Walking with leg blood flow restriction : wide-rigid cuffs vs. narrow-elastic bands

Blood flow restriction (BFR) training is becoming a popular form of exercise. The concept is that light-load exercise performed with BFR elicits similar adaptations achieved with traditional heavy-load exercise. Walking exercise in combination with pressurized wide-rigid (WR) cuffs elicits higher cardiac workload and a vascular dysfunction due presumably to reperfusion injury to the endothelium. In contrast, narrow-elastic (NE) BFR bands may elicit different hemodynamic effects, as the limb is able to increase in diameter with increased blood flow accompanying exercise. Purpose: To compare the acute cardiovascular responses to two distinct forms of BFR training during light-intensity exercise. Methods: 15 young healthy participants (M=9, F=6) performed 5 bouts of 2-minute walking intervals at 0.9 m/s with a 1-minute rest and deflation period between bouts with either WR, NE, or no bands placed on both upper thighs. Cuff pressure was inflated to 160 mmHg in WR cuffs and 300 mmHg in NE bands while no cuffs were used for the control. Beat-by-beat blood pressure and heart rate were measured continuously using finger plethysmography. Blood lactate concentration, rating of perceived exertion (RPE), flow-mediated dilation (index of endothelium-dependent vasodilation), and cardio-ankle vascular index (measure of arterial stiffness) were assessed before and after the walking exercise. Results: At baseline, no significant differences existed in any of the variables between the three conditions. Increases in heart rate were greater (p0.05) in arterial stiffness or endothelial function in all three trials. Conclusion: Use of wide-rigid BFR cuffs result in a marked increase in blood pressure and myocardial oxygen demand compared with narrow-elastic BFR bands, suggesting that narrow-elastic bands present a safer alternative for at-risk populations to perform BFR exercise.Kinesiology and Health Educatio

Impaired Erythropoietin Response to a Single Session of Intermittent Hypoxia in Patients with Type 2 Diabetes

Patients with type 2 diabetes (T2D) exhibit, on average, a 20% decline in maximal oxygen consumption when compared to healthy adults. Hemoglobin mass strongly correlates to maximal oxygen consumption. A reduced total blood volume has been observed in patients with T2D, suggesting that a reduced hemoglobin mass contributes to the decreased maximal oxygen consumption in this population. Hypoxia stimulates the release of erythropoietin (EPO), the hormone regulating red blood cell production. We previously showed that intermittent hypoxia, consisting of alternating short bouts of breathing hypoxic and normoxic air, increases EPO levels. PURPOSE: To determine the effect of a single session of intermittent hypoxia on serum EPO levels and hemoglobin mass in patients with T2D. We hypothesized that a single session of intermittent hypoxia would raise serum EPO levels and lead to an increase in hemoglobin mass in patients with T2D. METHODS: Ten patients with T2D (4 women, age: 53 ± 10 years, body mass index: 36.2 ± 8.5 kg/m2, HbA1c: 7.2 ± 1.2%) were exposed to an intermittent hypoxia protocol consisting of eight 4-min cycles at a targeted oxygen saturation of 80% interspersed with normoxic cycles to resaturation. Air was made hypoxic by titrating nitrogen into a breathing circuit. Pulmonary gas exchange, oxygen saturation, and hemodynamics were continuously measured throughout the protocol. EPO levels were measured before and 4.5 hours after the beginning of the protocol. Hemoglobin mass was assessed via carbon monoxide rebreathing before and seven days following intermittent hypoxia. RESULTS: Intermittent hypoxia lowered oxygen saturation (­­97 ±­ 2 to 81 ± 2%, p\u3c0.01), which resulted from a lower fraction of inspired oxygen (20.8 ±­ 0.1 to 11.1 ± 1.0%, p\u3c0.01). There was no significant change in EPO levels following exposure to intermittent hypoxia (11.9 ± 5.3­ to 12.1 ± 4.3 mU/ml, p=0.83). There was also no change in hemoglobin mass in response to intermittent hypoxia (864 ± 152­ to 850 ± 150 g, p=0.64). Intermittent hypoxia did not affect mean arterial pressure (94 ± 5 to 97 ± 7 mmHg, p=0.18) but increased cardiac output (9.1 ± 2.7 to 9.8 ± 2.8 L/min, p=0.03) due to an increase in heart rate (78 ± 9 to 84 ± 10 bpm, p\u3c0.01). CONCLUSION: A single session of intermittent hypoxia did not increase serum EPO levels or hemoglobin mass in patients with T2D. These findings suggest an impaired EPO response to decreased oxygen levels in patients with T2D, which may contribute to the reduced hemoglobin mass and total blood volume observed in this population

The Influence of Intermittent Hypoxia on Erythropoietin Levels in Older Adults

Few minutes of hypoxia exposure stabilizes hypoxia-inducible factors, resulting in erythropoietin (EPO) gene transcription and production. A brief intermittent hypoxia exposure increased EPO levels in young healthy adults, suggesting that a single session of intermittent hypoxia has the potential to increase oxygen-carrying capacity. PURPOSE: To determine the effect of a single session of intermittent hypoxia on serum EPO levels and hemoglobin mass among older adults. We hypothesized that a single session of intermittent hypoxia would raise serum EPO levels and lead to an increase in hemoglobin mass in older adults. METHODS: Seventeen participants (8 women, age: 54 ± 8 years, height: 177 ± 10 cm, weight: 76 ± 14 kg, BMI: 24 ± 4 kg/m2) were randomly assigned to an intermittent hypoxia group (IH, n=11) or an intermittent normoxia group (IN, n=6). Intermittent hypoxia consisted of eight 4-minute cycles at a targeted arterial oxygen saturation of 80% interspersed with normoxic cycles to resaturation. Air was made hypoxic by titrating nitrogen into the breathing circuit. Intermittent normoxia consisted of the same protocol, but nitrogen was not added to the breathing circuit. Pulmonary gas exchange, arterial oxygen saturation, and hemodynamics were continuously measured throughout both protocols. EPO levels were measured before and 4.5 hours after the beginning of each protocol. Hemoglobin mass was assessed via carbon monoxide rebreathing the day before and seven days following intermittent hypoxia or normoxia. RESULTS: Intermittent hypoxia lowered arterial oxygen saturation (­­98 ±­ 1 to 82 ± 3 %, p\u3c0.01), which resulted in a lower fraction of inspired oxygen (20.8 ±­ 0.1 to 10.9 ± 1.0 %, p\u3c0.01). There was no significant change in EPO levels in either condition (IH:10.4 ±­ 2.9 to 13.3 ± 4.2; IN: 5.6 ±­ 2.4 to 6.5 ± 2.9 mU/ml, main effect for time p=0.12). Similarly, there was no change in hemoglobin mass in response to both conditions (IH: 752 ±­ 189 to 754 ± 189; IN: 858 ± 177 to 879 ± 157 g, main effect for time p=0.87). Intermittent hypoxia did not affect mean arterial pressure (87 ± 15 to 88 ± 14 mmHg, p=0.18) or cardiac output (5.5 ± 1.5 to 5.7 ± 1.5 L/min, p=0.22), but increased heart rate (62 ± 9 to 68 ± 9 bpm, p\u3c0.01). CONCLUSION: A single session of eight 4-minute cycles of intermittent hypoxia did not increase serum EPO levels in older adults

Intermittent Hypoxia Increases Erythropoietin Levels in Healthy Individuals

Few minutes of hypoxic exposure stabilizes hypoxia-inducible factor-1α, resulting in erythropoietin (EPO) gene transcription and production. PURPOSE: The objective of this study was to identify the shortest intermittent hypoxia protocol necessary to increase serum EPO levels in healthy individuals. We hypothesized that two separate intermittent hypoxia protocols would significantly increase EPO levels in healthy individuals. METHODS: A total of seven individuals (4 women and 3 men, age: 28±7 years, height: 177±9 cm, weight: 79.7±18.4 kg) participated in the study. In Experiment 1, the spontaneous EPO changes under normoxia (NORM) and the EPO response to five 4-minute cycles of intermittent hypoxia (IH5) were determined in six individuals. In Experiment 2, the EPO response to eight 4-minute cycles of intermittent hypoxia (IH8) and 120 minutes of continuous hypoxia (CONT) was determined in six individuals. All hypoxic protocols were performed at a targeted arterial oxygen saturation of 80%. Air was made hypoxic by titrating nitrogen into a breathing circuit. Pulmonary gas exchange, arterial oxygen saturation, and hemodynamics obtained by finger plethysmography were continuously monitored throughout all hypoxic protocols. In Experiment 1, EPO levels were measured before, 2.5 and 4.5 hours after the beginning of the IH5 and NORM protocols. In Experiment 2, EPO levels were measured before, 4.5 and 6 hours after the beginning of the IH8 and CONT protocols. RESULTS: There was no significant change in EPO levels in response to normoxia or in response to five cycles of intermittent hypoxia (NORM: 9.5±1.8 to 10.5±1.8, IH5: 11.4±2.3 to 13.4±2.1 mU/ml, main effect for time p=0.35). There was an increase in EPO levels in response to eight cycles of intermittent hypoxia and 120 minutes of continuous hypoxia, with peak levels observed 4.5 hours after the onset of hypoxia (IH8: 11.2±2.0 to 16.7±2.2, CONT: 11.1±3.8 to 19.4±3.8 mU/ml, main effect for time p˂0.01). Eight cycles of intermittent hypoxia increased EPO levels to a similar extent as 120 minutes of continuous hypoxia (main effect for condition p=0.36). Intermittent hypoxia did not affect mean arterial pressure (IH5: 88±7 to 87±7, IH8: 90±7 to 88±7 mmHg, p\u3e0.05). CONCLUSION: Eight 4-minute cycles of intermittent hypoxia represent the shortest protocol to increase serum EPO levels in healthy individuals

Hypoxic Preconditioning Attenuates Ischemia-reperfusion Injury in Older Adults

Sudden restoration of blood flow to an ischemic vessel paradoxically damages endothelial cells. In young healthy adults, ischemic preconditioning, caused by repeated periods of brief ischemia induced by local cuff inflation prior to reperfusion, attenuates endothelial dysfunction following an ischemia-reperfusion injury. However, ischemic preconditioning does not consistently protect against ischemia-reperfusion injury in older adults. Intermittent systemic hypoxemia, induced via brief bouts of breathing low levels of oxygen, attenuates endothelial dysfunction following an ischemia-reperfusion injury in young adults. PURPOSE: To determine whether intermittent hypoxia protects against ischemia-reperfusion injury in older adults. METHODS: Twelve older adults (5 women, age: 57 ± 9 years, height: 173 ± 8 cm, body weight: 75.8 ± 13.4 kg) visited the laboratory on two separate occasions. Endothelium-dependent vasodilation was assessed by brachial artery flow-mediated dilation using a semiautomated diagnostic ultrasound system before and after 20 minutes of upper arm blood flow occlusion to induce an ischemia-reperfusion injury. Blood flow occlusion was preceded by either intermittent hypoxia, consisting of three 4-minute hypoxic cycles at a targeted arterial oxygen saturation of 80% interspersed with 4-minute room air cycles, or intermittent normoxia, consisting of three 4-minute normoxic cycles separated by 4-minute room air cycles. RESULTS: Intermittent hypoxia resulted in an arterial oxygen saturation of 80 ± 2%, which corresponded to oxygen levels of 11.4 ± 0.7%. When preceded by intermittent normoxia, blood flow occlusion reduced flow-mediated dilation by 4.1 ± 2.6% (6.5 ± 1.7 to 2.4 ± 1.7%). In contrast, flow-mediated dilation was reduced by 2.0 ± 1.5% when blood flow occlusion was preceded by intermittent hypoxia (5.6 ± 1.7 to 3.6 ± 2.3%, P = 0.03). When compared to intermittent normoxia, intermittent hypoxia resulted in a greater heart rate (60 ± 10 vs. 68 ± 10 bpm, P \u3c 0.01) but did not affect cardiac output (5.1 ± 1.4 vs. 5.8 ± 1.8 L/min, P = 0.11). CONCLUSION: Hypoxic preconditioning attenuated the reduction in flow-mediated dilation induced by a 20-minute blood flow occlusion in older adults. Thus, exposure to intermittent hypoxia represents a promising strategy to protect against ischemia-reperfusion injury in populations at risk for ischemic events

Discrepancy between cardiorespiratory system and skeletal muscle in elite cyclists after hypoxic training

BACKGROUND: The purpose of this study was to determine the effects of hypoxic training on the cardiorespiratory system and skeletal muscle among well-trained endurance athletes in a randomized cross-over design. METHODS: Eight junior national level competitive cyclists were separated into two groups; Group A trained under normoxic condition (21% O(2)) for 2 hours/day, 3 days/week for 3 weeks while Group B used the same training protocol under hypoxic condition (15% O(2)). After 3 weeks of each initial training condition, five weeks of self-training under usual field conditions intervened before the training condition was switched from NT to HT in Group A, from HT to NT in Group B. The subjects were tested at sea level before and after each training period. O(2 )uptake ([Image: see text] O(2)), blood samples, and muscle deoxygenation were measured during bicycle exercise test. RESULTS AND DISCUSSION: No changes in maximal workload, arterial O(2 )content, [Image: see text] O(2 )at lactate threshold and [Image: see text] O(2max )were observed before or after each training period. In contrast, deoxygenation change during submaximal exercise in the vastus lateralis was significantly higher at HT than NT (p < 0.01). In addition, half time of oxygenation recovery was significantly faster after HT (13.2 ± 2.6 sec) than NT (18.8 ± 2.7 sec) (p < 0.001). CONCLUSIONS: Three weeks of HT may not give an additional performance benefit at sea level for elite competitive cyclists, even though HT may induce some physiological adaptations on muscle tissue level

Defining the Dose of Altitude Training: How High to Live for Optimal Sea Level Performance Enhancement

Defining the dose of altitude training: how high to live for optimal sea level performance enhancement. J Appl Physiol 116: 595-603, 2014. First published October 24, 2013; doi:10.1152/japplphysiol.00634.2013.-Chronic living at altitudes of 2,500 m causes consistent hematological acclimatization in most, but not all, groups of athletes; however, responses of erythropoietin (EPO) and red cell mass to a given altitude show substantial individual variability. We hypothesized that athletes living at higher altitudes would experience greater improvements in sea level performance, secondary to greater hematological acclimatization, compared with athletes living at lower altitudes. After 4 wk of group sea level training and testing, 48 collegiate distance runners (32 men, 16 women) were randomly assigned to one of four living altitudes (1,780, 2,085, 2,454, or 2,800 m). All athletes trained together daily at a common altitude from 1,250-3,000 m following a modified live high-train low model. Subjects completed hematological, metabolic, and performance measures at sea level, before and after altitude training; EPO was assessed at various time points while at altitude. On return from altitude, 3,000-m time trial performance was significantly improved in groups living at the middle two altitudes (2,085 and 2,454 m), but not in groups living at 1,780 and 2,800 m. EPO was significantly higher in all groups at 24 and 48 h, but returned to sea level baseline after 72 h in the 1,780-m group. Erythrocyte volume was significantly higher within all groups after return from altitude and was not different between groups. These data suggest that, when completing a 4-wk altitude camp following the live high-train low model, there is a target altitude between 2,000 and 2,500 m that produces an optimal acclimatization response for sea level performance

Post-exercise hot water immersion induces heat acclimation and improves endurance exercise performance in the heat

We examined whether daily hot water immersion (HWI) after exercise in temperate conditions induces heat acclimation and improves endurance performance in temperate and hot conditions. Seventeen non-heat-acclimatized males performed a 6-day intervention involving a daily treadmill run for 40 min at 65% VO2max in temperate conditions (18 degrees C) followed immediately by either HWI (N = 10; 40 degrees C) or thermoneutral (CON, N = 7; 34 degrees C) immersion for 40 min. Before and after the 6-day intervention, participants performed a treadmill run for 40 min at 65% VO2max followed by a 5-km treadmill time trial (TT) in temperate (18 degrees C, 40% humidity) and hot (33 degrees C, 40% humidity) conditions. HWI induced heat acclimation demonstrated by lower resting rectal temperature (Tre , mean, -0.27 degrees C, P < 0.01), and final Tre during submaximal exercise in 18 degrees C (-0.28 degrees C, P < 0.01) and 33 degrees C (-0.36 degrees C, P < 0.01). Skin temperature, Tre at sweating onset and RPE were lower during submaximal exercise in 18 degrees C and 33 degrees C after 6 days in HWI (P < 0.05). Physiological strain and thermal sensation were also lower during submaximal exercise in 33 degrees C after 6 days in HWI (P < 0.05). HWI improved TT performance in 33 degrees C (4.9%, P < 0.01) but not in 18 degrees C. Thermoregulatory measures and performance did not change in CON. Hot water immersion after exercise on 6 days presents a simple, practical, and effective heat acclimation strategy to improve endurance performance in the heat

Life Satisfaction, Positive Affect, and Sleep Impairment in Masters Athletes: Modulation by Age, Sex, and Exercise Type

ntroduction: The masters athlete has been proposed as a model of successful aging. Research studies investigating psychological outlook in older athletes have primarily addressed negative affects including depression, anxiety, and stress. The impact of lifelong exercise on positive affect and life satisfaction as well as sleep impairment that could impact on these psychological states is largely unknown. Methods: A series of questionnaires (general life satisfaction, positive affect, and sleeprelated impairment) were administered to 240 masters athletes participating in the World Masters Athletics Championships. Total raw scores were converted into T scores for comparison with the general population. Meaningful difference was defined by the PROMISR as one-half standard deviation from the centering sample. Results: Meaningful differences were observed for improved general life satisfaction and reduced sleep impairment for all masters athletes. Positive affect did not reach the meaningful difference threshold. No significant sex differences were found for any of the questionnaires (all p > 0.05). Similarly, no significant differences were found between endurance, sprint, and strength/power sports for general life satisfaction (p = 0.18), positive affect (p = 0.46), and sleep impairment (p = 0.77). In general, life satisfaction increased with age (r = 0.15, p = 0.02), and sleep impairment trended towards reduction with age (r = −0.13, p = 0.05). Positive affect demonstrated no correlation with age (r = 0.09, p = 0.18). Conclusion: This study demonstrates that the lifestyles of masters athletes contribute to improved general life satisfaction and reduced sleep impairment but not improved positive affect. The beneficial effects were observed irrespective of age, gender, and sporting type