This study was designed to test the hypothesis that the electromyographic signal recorded from a working muscle reflects changes in blood lactate concentrations. A group of trained cyclists performed two incremental exercise tests on a cycle ergometer. The Control Trial was a incremental test with power increments of 23.5 watts per minute. Cadence was monitored and maintained at 90+/-1 revolutions per minute. The Experimental Trial consisted of a high intensity arm exercise protocol designed to elevate blood lactate above 8 mmol/1. The arm protocol was followed by five minutes of rest and the incremental exercise protocol used in the Control Trial. Expired gases were sampled every fifteen seconds and calculated values for oxygen uptake, ventilation, excess CO₂, and R.Q. were averaged to give a mean value for each minute in both trials. Heart rate was monitored and recorded every minute for both trials. Electromyographic data were sampled from the vastus lateralis of the right leg for the final eight seconds of each workload in both trials. The data were integrated for each pedal cycle and averaged to give a mean integrated value for each cycle (CIEMG) for each workload. During both trials blood samples were drawn from the cephalic vein of the left arm during the last ten seconds of each workload. The anaerobic threshold (Tlac) was determined using the log-log transformation as outlined by Beaver et al., (1985). Control Trial lactate concentration showed a marked inflection point after an initial slow increase. The mean maximal lactate concentration was 18.21 +/- 5.54 in the Control Trials. This inflection point occurred at a mean lactate concentration of 5.58 +/- 1.05 mmol/1. The mean oxygen uptake at the inflection point was 2.28 +/- 0.37 1/min which represented a mean of 72.6 +/- 7.20 % of maximum. Experimental Trial mean plasma lactate at the beginning of incremental exercise was 26.61 +/- 8.86 mmol/1. The plasma lactate concentration decreased steadily for the initial loads to a mean low concentration of 10.78 +/- 5.78 mmol/1 at Tlac and then increased to a mean of 19.08 +/- 6.66 mmol/1 at test completion. Plasma lactate concentration was greater in the Experimental Trial at all workloads though the values tended to converge once Tlac was surpassed. No visually identifiable inflection point in the plot of CIEMG vs Power could be determined in any of the plots. An analysis of the slope of the CIEMG vs. Power relationship was therefore performed. An analysis of variance demonstrated no significant difference in the slope of the relationship within or between trials in three different comparisons. The slope of the line was not statistically different when compared over: (a) the entire sample (b) pre Tlac and (c) post Tlac. Correlations performed between plasma lactate concentrations and CIEMG were significant in five of six subjects during the Control Trial (r = 0.57 to 0.97). During the Experimental Trial only three of the six subjects showed significant correlations and they were in the opposite direction (r = -0.62 to -0.96). Correlations between power output and CIEMG were for all subjects in both trials (r = 0.92 to 0.99 Control, r = 0.91 to 0.99 Experimental). The increase seen in CIEMG with increased power output reflects poorly the changes in blood lactate concentrations under the conditions of this investigation. Plasma lactate showed a dramatic increase in the Control Trial and a steady decrease from an initial high concentration followed by a marked increase in the final workloads of the Experimental Trial. In contrast the CIEMG increased in a near linear fashion for all subjects in both trials. The changes in CIEMG showed highly significant correlations with changes in VO₂ or power output in both trials for all subjects. These results indicate that changes in the surface electromyogram are highly related to changes in power output. However the surface electromyogram changes are not driven by changes in lactate concentration under the conditions of this investigation and may not be a sensitive enough indicator of these changes to be employed in the determination of Tlac. / Education, Faculty of / Curriculum and Pedagogy (EDCP), Department of / Graduate

No description available.

Graduation date: 1995

Thesis (M.S.)--Eastern Illinois University. / Vita. Includes bibliographical references (leaves 40-42).

The effects of differing recovery patterns following intermittent exercise on blood lactate and subsequent performance were examined. Fourteen male subjects completed three randomly assigned experimental protocols. Each protocol consisted of eight 45s-bouts of cycling on a Monark cycle ergometer at 120% of VO$ sb2$ max interposed with five minute recovery periods. Each protocol ended with a maximal performance task consisting of a 45s all-out cycling test. Recovery patterns included passive, cycling (45% of VO$ sb2$ max), and arm cranking (45% of VO$ sb2$ max). Results revealed similar blood lactate concentrations in the passive and arm cranking conditions but significantly lower (p $<$.05) levels in the cycling condition. Mean power outputs measured from the performance task were significantly higher (p $<$.05) in the cycling and arm cranking recovery conditions. The correlation between blood lactate levels and mean power output was low (r = $-$0.28), suggesting that other factors were influencing subsequent performance.

This study was designed to characterize the cardiac output (Q$ sb{ rm c}$) response to progressive submaximal upright (U) exercise in CF patients. Secondly, the Q$ sb{ rm c}$ adjustments were compared to those of similar supine (S) exercise, in an attempt to assess myocardial accommodation to the enhanced ventricular preload in the S posture. Q$ sb{ rm c}$ generally increased with exercise intensity in both U and S positions, although gr.IV plateaued at 50% VO$ sb2$max (S). Maximal stroke volume index (SI) was achieved at 50% VO$ sb2$max (U) in all groups, except gr.IV and at 30% VO$ sb2$max (S) in all groups. The change from U to S posture resulted in a significant (p $ le$.05) increase in SI at rest and for every submaximal exercise in gr.I, but not in CF patients, independent of disease severity eg(Rest:gr.I:27 $ pm$ 7(U) vs 39 $ pm$ 8(S); gr.II:24 $ pm$ 5vs28 $ pm$ 10; gr.III:18 $ pm$ 4 vs 22 $ pm$ 5; gr.IV:17 $ pm$ 4 vs 20 $ pm$ 6 ml/bt/m$ sp2$). These observations suggest a limitation in ventricular volume accommodation in CF patients which becomes apparent under the S exercise conditions.

Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1999. / Bibliography: leaves 246-280.

Thesis (M.S. Ed.)--Virginia Polytechnic Institute and State University, 1991. / Vita. Abstract. Includes bibliographical references (leaves 64-68). Also available via the Internet.

Thesis (M.S.)--Virginia Polytechnic Institute and State University, 1992. / Vita. Abstract. Includes bibliographical references (leaves 79-82). Also available via the Internet.

Thesis (M.A.)--University of North Carolina at Chapel Hill, 2002. / Includes bibliographical references (leaves 44-46).