This study aimed to elucidate whether muscle blood flow restriction during maximal exercise is associated with alterations in hemodynamics, cerebral oxygenation, cerebral activation, and deterioration of exercise performance in male participants. Thirteen healthy males, cyclists (age 33 ± 2 yrs., body mass: 78.6 ± 2.5 kg, and body mass index: 25.57 ± 0.91 kg·m⁻¹), performed a maximal incremental exercise test on a bicycle ergometer in two experimental conditions: (a) with muscle blood flow restriction through the application of thigh cuffs inflated at 120 mmHg (with cuffs, WC) and (b) without restriction (no cuffs, NC). Exercise performance significantly deteriorated with muscle blood flow restriction, as evidenced by the reductions in $\dot{V}$O_2max (−17 ± 2%, p < 0.001), peak power output (−28 ± 2%, p < 0.001), and time to exhaustion (−28 ± 2%, p < 0.001). Muscle oxygenated hemoglobin (Δ[O₂Hb]) during exercise declined more in the NC condition (p < 0.01); however, at exhaustion, the magnitude of muscle oxygenation and muscle deoxygenation were similar between conditions (p > 0.05). At maximal effort, lower cerebral deoxygenated hemoglobin (Δ[HHb]) and cerebral total hemoglobin (Δ[THb]) were observed in WC (p < 0.001), accompanied by a lower cardiac output, heart rate, and stroke volume vs. the NC condition (p < 0.01), whereas systolic blood pressure, rating of perceived exertion, and cerebral activation (as assessed by electroencephalography (EEG) activity) were similar (p > 0.05) between conditions at task failure, despite marked differences in exercise duration, maximal aerobic power output, and $\dot{V}$O_2max. In conclusion, in trained cyclists, muscle blood flow restriction during an incremental cycling exercise test significantly limited exercise performance. Exercise intolerance with muscle blood flow restriction was mainly associated with attenuated cardiac responses, despite cerebral activation reaching similar maximal levels as without muscle blood flow restriction.

This study tested the hypothesis that muscle blood flow restriction reduces muscle and cerebral oxygenation at rest. In 26 healthy males, aged 33 ± 2 yrs, physiological variables were continuously recorded during a 10-min period in 2 experimental conditions: a) with muscle blood flow restriction through thigh cuffs application inflated at 120 mm Hg (With Cuffs, WC) and b) without restriction (No Cuffs, NC). Muscle and cerebral oxygenation were reduced by muscle blood flow restriction as suggested by the increase in both muscle and cerebral deoxygenated hemoglobin (Δ[HHb]; p < 0.01) and the decrease of muscle and cerebral oxygenation index (Δ[HbDiff]; p < 0.01). Hemodynamic responses were not affected by such muscle blood flow restriction, whereas baroreflex sensitivity was reduced (p = 0.009). The perception of leg discomfort was higher (p < 0.001) in the WC than in the NC condition. This study suggests that thigh cuffs application inflated at 120 mm Hg is an effective method to reduce muscle oxygenation at rest. These changes at the muscular level seem to be sensed by the central nervous system, evoking alterations in cerebral oxygenation and baroreflex sensitivity. Novelty: Thigh cuffs application inflated at 120 mm Hg effectively reduces muscle oxygenation at rest. Limiting muscle oxygenation appears to reduce cerebral oxygenation, and baroreflex sensitivity, at rest. Even in healthy subjects, limiting muscle oxygenation, at rest, affects neural integration.

Purpose: Integrated physiological responses during maximal whole-body exercise, such as cycling, under additive hypoxemia (anemia + hypoxia) are not adequately studied. Therefore, we investigated cardiovascular, muscular and cerebral oxygenation responses in chronic mildly iron-deficient and control women under normoxic and moderate hypoxic conditions during maximal whole-body exercise. Methods: In a randomized and counterbalanced order, 16 females performed incremental exercise to exhaustion under normoxia (N; FIO ₂ :20.94%) and hypoxia (H; FIO ₂ :13.6%). The participants were divided into two groups matched for age and anthropometric characteristics, but intentionally varying in [Hb] ( p < 0.001) and V̇O _2max ( p < 0.01); iron-deficient (A; n = 8; [Hb]:11.3 ± 0.4 g/dl; V̇O _2max :37.3 ± 2.8 ml/kg/min) and healthy controls (C; n = 8; [Hb]:13.3 ± 0.4 g/dl; V̇O _2max :40.8 ± 1.9 ml/kg/min). Results: During exercise in hypoxia compared to normoxia, the A exhibited greater decrement in V̇O _2max (5.0%; p = 0.02) and peak power output (5.4%; p = 0.004) than C. Maximal mean arterial pressure was reduced ( p < 0.05) due to lower total peripheral resistance ( p < 0.05) and unchanged maximal cardiac output ( p > 0.05). Enhanced O ₂ utilization under H was observed only in C, based on ΔHHb ( p < 0.05). Cerebral oxygenation was reduced linearly with CaO ₂ ( r = 0.95, p < 0.001). Conclusion: Collectively, moderate hypoxia induced greater reduction of V̇O _2max , peak power output and cerebral oxygenation leading to exercise intolerance in A compared to C. These responses were accompanied by an inability of skeletal muscle to increase O ₂ utilization at maximal effort in H and by a failure of the cardiovascular system to compensate and counteract convective and diffusion limitations during maximal whole-body exercise in anemic women.

The effects of two short‐haul air travel (SHAT) of different durations on sport‐specific performance, sleep, and psychophysiological indices in highly trained football players were examined. Nineteen participants completed, in a randomized order, two simulated SHAT, 1 week apart, each lasting 4 h and 2 h, followed by a control condition (CON). Generic (10‐m sprint, repeated sprint ability; RSA, countermovement jump; CMJ), sport‐specific performance (Hoff Test, Loughborough Soccer Passing Test; LSPT), and psychophysiological responses (sleep, heart rate variability [HRV], salivary cortisol and immunoglobulin‐A [sIgA], and perceptual recovery) were evaluated before (Baseline) and after each condition. Compared to Baseline, RSA and 10‐m sprint declined by 3.5% and 6%, respectively, on the day after travel (D + 1) ( p < 0.001 and p < 0.01). Likewise, CMJ and total distance covered during the Hoff test decreased by 5.5% at D + 1 ( p < 0.001). LSPT performance decreased only after the 4 h flight ( p < 0.05). Total sleep time was reduced the night before SHAT ( p < 0.001) compared to Baseline. sIgA was reduced on the day of the travel (DT) and D + 1 after both SHAT, while HRV was decreased at DT only after the 4 h SHAT ( p < 0.05). Mood states remained unaffected by travel, regardless of duration. We currently suggest that short‐haul air travel, whether 4 or 2 h, induces psychophysiological perturbations and performance deterioration, likely due to the travel restrictive conditions and the inadequate sleep obtained the night before the flight. Since both flights were conducted early in the morning, more research is warranted to investigate the role of departure time on football performance.

We examined the effects of carbohydrate ingestion on endurance performance and fatigue during a soccer simulation in adolescent soccer players and evaluated the protocol’s reliability. Nine (13.5 ± 0.4 years pre-PHV) soccer players performed two soccer simulation intermittent exercise sessions on the treadmill (60 min) while consuming 4 boluses of either a CHO or PLC beverage in random, counterbalanced order. Before and immediately after each exercise session, MVC was measured for the quadriceps and the hand. Participants also performed a TTE on a cycle ergometer on three occasions, after each simulation exercise session (CHO and PLC), and on another day in a rested state (CON). The simulation protocol produced an ICC of 0.96 ([0.77–0.98 95%CI], p = 0.01) for VO₂, with 2.24%CV between trials, suggesting strong reliability. TTE was higher (p = 0.01) in the CHO condition (123 ± 33 s) compared to PLC (85 ± 5 s) by 29%. The relative reduction in MVC_LEG was more pronounced in the PLC (22 ± 11%) condition than in CHO (14 ± 6%) (p = 0.05). Compared to the PLC, CHO resulted in lower RPE_local during the second half of the simulation protocol (p < 0.05). Carbohydrate ingestion can improve endurance performance and reduce peripheral fatigue during a reliable soccer simulation that resembles the physiological demands of a youth soccer match.

Background/Objective: Temperature regulation is impaired in iron deficient anemic humans and rats at rest during cold exposure. However, there is a paucity of data regarding the interplay of cold exposure, anemia and exercise on thermal and cardiovascular responses. Therefore, we aimed to explore thermal and cardiovascular responses of individuals with chronic mild iron deficient anemia during exercise in the cold compared to controls. Methods: Nine anemic (5 F, 4 M) and 9 control (5 F, 4 M) individuals, matched for body fat, size, mass but different by design in hematological parameters and physical fitness, participated in the study. The participants cycled in cold (11 °C, 40% RH) and neutral (22 °C, 40% RH) conditions at an intensity ~10% below the respiratory threshold until 1 °C increase in Tre or 1h exercise, whichever occurred first. Results: In the cold, the anemic individuals showed a lower rate of Tre rise compared to controls (p=0.047) and only controls increased heat production (V̇O2) compared to the neutral condition (p=0.035). Moreover, in the cold, the anemic group exhibited lower Tsk than controls (p=0.03) and exaggerated blood pressure response compared to the neutral environment (p<0.05) due to heightened total peripheral resistance (p<0.05) and vasomotor response (p<0.001). Conclusions: In summary, chronic mild iron deficient anemia impaired temperature regulation as judged from the lower rate of Tre rise and an inability to activate further the metabolism at cold. Concomitantly, the anemic participants demonstrated increased cardiovascular strain. This is notable because anemia and these environmental conditions are encountered in the workplace, recreational activities and athletic endeavors.