For both different individuals and modes of locomotion, the external forces determining all-out sprinting performances fall predictably with effort duration from the burst maximums attained for 3 s to those that can be supported aerobically as trial durations extend to roughly 300 s. The common time course of this relationship suggests a metabolic basis for the decrements in the force applied to the environment. However, the mechanical and neuromuscular responses to impaired force production (i.e., muscle fatigue) are generally considered in relation to fractions of the maximum force available, or the maximum voluntary contraction (MVC). We hypothesized that these duration-dependent decrements in external force application result from a reliance on anaerobic metabolism for force production rather than the absolute force produced. We tested this idea by examining neuromuscular activity during two modes of sprint cycling with similar external force requirements but differing aerobic and anaerobic contributions to force production: one- and two-legged cycling. In agreement with previous studies, we found greater peak per leg aerobic metabolic rates [59% (+/-6 SD)] and pedal forces at VO2 peak [30% (+/-9)] during one- vs. two-legged cycling. We also determined downstroke pedal forces and neuromuscular activity by surface electromyography during 15 to 19 all-out constant load sprints lasting from 12 to 400 s for both modes of cycling. In support of our hypothesis, we found that the greater reliance on anaerobic metabolism for force production induced compensatory muscle recruitment at lower pedal forces during two- vs. one-legged sprint cycling. We conclude that impaired muscle force production and compensatory neuromuscular activity during sprinting are triggered by a reliance on anaerobic metabolism for force production.

Humans walk with exceptional economy, expending roughly half as much energy to walk a mile as to run one, and only three-fourths that expected of a 70 kg animal. The lower mass-specific metabolic rates of larger vs. smaller terrestrial animals have been attributed to their longer periods of foot-ground contact during locomotion. Here, we hypothesized that relatively long periods of foot-ground contact allow humans to walk economically. PURPOSE We specifically wished to assess whether reductions in periods of foot-ground contact during human walking would result in increases in the metabolic rates of human walkers. METHODS Metabolic rates were determined from steady-state rates of oxygen uptake while four humans (3 male, 1 female 71.0 ± 2.3 kg) walked on a motorized treadmill at 5 different speeds (range: 0.4–1.8 m/s). Measurements were taken under two conditions: 1) normal walking and 2) walking with wooden foot supports that shortened effective foot length. We expected that reductions in effective foot length would reduce periods foot-ground contact by eliminating the heel-to-toe stance shift that occurs in normal human walking. RESULTS Mass-specific metabolic rates were significantly greater (p. < 0.05), and periods of foot-ground contact were significantly shorter at every speed while subjects walked on shorter effective feet. CONCLUSIONS We conclude that humans prolong periods of foot-ground contact during walking by using a heel-to-toe stance shift. These prolonged periods of foot-ground contact economize human walking by allowing ground force to be applied more slowly and therefore economically.

We compared backward with forward running to test the idea that the application of ground force to support the weight of the body determines the energetic cost of running. We hypothesized that higher metabolic rates during backward versus forward running would be directly related to greater rates of ground force application and the volume of muscle activated to apply support forces to the ground. Four trained males ran backward and forward under steady-state conditions at eight treadmill speeds from 1.75 to 3.50 m x s(-1). Rates of oxygen uptake were measured to determine metabolic rates, and inverse periods of foot-ground contact (1/tc) were measured to estimate rates of ground force application. As expected, at all eight speeds, both metabolic rates and estimated rates of ground force application were greater for backward than for forward running. At the five slowest speeds, the differences in rates of ground force application were directly proportional to the differences in metabolic rates between modes (paired t-test, P<0.05), but at the three highest speeds, small but significant differences in proportionality were present in this relationship. At one of these three higher speeds (3.0 m x s(-1)), additional measurements to estimate muscle volumes were made using a non-invasive force plate/video technique. These measurements indicated that the volume of muscle active per unit of force applied to the ground was 10+/-3% greater when running backward than forward at this speed. The product of rates of ground force application and estimated muscle volumes predicted a difference in metabolic rate that was indistinguishable from the difference we measured (34+/-6% versus 35+/-6%; means +/- s.e.m., N=4). We conclude that metabolic rates during running are determined by rates of ground force application and the volume of muscle activated to apply support forces to the ground.

We twice tested the hypothesis that top running speeds are determined by the amount of force applied to the ground rather than how rapidly limbs are repositioned in the air. First, we compared the mechanics of 33 subjects of different sprinting abilities running at their top speeds on a level treadmill. Second, we compared the mechanics of declined (-6 degrees ) and inclined (+9 degrees ) top-speed treadmill running in five subjects. For both tests, we used a treadmill-mounted force plate to measure the time between stance periods of the same foot (swing time, t(sw)) and the force applied to the running surface at top speed. To obtain the force relevant for speed, the force applied normal to the ground was divided by the weight of the body (W(b)) and averaged over the period of foot-ground contact (F(avge)/W(b)). The top speeds of the 33 subjects who completed the level treadmill protocol spanned a 1.8-fold range from 6.2 to 11.1 m/s. Among these subjects, the regression of F(avge)/W(b) on top speed indicated that this force was 1.26 times greater for a runner with a top speed of 11.1 vs. 6.2 m/s. In contrast, the time taken to swing the limb into position for the next step (t(sw)) did not vary (P = 0.18). Declined and inclined top speeds differed by 1.4-fold (9.96+/-0.3 vs. 7.10+/-0.3 m/s, respectively), with the faster declined top speeds being achieved with mass-specific support forces that were 1.3 times greater (2.30+/- 0.06 vs. 1.76+/-0.04 F(avge)/ W(b)) and minimum t(sw) that were similar (+8%). We conclude that human runners reach faster top speeds not by repositioning their limbs more rapidly in the air, but by applying greater support forces to the ground.

We tested the importance of aerobic metabolism to human running speed directly by altering inspired oxygen concentrations and comparing the maximal speeds attained at different rates of oxygen uptake. Under both normoxic (20.93% O-2) and hypoxic (13.00% O-2) conditions, four fit adult men completed 15 all-out sprints lasting from 15 to 180 s as well as progressive, discontinuous treadmill tests to determine maximal oxygen uptake and the metabolic cost of steady-state running. Maximal aerobic power was lower by 30% (1.00 +/- 0.15 vs. 0.77 +/- 0.12 ml O-2.kg(-1).s(-1)) and sprinting rates of oxygen uptake by 12-25% under hypoxic vs. normoxic conditions while the metabolic cost of submaximal running was the same. Despite reductions in the aerobic energy available for sprinting under hypoxic conditions, our subjects were able to run just as fast for sprints of up to 60 s and nearly as fast for sprints of up to 120 s. This was possible because rates of anaerobic energy release, estimated from oxygen deficits, increased by as much as 18%, and thus compensated for the reductions in aerobic power. We conclude that maximal metabolic power outputs during sprinting are not limited by rates of anaerobic metabolism and that human speed is largely independent of aerobic power during all-out runs of 60 s or less.

To determine the diagnostic value of exerciseinduced R-wave changes in adolescents with congenital heart disease, the responses of 50 adolescents without significant heart disease were compared with those of 72 patients with either a left ventricular (LV) pressure or volume overload lesion. Among the pressure overload group, 24 patients had valvular aortic stenosis (AS) and 27 had coarctation of the aorta. The volume overload group included 12 patients with mitral regurgitation (MR) and 9 with aortic regurgitation (AR). Severity of the cardiac lesion was assessed using cardiac catheterization in patients with AS, physical examination in patients with coarctation of the aorta and clinical or angiographiec criteria, or both, in patients with valvular regurgitation. The R wave was measured in 10 consecutive QRS complexes in leads II, aVF and V5 at rest, maximal exercise and 1-minute recovery. At maximal exercise, control subjects had a mean decrease in amplitude (ΔR) of −3.6 mm (p < 0.0001). Compared with the control group, the AS group had a similar decrease of −3.5 mm, but the coarctation group had a ΔR of −1.4 (p < 0.005) and the volume overload group a ΔR of −1.1 mm (p < 0.003). Patients with AS and ischemic ST-segment changes during exercise (n = 12) had greater decreases in R-wave amplitude than did those with no ST changes (n = 12) (p < 0.04). In patients with AS and an LV end-diastolic pressure ⪢ 12 mm Hg (n = 7), the decrease in ΔR was also greater than that in patients with LV end-diastolic pressure ≤ 12 mm Hg (n = 14) (p < 0.006). Among patients with volume overload, more severe valvular regurgitation was associated with a smaller ΔR (p < 0.03). In patients with AS an increased ΔR reflects ischemia or diminished LV compliance, or both, whereas in patients with volume overload a decrease in ΔR is an indicator of the severity of regurgitation.