Metabolic Power and Efficiency for an Amputee Cyclist: Implications for Cycling Technique

Cycling technique is steeped in cultural lore. One deeply held belief is that "pulling-up" to lift the leg (increased muscular leg flexion) will optimize technique and improve efficiency. In contrast, scientific evidence suggests that when cyclists are instructed to pull-up efficiency decreases. However, such interventions may not have allowed sufficient time for cyclists to adapt and refine their technique. This case study documented how a cyclist with a complete unilateral limb amputation consumed metabolic power to produce mechanical power during single-leg cycling. The cyclist was a 4-time U.S. National Paralympic Champion who performed single-leg cycling for 7yrs and thus was fully adapted to pull-up. We hypothesized that a counterweight system, which reduced the requirement to pull-up, would decrease metabolic power and increase efficiency for this cyclist. The cyclist performed submaximal cycling (100, 135, 170, 205W, 80rpm, 5min) with and without a counterweight (10kg) on the unused crank. Expired gasses were measured, and metabolic power and gross efficiency were calculated. Metabolic power decreased on average by 87±7W (p<0.001) and gross efficiency increased from 16.3±1.9 to 18.0±1.8% (p<0.001) when cycling with the counterweight. During counterweighted single-leg cycling, the metabolic power of unloaded cycling decreased (317 vs. 238W) and delta efficiency was similar (25.2 vs. 25.5%). Results demonstrated that significant metabolic power was associated with pulling-up to produce muscular leg flexion power even in a cyclist who pulled-up substantially during cycling. Our findings confirm observations from previous studies that altered pedaling technique acutely and indicate that pulling-up during cycling is less efficient.

Highly Accurate Delta Efficiency Measurements at the Large Scale Turbine Rig

High pressure turbines are nowadays designed to a point where most design enhancements only yield marginal efficiency improvements. This challenges research facilities to reliably resolve ever smaller differences in efficiency caused by individual design changes. In recent years, immense efforts towards such highly accurate delta-efficiency measurements have been undertaken at the Large Scale Turbine Rig (LSTR). This paper comprises an overview of the applied methodology and the achievements on the basis of various validation cases. By thoroughly controlling the operation point and accounting for all variables affecting the efficiency η, the rig can resolve efficiency-differences Δη of ±0.1 % for a single day measurement. Four benchmark cases are investigated to validate the rig’s capabilities. First, the influence of tip clearance is investigated for a squealer-type geometry for swirling inflow. It is found that for an increase in tip clearance of 1 %, η is decreased by 2.68 %. Then, it is shown that a winglet-type tip geometry may improve the efficiency by Δη 0.33% in comparison to the squealer tip. Third, it is shown that these trends are similar for plain inflow, however swirl decreases efficiency by up to 1.25 % in comparison to plain inflow. Finally, the clocking-position of the combustor-module relative to the nozzle guide vanes is varied leading to efficiency differences of up to 0.52 %.

Variation in the uncoupling protein 2 and 3 genes and human performance

Uncoupling proteins 2 and 3 (UCP2 and UCP3) may negatively regulate mitochondrial ATP synthesis and, through this, influence human physical performance. However, human data relating to both these issues remain sparse. Examining the association of common variants in the UCP3/2 locus with performance phenotypes offers one means of investigation. The efficiency of skeletal muscle contraction, delta efficiency (DE), was assessed by cycle ergometry in 85 young, healthy, sedentary adults both before and after a period of endurance training. Of these, 58 were successfully genotyped for the UCP3-55C>T (rs1800849) and 61 for the UCP2-866G>A (rs659366) variant. At baseline, UCP genotype was unrelated to any physical characteristic, including DE. However, the UCP2-866G>A variant was independently and strongly associated with the DE response to physical training, with UCP2-866A allele carriers exhibiting a greater increase in DE with training (absolute change in DE of −0.2 ± 3.6% vs. 1.7 ± 2.8% vs. 2.3 ± 3.7% for GG vs. GA vs. AA, respectively; P = 0.02 for A allele carriers vs. GG homozygotes). In multivariate analysis, there was a significant interaction between UCP2-866G>A and UCP3-55C>T genotypes in determining changes in DE (adjusted R2 = 0.137; P value for interaction = 0.003), which was independent of the effect of either single polymorphism or baseline characteristics. In conclusion, common genetic variation at the UCP3/2 gene locus is associated with training-related improvements in DE, an index of skeletal muscle performance. Such effects may be mediated through differences in the coupling of mitochondrial energy transduction in human skeletal muscle, but further mechanistic studies are required to delineate this potential role.

The effect of training volume and intensity on competitive cyclists’ efficiency

The impact of different intensity training on cycling efficiency in competitive cyclists is unknown. Twenty-nine endurance-trained competitive male cyclists completed 3 laboratory visits during a 12-week training period. At each visit, their cycling efficiency and maximal oxygen uptake were determined. After the first visit, cyclists were randomly split into 2 groups (A and B). Over the first 6 weeks, between tests 1 and 2, group A was prescribed specific high-intensity training sessions, whereas group B was restricted in the amount of intensive work undertaken. After test 2 and for the second 6-week period, group B was allowed to conduct high-intensity training. Gross efficiency (GE) increased in group A (+1.6 ± 1.4%; p < 0.05) following the high-intensity training, whereas no significant change was seen in group B (+0.1 ± 0.7%; p > 0.05). Group B cyclists increased their GE between tests 2 and 3 (+1.4 ± 0.8%; p < 0.05) but no changes in GE were observed in group A over this period (+0.4 ± 0.4%; p > 0.05). Delta efficiency (DE) did not change significantly in either group across the study period. This study demonstrates that GE is increased following high-intensity training in competitive male cyclists after 12 weeks.

Bradykinin receptor gene variant and human physical performance

Accumulating evidence suggests that athletic performance is strongly influenced by genetic variation. One such locus of influence is the gene for angiotensin-I converting enzyme (ACE), which exhibits a common variant [ACE insertion (I)/deletion (D)]. ACE can drive formation of vasoconstrictor ANG II but preferentially degrades vasodilator bradykinin. The ACE I allele is associated with higher kinin activity. A common gene variant in the kinin β2 receptor (B2R) exists: the -9 as opposed to +9 allele is associated with higher receptor mRNA expression. We tested whether this variant was associated with the efficiency of muscular contraction [delta efficiency (DE)] in 115 healthy men and women, or with running distance among 81 Olympic standard track athletes. We further sought evidence of biological interaction with ACE I/D genotype. DE was highly significantly associated with B2R genotype (23.84 ± 2.41 vs. 24.25 ± 2.81 vs. 26.05 ± 2.26% for those of +9/+9 vs. +9/-9 vs. -9/-9 genotype; n = 25, 61, and 29, respectively; P = 0.0008 for ANOVA adjusted for sex). There was evidence for interaction with ACE I/D genotype, with individuals who were ACE II, with B2R -9/-9 having the highest DE at baseline. The ACE I/B2R -9 “high kinin receptor activity” haplotype was significantly associated with endurance (predominantly aerobic) event among elite athletes ( P = 0.003). These data suggest that common genetic variation in the B2R is associated with efficiency of skeletal muscle contraction and with distance event of elite track athletes and that at least part of the associations of ACE and fitness phenotypes is through elevation of kinin activity.