Gain with no pain; just a little strain – physical conditioning for people with cardio-pulmonary impairments.
1. Introduction:
As a basic grade occupational therapist, I frequently encounter people for whom exercise tolerance is the limiting factor of occupational performance. Usually, this is due to physical de-conditioning secondary to inactivity, but occasionally it is due to pathology. This can often be obvious in people with pulmonary or cardiovascular impairments, but less obvious for those with neurological or renal pathology. Reflecting on my undergraduate occupational therapy training, it has not informed me of how best to manage these people as patients. If I knew no better, I might be hesitant to stress people with cardio-pulmonary pathology for fear of straining their already compromised organs. I might just issue loads of equipment and re-organise tasks to reduce occupational stress. Luckily, from previous experience I know that peripheral physiological adaptations contribute grately to increased performance capacity, and can therefore reduce the overall daily load placed on a compromised heart or lungs. When cleaning out my hard-drive this weekend I found a piece of work I did 9 years ago that has influenced my own physical training and the way I have viewed people with reduced exercise tolerance since. I thought I might as well share it here before deleting it along with the rest of my junk.
2. What limits physiological (not psychological) exercise tolerance?
Aerobic performance (exercise with oxygen) depends on the ability to utilise oxygen relative to demand (l·min-1kg-1). Thus VO2max (maximal oxygen uptake) is a performance indicator. In twelve year old males, Counil et al[1] found that asthmatics achieve only 79% of normal VO2max. At first this appears to suggest respiratory function is the limiting factor, but asthmatics also have decreased cardiac stroke volume[1] and lung function is known not to limit VO2max in healthy subjects. Lung perfusion (circulation of blood through the lungs), red blood cell count and haemoglobin concentration[2] are determinants of oxygen uptake.
Cardiac output affects systolic blood pressure and rate of oxygen carriage between the lungs and muscles. Stroke volume is therefore a determinant of VO2max[3]. Forceful skeletal muscle contractions occlude blood flow[4], so perfusion (circulation of blood through the mucles) is dependant on blood pressure[5] sufficient to overcome this resistance. Local vasodilation occurs in response to muscle activity, but if a large mass of muscle is working, the sympathetic nervous system overrides this reflex to prevent hypotension (low blood pressure)[5]. Thus blood pressure and circulating volume affect performance.
Muscle mitochondria (the site of aerobic respiration) are the last factor of VO2max[6, 3], and some think, the limiting factor[5]. Skeletal muscle characteristics may also influence blood pressure control during exercise[7]. Type I (slow twitch) fibres have greater vascularity and therefore, offer less peripheral resistance than type II (fast twitch) fibres[7], contributing to higher VO2max[5].
The validity of VO2max in performance prediction is questionable. Lactic acid accumulation (which causes muscle pain when you exercise too hard) occurs at activity levels below VO2max, and correlates more closely with ventilatory threshold[8]. Ventilatory threshold is the point at which ventilations increase disproportionately to oxygen uptake, and is also a performance indicator[8]. Ventilatory threshold and point of onset of blood lactate accumulation have been used as indicators of anaerobic threshold[8] - the point of oxygen debt. It is unclear whether there is a causal link between ventilatory threshold and onset of blood lactate accumulation, and whether onset of blood lactate accumulation lactate concentration is fixed, or varies between individuals[8].
The belief that aerobic fatigue results from neuro-transmitter depletion has been disproved[9]. Fatigue can result from fuel depletion[10], so endurance below onset of blood lactate accumulation depends on glycogen and fat storage. Patients are unlikely to experience this unless they are malnourished or have poorly managed diabetes. Anaerobic capacity (the ability to exercise without oxygen) correlates with lean body mass[11], and is limited by the ability to buffer the pH[12, 4] of lactic acid accumulation[10].
3. Physical conditioning to remedy poor exercise tolerance:
Effects of training on the respiratory and cardiovascular systems can be determined by two methods; comparison of physiological measurements in trained and untrained subjects, or comparison of physiological measurements in subjects before and after a training program. The former approach confirms nothing, as it fails to account for genetics, but it provides insight for further research.
3.1. Cardiovascular response to training:
3.1.1. Cardiac output: Gregoire et al[13] compared aerobically trained and untrained young and middle-aged subjects, and noticed reduced sympathetic- and increased parasympathetic- nervous activity, at rest and during exercise in the trained groups, which could be due to changes in central integration of muscle afferent information[14]. Trained middle aged individuals had greater resting heart rate variability than matched untrained subjects[13], but there was no significant heart rate variability difference in the young[13]. Endurance training increased heart rate variability in nine out of eleven young males tested by Al-Ani et al.[15], whose methodology was more valid.
Aerobic training increases maximal cardiac output[16], reduces resting pulse rate[17, 3] and heart rate during sub-maximal exercise[18, 19]. Sprinters respond to isometric exercise with a larger heart rate increase than distance runners[7]. Differences are thought to be due to increased vagal tone[18], and/or decreased sympathetic tone[3], though some have proposed changes of intrinsic heart rate[18].
Di Bello et al.[3] compared male endurance athletes to sedentary males matched by age, height, weight and relative body surface. The athletes had larger resting stroke volumes, resting- and exercise- left ventricular end diastolic volumes. Athletes' ejection fractions increased during exercise as did stroke volume, significantly more than sedentary subjects'[3]. Non-invasive measures of heart volume were used, so reliability of this data is questionable, but ejection fraction increase is supported by the findings of Kavanagh et al.[17] with chronic heart failure patients.
Di Bello et al.[3], found athletes have greater end diastolic volumes than sedentary subjects during recovery from exercise. This depends on venous return and heart rate. Heart rate returns to resting values quicker in trained subjects, so there is more time for filling between each stroke.
3.1.2. Blood Pressure: Endurance athletes have larger blood volumes than matched sedentary subjects[3], but comparable resting blood pressure. Isometric[14] and endurance[20, 21] training lower resting blood pressure. Muscle capillary beds enlarge in response to training[5], but resistance (muscle) training has been shown to have no effect on blood pressure in subjects over seventy years old[20]. This may indicate that muscle plasticity decreases with age and physical conditioning may be less effective for older patients. Torok et al.[7] found sprinters respond to isometric exercise, with greater increases in blood pressure than distance runners. No significant difference was found in dynamic exercise blood pressures, though distance runners exhibited greater vasodilation[7].
Endurance athletes have a greater increase in mean arterial blood pressure than matched sedentary subjects during maximal exercise[3], but the maximum pressures are comparable. Regular exercise may cause baroreceptor resetting[22, 14], decreased sympathetic nervous system activity[13], and reduced catecholamine release[23], thereby decreasing peripheral resistance. McArdle et al.[24] proposed that exercise may facilitate sodium elimination from kidneys, but cited no evidence.
3.1.3. Structural adaptations: Structural cardiac adaptations and physiological changes, are specific to posture[25] and activity. Weight lifters have thickened cardiac muscle, with minimal increase in ventricular volume[24], whereas endurance athletes have increased internal atrial[5] and ventricular[24] volumes.
Athletes' hearts have thicker septums, and higher left ventricular mass indexes than sedentary subjects'[3]. Resting end diastolic left ventricular diameter is increased in endurance athletes[3]. This accounts for the increased ejection fraction and stroke volume, in accordance with the Frank Starling mechanism[3] - increased mechanical efficiency due to altered relative positions of actin- and myosin-filaments (resulting in more forceful muscle contraction). Trained skeletal muscles facilitate venous return better than untrained[3].
3.2. Pulmonary response to training:
According to McArdle et al[24], ventilatory muscles develop increased endurance in response to aerobic training, thereby allowing a higher maximal respiratory rate and larger exercise tidal volume and, athletes have higher maximum ventilation rates (l·min-1) than untrained subjects, but evidence of pulmonary changes is lacking. Three months of aerobic training improved lung function, as assessed by forced vital capacity, forced expiratory volume in one second and peak expiratory flow rate, of a subject with acid maltase deficiency, in a single case study by Leutholtz and Ripoll[21]. The subject was treated with Depo-Testosterone[21], which may have enhanced beneficial training effects[26] while preventing detrimental effects of training and pathology[27]. Validity of generalisations may be poor due to the unique pathology, and the specific nature of the study[28]. Clark et al.[29] concluded there is no relationship between ventilatory variables and exercise capacity in healthy individuals, having measured the effects of 19 weeks of aerobic training on ventilatory performance in 27 subjects.
Some advocate specific training when respiratory muscle function is a limiting factor of performance[30, 31], but Berry et al[32] found that inspiratory muscle training with a general exercise program, was no more beneficial than a general exercise program alone. Various studies indicate respiratory muscle training may be of benefit in chronic obstructive pulmonary disease[33]. Performance in chronic obstructive pulmonary disease is ventilatory limited[34], not cardiovascular limited as is the norm, so findings may have no bearing on people with normal respiratory function.
Torok et al[7] found no difference in maximum oxygen uptake (VO2max l·min-1) between sprinters and long distance runners, but when adjusted for body mass (ml·kg-1min-1) distance runners had greater relative VO2max. For previously mentioned reasons, extrapolations from this data, on the effects of training may not be valid, but other research has confirmed endurance training increases VO2max[6]. Ventilatiory equivalent for oxygen (the ratio of the volume of air passing through the lungs to the volume of oxygen uptake) decreases with endurance training[24]. If anything, this shows that adaptations take place outside the respiratory system.
In people with chronic obstructive pulmonary disease, endurance training reduces VO2(volume of oxygen consumed l min-1) at standardised sub-maximal power outputs[30]. Training improves efficiency, and economy of oxygen consumption and ventilation (reduces ventilatiory equivalent). Trained subjects expire relatively less oxygen than untrained[24], but training only reduces ventilatiory equivalent for exercise of the trained muscles[5]. This is because adaptations (increased aerobic enzyme concentrations and number of mitochondria) take place in muscles, rather than the respiratory system[30].
4. Conclusion:
The validity to rehabilitation of much of the research looked at here[3, 13, 25, 7] is questionable, as differences between athletes and sedentary people may not all be due to training. Also, findings in disease[32, 24, 17] may have no bearing on people without those specific diseases. All things considered, evidence suggests that cardio-respiratory adaptations to training are; left ventricular physiological hypertrophy[35], increased: stroke volume, blood volume, sympathetic nervous system modulation[3], vascularity[36] and ventilatory muscle endurance[37].
We can extrapolate from adaptations to training, that ,VO2max[18], heart size and shape[5], blood volume[3], lean body mass[11] and muscle fibre type ratio[6], contribute to performance. No one variable has proved more critical than the rest[5]. While people with compromised cardio-pulmonary systems may not be able to produce cardio-pulonary adaptations there is adequate evidence that adaptations of skeletal muscle and peripheral circulation in response to training can contribute to increased exercise tolerance and reduced resting loads on the heart and lungs. Occupational therapists should therefore consider rehabilitation for these people instead of just compensatory interventions. Obviously, any conditioning programs should be graduated sufficiently to avoid dangerous physiological stress.
This work is now nearly ten years out of date and I got a bad mark for it at the time, so feel free to recycle it with newer information. Modern guildines such as Chapter 7 of the Cornary Heart Disease National Service Framework[38] are available from: http://www.cardiacrehabilitation.org.uk/ It is also worth noting that this document only focuses on the cardiovascular and pulmonary systems though studies of the effects of exercise on other systems relevant to occupational therapy have been conducted[39].
V
5. References:
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