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Symposium Reports |
1 Centre for Sport and Exercise Sciences, Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK Email: s.a.ward{at}leeds.ac.uk
This collection of articles forms the basis of a symposium entitled Muscle-energetic and Cardio-pulmonary Determinants of Exercise Tolerance in Humans, which took place at the Physiological Society's meeting at University College London in July 2006. Recognizing that reduced exercise tolerance is a cardinal feature of ageing and of many cardiorespiratory and metabolic disease states, the purpose of this symposium was to critically address putative mechanisms that might contribute to fatigue during whole-body exercise.
Based on analysis of microdissected human muscle fibres, Professor Tony Sargeant presented a critical analysis of the relative contributions of different skeletal muscle fibre types to force generation and fatigue in the context of the muscles' power–velocity relationships (Sargeant, 2007). These techniques are valuable, because they allow investigations of the responses to different exercise intensities and modalities (eccentric, concentric and isometric contractions), and also the analysis of key energetic metabolites. Of particular interest in the context of the performance of high-intensity exercise was the demonstration that a relatively small population of fast fatigue-sensitive fibres expressing the IIX myosin heavy chain isoform, whose contribution to overall force generation is appreciable, may be particularly influential in the fatigue process.
The energetic basis for the support of force generation was then addressed by Professor Kevin Conley, who focused on the phosphorylative coupling efficiency of human skeletal muscle mitochondria in vivo (i.e. the P:O ratio) with ageing (Conley et al. 2007). Using innovative optical and magnetic resonance spectroscopic techniques, the heterogeneous nature of muscle was reinforced by the demonstration that mitochondrial coupling varies between different muscles, ranging from well-coupled oxidative phosphorylation in a hand muscle to mild uncoupling in a leg muscle. Also, in contrast to leg muscles, hand muscles demonstrated an appreciable degree of uncoupling and loss of ATP in elderly subjects, consistent with age-related mitochondrial dysfunction being more striking in muscles with a greater proportion of slow, fatigue-resistant type II muscle fibres; findings which may have implications for the sarcopenia of ageing.
The emphasis on ageing was continued by Professor David Poole in the context of the skeletal muscle microcirculation and its role in supporting O2 delivery and consumption (Poole & Ferreira, 2007). Intramuscular factors related to high-energy phosphate turnover are the most likely candidates for the control of O2 consumption kinetics following exercise onset, at least in young adults undergoing moderate-intensity exercise. This may not be the case in the elderly. In aged rats (Fisher 344 Brown Norway hybrids), for example, blood flow during exercise was found to be distributed preferentially towards low- (rather than high-) oxidative muscle regions, in contrast to the findings in young adult rats. Also, red cell flux within individual capillaries showed only a modest increase in response to muscle contractions. Furthermore, the pronounced fall of muscle microvascular O2 tension at exercise onset (measured by phosphorescence quenching) reflects a sluggish recruitment of perfusion relative to O2 consumption. Collectively, these observations indicate that muscle microcirculatory factors have the potential to contribute to exercise intolerance in the elderly, through their effects on blood–myocyte O2 exchange dynamics.
Professor Brian Whipp extended the scope of these considerations to how the functional linkages between muscle and pulmonary dynamics for pulmonary CO2 exchange differ from those for O2 exchange (Whipp, 2007). Even for moderate exercise (below the lactate threshold), pulmonary CO2 output dynamics are dissociated from those of O2 uptake by the influence of the local high-capacitance CO2 stores. At suprathreshold work rates, the breakdown rates of muscle and blood bicarbonate and the compensatory hyperventilation for the metabolic acidosis introduce further complexities into these CO2 exchange dynamics. A practical consequence of this behaviour is that the increased rate of CO2 output attributable to the falling bicarbonate levels, relative to O2 uptake, can be used to provide a valid estimate of the lactate threshold non-invasively during incremental exercise. However, when there is depletion of CO2 stores prior to exercise, as a result of volitional or anticipatory hyperventilation or when the work rate is incremented very rapidly, a ‘false-positive’ or ‘pseudo-threshold’ may result early in the test as a result of the subsequent slowing of the rapid rate of transient CO2 stores wash-in. A criterion to signal the presence of such a response was presented.
Finally, the expression of the gas exchange responses as requirements for pulmonary ventilation was addressed by Professor Susan Ward, with an emphasis on potential constraints and limitations (Ward, 2007). At very high work rates, these requirements can assume limiting proportions because of the high demands for pulmonary CO2 clearance, the compensatory hyperventilation for the metabolic acidosis and, in some highly fit endurance athletes, the presence of exercise-induced arterial hypoxaemia. While the increase in end-expiratory lung volume seen in elderly subjects allows the limiting airflow to be increased, it has the adverse effect of causing the inspiratory muscles to work over a less optimal length range. The high airflow requirements, coupled with this reduction in contractile efficiency, predispose to diaphragmatic fatigue. This has been proposed to evoke a reflex redistribution of the cardiac output away from the locomotor muscles to the respiratory muscles to support their high metabolic requirements. The high cardiac output can also impose limitations: the pulmonary capillary transit time may become sufficiently reduced that oxygenation is impaired; and it has been suggested that the high pulmonary capillary pressures may lead to pulmonary interstitial oedema and even pulmonary capillary stress failure. These several influences all predispose to premature cessation of exercise.
In conclusion, these wide-ranging physiological-system perspectives illustrate the multifactorial nature of exercise intolerance and have the potential to provide insights into possible means of ameliorating the functional declines associated with chronic sedentarity, ageing and disease.
References
Conley KE, Amara CE, Jubrias SA & Marcinek DJ (2007). Mitochondrial function, fibre types and ageing: new insights from human muscle in vivo. Exp Physiol 92, 333–339.
Poole DC & Ferreira LF (2007). Oxygen exchange in the young and old mammal: muscle–vascular–pulmonary coupling. Exp Physiol 92, 341–346.
Sargeant AJ (2007). Structural and functional determinants of human muscle power. Exp Physiol 92, 323–331.
Ward SA (2007). Ventilatory control in humans: constraints and limitations. Exp Physiol 92, 357–366.
Whipp BJ (2007). Physiological mechanisms dissociating pulmonary CO2 and O2 exchange dynamics during exercise. Exp Physiol 92, 347–355.
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