V02 'overshoot' during moderate-intensity exercise in endurance-trained athletes: the influence of exercise modality.
ABSTRACT The purpose of this study was to investigate the influence of exercise modality on the 'overshoot' in V(O2) that has been reported following the onset of moderate-intensity (below the gas exchange threshold, GET) exercise in endurance athletes. Seven trained endurance cyclists and seven trained endurance runners completed six square-wave transitions to a work-rate or running speed requiring 80% of mode-specific GET during both cycle and treadmill running exercise. The kinetics of V(O2) was assessed using non-linear regression and any overshoot in V(O2) was quantified as the integrated volume (IV) of O(2) consumed above the steady-state requirement. During cycling, an overshoot in V(O2) was evident in all seven cyclists (IV = 136 +/- 41 ml) and in four runners (IV = 81 +/- 94 ml). During running, an overshoot in V(O2) was evident in four runners (IV = 72 +/- 61 ml) but no cyclists. These data challenge the notion that V(O2) always rises towards a steady-state with near-exponential kinetics in this exercise intensity domain. The greater incidence of the V(O2) overshoot during cycling (11/14 subjects) compared to running (4/14 subjects) indicates that the overshoot phenomenon is related to an interaction between high levels of aerobic fitness and exercise modality. We speculate that a transient loss in muscle efficiency as a consequence of a non-constant ATP requirement following the onset of constant-work-rate exercise or an initially excessive recruitment of motor units (relative to the work-rate) might contribute to the overshoot phenomenon.
- SourceAvailable from: David Poole[Show abstract] [Hide abstract]
ABSTRACT: The tolerable work duration (t) for high-intensity cycling is well described as a hyperbolic function of power (W): W = (W'.t-1) + Wa, where Wa is the upper limit for sustainable power (lying between maximum W and the threshold for sustained blood [lactate] increase, theta lac), and W' is a constant which defines the amount of work which can be performed greater than Wa. As training increases the tolerable duration of high-intensity cycling, we explored whether this reflected an alteration of Wa, W' or both. Before and after a 7-week regimen of intense interval cycle-training by healthy males, we estimated ( ) theta lac and determined maximum O2 uptake (mu VO2); Wa; W'; and the temporal profiles of pulmonary gas exchange, blood gas, acid-base and metabolic response to constant-load cycling at and above Wa. Although training increased theta lac (24%), mu VO2 (15%) and Wa (15%), W' was unaffected. For exercise at Wa, a steady state was attained for VO2, [lactate] and pH both pre- and post-training, despite blood [norepinephrine] and [epinephrine] ([NE], [E]) and rectal temperature continuing to rise. For exercise greater than Wa, there was a progressive increase in VO2 (resulting in mu VO2 at fatigue), [lactate], [NE], [E] and rectal temperature, and a progressive decrease for pH. We conclude that the increased endurance capacity for high-intensity exercise following training reflects an increased W asymptote of the W-t relationship with no effect on its curvature; consequently, there is no appreciable change in the amount of work which can be performed above Wa.(ABSTRACT TRUNCATED AT 250 WORDS)European Journal of Applied Physiology and Occupational Physiology 02/1990; 59(6):421-9. DOI:10.1007/BF02388623
- [Show abstract] [Hide abstract]
ABSTRACT: The purpose of this paper is to provide an introduction to the study of oxygen uptake (VO(2)) dynamics or kinetics. Following the onset of exercise, both muscle and pulmonary VO(2) rise in a near-exponential fashion towards the anticipated "steady-state" VO(2) demand. However, it can take 2-4 min, or even longer at higher work rates, before this steady state is attained. Slow VO(2) kinetics increase the so-called O(2) deficit and obligate a greater contribution from anaerobic mechanisms of ATP production (involving the breakdown of muscle high energy phosphates and lactate production from glycogen) to meet the ATP requirement of the exercise task. A primary goal in this area of research is therefore to elucidate the physiological mechanisms which control and/or limit the rate at which muscle VO(2) increases following the onset of exercise. At higher intensities of exercise, a continued increase in both muscle and pulmonary VO(2) is observed with time despite the external work rate remaining constant. This continued rise in VO(2), beyond the anticipated steady-state requirement for the work rate, has been termed the VO(2) "slow component," and establishing the mechanistic basis for this phenomenon is another important goal of research in this field. This paper provides an overview of some of the factors which might contribute to both the fundamental and slow phases of the VO(2) kinetics and, in so doing, provides general background material for the more specific papers that follow.Medicine & Science in Sports & Exercise 10/2005; 37(9):1542-50. DOI:10.1249/01.mss.0000177466.01232.7e · 4.46 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: This paper offers a brief synopsis of the five preceding papers which constitute the proceedings of the symposium "Mechanistic basis of the slow component of VO2 kinetics during heavy exercise." The key features have been taken from each paper and a coherent position regarding the site and potential underlying mechanisms for the "excess" VO2 is presented. The hypothesis is developed that some aspect of fiber type recruitment patterns might be responsible for this phenomenon. Elucidation of the precise determinants of VO2 during heavy exercise is fundamental to our understanding of muscle energetics. Furthermore, certain patient populations, whose exercise tolerance is limited by impaired cardiovascular and/or respiratory capacity, may benefit from interventions designed to constrain the magnitude of the VO2 slow component.Medicine & Science in Sports & Exercise 12/1994; 26(11):1354-8. · 4.46 Impact Factor