During dynamic exercise, mechanisms controlling the cardiovascular apparatus operate to provide adequate oxygen to fulfill metabolic demand of exercising muscles and to guarantee metabolic end-products washout. Moreover, arterial blood pressure is regulated to maintain adequate perfusion of the vital organs without excessive pressure variations. The autonomic nervous system adjustments are characterized by a parasympathetic withdrawal and a sympathetic activation. In this review, we briefly summarize neural reflexes operating during dynamic exercise. The main focus of the present review will be on the central command, the arterial baroreflex and chemoreflex, and the exercise pressure reflex. The regulation and integration of these reflexes operating during dynamic exercise and their possible role in the pathophysiology of some cardiovascular diseases are also discussed.

Ischemic preconditioning (IPC) has been shown to improve performance of exercises lasting 10–90 s (anaerobic) and more than 90 s (aerobic). However, its effect on repeated sprint performance has been controversial, placebo effect has not been adequately controlled, and nocebo effect has not been avoided. Thus, the IPC effect on repeated sprint performance was investigated using a swimming task and controlling placebo/nocebo effects. Short-distance university swimmers were randomized to two groups. One group (n = 15, 24 ± 1 yr [mean ± SEM]) was exposed to IPC (ischemia cycles lasted 5 min) and control (CT) (no ischemia); another (n = 15, 24 ± 1 yr) to a placebo intervention (SHAM) (ischemia cycles lasted 1 min) and CT. Seven subjects crossed over groups. Subjects were informed IPC and SHAM would improve performance compared with CT and would be harmless despite circulatory occlusion sensations. The swimming task consisted of six 50-m all-out efforts repeated every 3 min. IPC, in contrast with SHAM, reduced worst sprint time (IPC, 35.21 ± 0.73 vs CT, 36.53 ± 0.72 s; P = 0.04) and total sprints time (IPC, 203.7 ± 4.60 vs CT, 206.03 ± 4.57 s; P = 0.02), moreover augmented swimming velocity (IPC, 1.45 ± 0.03 vs CT, 1.44 ± 0.03 m·s−1; P = 0.049). Six of seven subjects who crossed over groups reduced total sprints time with IPC versus SHAM (delta = −3.95 ± 1.49 s, P = 0.09). Both IPC and SHAM did not change blood lactate concentration (P = 0.20) and perceived effort (P = 0.22). IPC enhanced repeated sprint swimming performance in university swimmers, whereas a placebo intervention did not.

Recent studies have reported ischemic preconditioning (IPC) can acutely improve endurance exercise performance in athletes. However, placebo and nocebo effects have not been sufficiently controlled, and the effect on aerobic metabolism parameters that determine endurance performance (e.g., oxygen cost of running, lactate threshold, and maximal oxygen uptake [V˙O2max]) has been equivocal. Thus, we circumvented limitations from previous studies to test the effect of IPC on aerobic metabolism parameters and endurance performance in well-trained runners. Eighteen runners (14 men/4 women) were submitted to three interventions, in random order: IPC; sham intervention (SHAM); and resting control (CT). Subjects were told both IPC and SHAM would improve performance compared to CT (i.e., similar placebo induction), and IPC would be harmless despite circulatory occlusion sensations (i.e., nocebo avoidance). Next, pulmonary ventilation and gas exchange, blood lactate concentration, and perceived effort were measured during a discontinuous incremental test on a treadmill. Then, a supramaximal test was used to verify the V˙O2max and assess endurance performance (i.e., time to exhaustion). Ventilation, oxygen uptake, carbon dioxide output, lactate concentration, and perceived effort were similar among IPC, SHAM, and CT throughout the discontinuous incremental test (P > 0.05). Oxygen cost of running, lactate threshold, and V˙O2max were also similar among interventions (P > 0.05). Time to exhaustion was longer after IPC (mean ± SEM, 165.34 ± 12.34 s) and SHAM (164.38 ± 11.71 s) than CT (143.98 ± 12.09 s; P = 0.02 and 0.03, respectively), but similar between IPC and SHAM (P = 1.00). IPC did not change aerobic metabolism parameters, whereas improved endurance performance. The IPC improvement, however, did not surpass the effect of a placebo intervention.

Being overweight or obese is associated with a higher rate of survival in patients with advanced chronic obstructive pulmonary disease (COPD). This paradoxical relationship indicates that the influence of nutritional status on functional parameters should be further investigated. To investigate the impact of nutritional status on body composition, exercise capacity and respiratory muscle strength in severe chronic obstructive pulmonary disease patients. Thirty-two patients (nine women) were divided into three groups according to their body mass indices (BMI): overweight/obese (25 < or = BMI < or = 34.9 kg/m(2), n=8), normal weight (18.5 < or = BMI < or = 24.9 kg/m(2), n=17) and underweight (BMI <18.5 kg/m(2), n=7). Spirometry, bioelectrical impedance, a six-minute walking distance test and maximal inspiratory and expiratory pressures were assessed. Airway obstruction was similar among the groups (p=0.30); however, overweight/obese patients had a higher fat-free mass (FFM) index [FFMI=FFM/body weight(2) (mean+/-SEM: 17+/-0.3 vs. 15+/-0.3 vs. 14+/-0.5 m/kg(2), p<0.01)], exercise capacity (90+/-8 vs. 79+/-6 vs. 57+/-8 m, p=0.02) and maximal inspiratory pressure (63+/-7 vs. 57+/-5 vs. 35+/-8 % predicted, p=0.03) in comparison to normal weight and underweight patients, respectively. In addition, on backward multiple regression analysis, FFMI was the unique independent predictor of exercise capacity (partial r=0.52, p<0.01). Severe chronic obstructive pulmonary disease (COPD) patients who were overweight or obese had a greater FFM, exercise capacity and inspiratory muscle strength than patients with the same degree of airflow obstruction who were of normal weight or underweight, and higher FFM was independently associated with higher exercise capacity. These characteristics of overweight or obese patients might counteract the drawbacks of excess weight and lead to an improved prognosis in COPD.

Purpose: Some evidence suggests that sedentary women may be more vulnerable to cognitive task-induced mental fatigue. Mental fatigue, in turn, may worse aerobic exercise performance, presumably via increased perceived effort. However, it remains unclear whether acute mental fatigue induction increases perceived effort and worsens endurance performance in high-level professional athletes and whether such effects are influenced by sex. Methods: We studied 30 athletes (15 women and 16 men) in a single-blinded, randomized, controlled and crossover protocol. In separate visits, athletes either performed a 45-min cognitive task (Stroop’s color–word conflict test) to induce mental fatigue or watched a 45-min documentary as control. Then athletes performed a time-to-exhaustion test on a treadmill. Results: Perceptual measures and cognitive performance indicated that the prolonged cognitive task induced a similar mental fatigue state in women and men. Cardiorespiratory and metabolic responses to the TEE did not change with mental fatigue in both sexes. Mental fatigue increased perceived effort during the time-to-exhaustion test, anticipated attainment of maximal effort, and shortened time to exhaustion similarly in women and men (mean ± SE, −27.3 ± 20.9 s for women vs −26.7 ± 15.1 s for men; P = 0.98). Conclusions: The prolonged cognitive task provoked mental fatigue, anticipated attainment of maximal perceived effort, and worsened aerobic performance in professional runners with no sex differences. Although we did not contrasted athletes with nonathletes, our results suggest that being an athlete may somehow prevent women from developing greater mental fatigue and suffering more from its underlying effects compared with men.