflex that is associated with enhanced peripheral vasoconstriction.

While acute treatment with beetroot juice (BRJ) containing nitrate (NO3 (-)) can lower systolic blood pressure (SBP), afterload, and myocardial O2 demand during submaximal exercise, effects of chronic supplementation with BRJ (containing a relatively low dose of NO3 (-), 400 mg) on cardiac output (CO), SBP, total peripheral resistance (TPR), and the work of the heart in response to dynamic exercise are not known. Thus, in 14 healthy males (22 ± 1 yr), we compared effects of 15 days of both BRJ and nitrate-depleted beetroot juice (NDBRJ) supplementation on plasma concentrations of NOx (NO3 (-)/NO2 (-)), SBP, diastolic blood pressure (DBP), mean arterial pressure (MAP), CO, TPR, and rate pressure product (RPP) at rest and during progressive cycling exercise. Endothelial function was also assessed via flow-mediated dilation (FMD). BRJ supplementation increased plasma NOx from 83.8 ± 13.8 to 167.6 ± 13.2 μM. Compared with NDBRJ, BRJ reduced SBP, DBP, MAP, and TPR at rest and during exercise (P < 0.05). In addition, RPP was decreased during exercise, while CO was increased, but only at rest and the 30% workload (P < 0.05). BRJ enhanced FMD-induced increases in brachial artery diameter (pre: 12.3 ± 1.6%; post: 17.8 ± 1.9%). We conclude that 1) chronic supplementation with BRJ lowers blood pressure and vascular resistance at rest and during exercise and attenuates RPP during exercise and 2) these effects may be due, in part, to enhanced endothelium-induced vasodilation in contracting skeletal muscle. Findings suggest that BRJ can act as a dietary nutraceutical capable of enhancing O2 delivery and reducing work of the heart, such that exercise can be performed at a given workload for a longer period of time before the onset of fatigue.