Concurrent improvements in muscular strength and aerobic capacity by a single mode of exercise have been achieved after high-intensity, long-duration exercise training. For example, recumbent stepper training (75% of maximal heart rate reserve) improved maximal oxygen uptake (V[O.sub.2max]) and muscle strength in middle-aged adults (Hass et al., 2001). Furthermore, high-intensity (90% of V[O.sub.2max]) interval cycle training increased V[O.sub.2max] and isokinetic knee joint strength (Tabata et al., 1990). While significant improvements in muscular strength were observed in these studies, neither demonstrated significant muscular enlargement, leading to the conclusion that the increased strength was due mainly to neural adaptations. In contrast, low-intensity walk training (50 m x [min.sup.-1]) combined with leg blood flow reduction (BFR) results in both thigh muscle hypertrophy and increased muscular strength in young (Abe et al., 2006) and elderly (Abe et al., 2010) individuals. What remains to understand is if low-intensity walk training with BFR, which elicits muscle enlargement (unlike the studies reviewed), would also impact the metabolic and cardiovascular responses to continuous exercise leading to predictive conclusions about training effects on V[O.sub.2max].
The novelty of BFR appears to be the unique combination of venous blood volume pooling and restricted arterial blood inflow. While this clearly impacts the active muscle(s), this vascular occlusion and BFR would certainly impact venous return and the cardiovascular response to exercise. Further, the combination of BFR with low-intensity resistance exercise appears to alter muscle activation patterns and increase the apparent intensity of exercise (Yasuda et al., 2008; 2009) such that 20% one-repetition maximal (1-RM) intensity exercise in combination with BFR approximates muscle activation patterns observed during 60-70% 1-RM training without external compression and BFR. We concluded that apparent altered exercise intensity is the basis for the observed adaptations in muscle mass and muscular strength with minimal external loading and which are equivalent to those observed at higher training intensities (e.g. 60-70% 1RM; Abe et al., 2005; Fujita et al., 2008; Takarada et al., 2000). Hence, the present question includes whether BFR alters the apparent exercise intensity, and therefore the metabolic demand, of continuous exercise (e.g. walking, cycling, etc) as observed with resistance exercise. Indeed in a previous study (Abe et al., 2006) we reported significantly greater V[O.sub.2] (14%) and HR (20%) during low-intensity walking with BFR than that observed without BFR which indicate a greater metabolic demand. However, it is unknown whether the relationship between exercise intensity, metabolic demand and cardiovascular response is altered by BFR. Therefore, the purpose of the present study was to examine the metabolic (V[O.sub.2]) and cardiovascular responses to continuous exercise on a cycle ergometer with BFR at varying intensity of exercise (%V[O.sub.2max]) to ascertain if BFR alter the apparent intensity and metabolic demand of exercise.
Ten healthy young males volunteered to participate in the study. All subjects were habitually participating in recreational sports and exercise at the university. The subjects were informed of the procedures, risks, and benefits, and signed an informed consent documents before participation. The study was conducted according to the Declaration of Helsinki and was approved by the Ethics Committee for Human Experiments of the University of Tokyo, Japan.
Two weeks prior to the study V[O.sub.2max] was determined in all subjects. Subjects then participated in two cycle ergometer exercise tests with and without BFR in random order on separate days (one day between trials). The subjects reported to the laboratory in the morning (8:00-9:00 am) after a 12 hr fast. Subjects were instrumented and rested in the seated position. Following 30-min of rest respiratory and cardiovascular data was collected. Immediately following the resting measurements, subjects performed exercise at 20%, 40%, and 60% of V[O.sub.2max]. Exercise was continuously performed in 4-min stages at each workload. Pedal frequency was held at 70 rpm on a cycle ergometer (Monark, model-874E).
To establish the relationship between steady-state V[O.sub.2] and the exercise intensity for each subject, the following pretests were done. V[O.sub.2] during 8 min cycling exercise at a constant exercise intensity was determined at 8 or more different intensities below the maximal oxygen uptake (V[O.sub.2max]). The pedal frequency was kept at 70 rpm. The exercise intensity was increased by 13.7-34.3 W. The subjects were allowed to rest for approximately 10 minutes between these exercise bouts. Any subject who did not feel completely recovered to perform at the next higher exercise intensity was allowed more rest.
After a linear relationship between exercise intensity and steady state V[O.sub.2] was determined for each subject, V[O.sub.2] during several bouts of exercise at higher intensities was measured in order to ensure the leveling-off of the V[O.sub.2]. In these bouts, since some subjects could not keep the exercise intensity for the entire 8 min, V[O.sub.2] was measured every 30 s from the 3rd to 5th minute of exercise to the last. In these cases, the highest V[O.sub.2] value was adopted as the V[O.sub.2] at that intensity. V[O.sub.2max] was determined by the leveling-off criterion and a leveling-off of V[O.sub.2] was observed in all subjects. Then, the exercise intensities corresponding to 20%, 40%, and 60% V[O.sub.2max] were estimated individually by interpolating the linear relationship between V[O.sub.2] and the exercise intensity.
Blood flow restriction
Subjects wore pressure belts (KAATSU Master, Sato Sports Plaza, Tokyo, Japan) on both legs during BFR test. Prior to the test, the subjects were seated on a chair and the belt air pressure was repeatedly set (20 s) and then released (10 s) from initial (140 mmHg) to final (200 mmHg) pressure every 20 mmHg. The final belt pressure (testing pressure) was 200 mmHg.
Stroke volume (SV) was assessed by the Doppler echocardiographic technique (Rowland and Obert, 2002) using an ultrasound apparatus (Toshiba Model SSH-140A, Tokyo, Japan). A 1.9 MHz continuous wave transducer was directed inferiorly from the suprasternal notch to assess velocity of blood flow in the ascending aorta. The areas beneath highest and clearest velocity curves were traced offline to obtain the average velocity-time integral. The aortic cross-sectional area was calculated from the aortic diameter at the sinotubular junction, recorded at...