Biomedical subjects

Barry Drust

Publications and source records attributed to Barry Drust.

10 recordsLinked to original sources

PubMed2006

The impact of altered climatic conditions and altitude on circadian physiology.

Knowing the output of the "body clock" is fundamental to the science of chronobiology. As the clock resides within the suprachiasmatic nuclei, direct measurement is not feasible and therefore, characteristics of the clock are often inferred from the measurement of marker rhythms, one of which is core temperature. Core temperature is often the marker rhythm of choice due to ease of measurement, particularly in field conditions. However, if the output of the "body clock" is to be inferred from measurement of this variable, it is important to establish whether environmental conditions change or moderate the circadian rhythm of core temperature. Although the majority of circadian patterns do demonstrate independence from such exogenous influences, there does appear to be seasonal variation to their period. Given that humans can easily travel to environments of altered temperature and altitude, there is a need to ascertain the exact effect of such change on the rhythm of core temperature. This review will therefore outline the evidence that the circadian rhythm of core temperature is affected by ambient temperature and by hypoxia. Furthermore, the review will discuss whether these environmental factors act as zeitgebers (affecting the endogenous rhythm) or as masking influences of the inherent rhythm.

Acclimatization↗

PubMed2006

Time course and differential responses of the major heat shock protein families in human skeletal muscle following acute nondamaging treadmill exercise.

The exercise-induced expression of heat shock proteins (HSPs) in rodent models is relatively well defined. In contrast, comparable data from human studies are limited and the exercise-induced stress response of human skeletal muscle is far from understood. This study has characterized the time course and magnitude of the HSP response in the skeletal muscles of a healthy active, but untrained, young male population following a running exercise protocol. Eight subjects performed 45 min of treadmill running at a speed corresponding to their lactate threshold (11.7 +/- 0.5 km/h; 69.8 +/- 4.8% maximum O2 uptake). Muscle biopsies were obtained from the vastus lateralis muscle immediately before and at 24 h, 48 h, 72 h, and 7 days postexercise. Exercise induced a significant (P < 0.05) but variable increase in HSP70, heat shock cognate (HSC) 70, and HSP60 expression with peak increases (typically occurring at 48 h postexercise) to 210, 170, and 139% of preexercise levels, respectively. In contrast, exercise did not induce a significant increase in either HSP27, alphaB-crystallin, SOD 2 (MnSOD) protein content, or the activity of SOD and catalase. When examining baseline protein levels, HSC70, HSP27, and alphaB-crystallin appeared consistently expressed between subjects, whereas HSP70 and MnSOD displayed marked individual variation of up to 3- and 1.5-fold, respectively. These data are the first to define the time course and extent of HSP production in human skeletal muscle following a moderately demanding and nondamaging running exercise protocol. Data demonstrate a differential effect of aerobic exercise on specific HSPs.

Adult↗

PubMed2006

Environmental heat stress, hyperammonemia and nucleotide metabolism during intermittent exercise.

This study investigated the influence of environmental heat stress on ammonia (NH3) accumulation in relation to nucleotide metabolism and fatigue during intermittent exercise. Eight males performed 40 min of intermittent exercise (15 s at 306+/-22 W alternating with 15 s of unloaded cycling) followed by five 15 s all-out sprints. Control trials were conducted in a 20 degrees C environment while heat stress trials were performed at an ambient temperature of 40 degrees C. Muscle biopsies and venous blood samples were obtained at rest, after 40 min of exercise and following the maximal sprints. Following exercise with heat stress, the core and muscle temperatures peaked at 39.5+/-0.2 and 40.2+/-0.2 degrees C to be approximately 1 degrees C higher (P<0.05) than the corresponding control values. Mean power output during the five maximal sprints was reduced from 618+/-12 W in control to 558+/-14 W during the heat stress trial (P<0.05). During the hot trial, plasma NH3 increased from 31+/-2 microM at rest to 93+/-6 at 40 min and 151+/-15 microM after the maximal sprints to be 34% higher than control (P<0.05). In contrast, plasma K+ and muscle H+ accumulation were lower (P<0.05) following the maximal sprints with heat stress compared to control, while muscle glycogen, CP, ATP and IMP levels were similar across trials. In conclusion, altered levels of "classical peripheral fatiguing agents" does apparently not explain the reduced capacity for performing repeated sprints following intermittent exercise in the heat, whereas the augmented systemic NH3 response may be a factor influencing fatigue during exercise with superimposed heat stress.

Adult↗

PubMed2006

Thermoregulation in elite athletes.

PURPOSE OF REVIEW: Exercise causes body temperature to rise and the resulting heat stored becomes a factor limiting exercise performance in hot conditions. Loss of heat by evaporative processes leads to hypohydration which itself can eventually impair performance. This review focuses on thermoregulatory and behavioural processes during sustained exercise in the heat. RECENT FINDINGS: Several studies have implicated cerebral mechanisms in eschewing fatigue due to heat stress. Acclimatization improves performance by affecting heat loss mechanisms, implicating peripheral and central processes. Pharmacological methods of increasing heat tolerance are unacceptable strategies for the athlete, but appropriate precooling measures are effective. SUMMARY: This review highlights the combination of physiological processes that converge in heat stress during extended exercise. Pharmacological ergogenic aids are discouraged due to likely side effects in cerebral function whereas behavioural measures, including precooling the body, have practical support.

Acclimatization↗

PubMed2006

Chronobiological considerations for exercise and heart disease.

Although regular physical activity is beneficial for many clinical conditions, an acute bout of exercise might increase the risk of an adverse clinical event, such as sudden cardiac death or myocardial infarction, particularly in vulnerable individuals. Since it is also known that the incidence of these events peaks in the morning and that some cardiac patients prefer to schedule leisure-time physical activity before lunch, the question arises as to whether morning exercise is 'inherently' more risky than physical activity performed at other times of day. We attempt to answer this question by reviewing the relevant epidemiological data as well as the results of chronobiological and exercise-related studies that have concentrated on the pathophysiological mechanisms for sudden cardiac events. We also consider generally how chronobiology might impact on exercise prescription in heart disease. We performed a structured literature search in the PubMed and WEBofSCIENCE databases for relevant studies published between 1981 and 2004. The limited amount of published epidemiological data did not allow us to conclude that a bout of vigorous exercise in the morning increases the relative risk of either primary cardiac events in apparently healthy individuals, or secondary events in cardiac patients enrolled in supervised exercise programmes. Nevertheless, these data are not directly relevant to individuals who have a history of heart disease and perform uncontrolled habitual activities. It appears as though the influence of time of day on the cardiovascular safety of this type of exercise has not been examined in this population. There is evidence that several pathophysiological variables (e.g. blood pressure, endothelial function, fibrinolysis) vary in parallel with typical diurnal changes in freely chosen activity. Nevertheless, few studies have been designed to examine specifically whether such variables respond differently to a 'set' level of exercise in the morning compared with the afternoon or evening. Even fewer researchers have adequately separated the influences of waking from sleep, adopting an upright posture and physical exertion per se on these pathophysiological responses at different times of day. In healthy individuals, exercise is generally perceived as more difficult and functional performance is decreased in the morning hours. These observations have been confirmed for patients with heart disease in only one small study. It has also not been confirmed, using an adequately powered study involving cardiac patients, that the responses of heart rate and oxygen consumption (VO(2)) to a set bout of exercise show the highest reactivity in the afternoon and evening, which is the case with healthy individuals. Confirmation of this circadian variation would be important, since it would mean that exercise might be prescribed at too high an intensity in the morning if heart rate or VO(2) responses are employed as markers of exercise load. We conclude that there is some parallelism between the diurnal changes in physical activity and those in the pathophysiological mechanisms associated with acute cardiac events. Nevertheless, more studies are needed to ascertain whether the responses of endothelial function, fibrinolysis and blood pressure to a set exercise regimen differ according to time of day. The results of epidemiological studies suggest that morning exercise is just as safe as afternoon exercise for cardiac patients enrolled in a supervised rehabilitation programme. Nevertheless, it is unclear whether time of day alters the risk of a cardiac event occurring during spontaneous physical activity performed by individuals with established risk factors for heart disease.

Circadian Rhythm↗

PubMed2005

Reliability of maximal muscle force and voluntary activation as markers of exercise-induced muscle damage.

The loss of the ability of skeletal muscle to generate force is one of the most appropriate and valid means to quantify muscle damage. Routine measurements of maximal muscle force, however, include many potential sources of error, the most important of which may be a possible lack of central drive to the muscles. The aim of the present study was to determine the reliability of maximal isometric quadriceps muscle force and voluntary activation over a time scale that is typically employed to examine the aetiology of exercise-induced muscle damage. We also attempted to characterise the reliability of several twitch interpolation variables including the size of the interpolated twitch and the state (i.e. un-potentiated vs potentiated) and size of the resting twitch. Over a 7-day period, eight healthy active males performed repeated maximal voluntary isometric contractions (MVC) of the quadriceps (baseline and 2 h, 6 h, 24 h, 48 h, 72 h and 7 days post). Systematic variations in maximal muscle force, voluntary activation, interpolated twitch, un-potentiated twitch and potentiated twitch were not statistically significant (P>0.05) and 95% repeatability coefficients of +/-76.03 N, +/-4.42%, +/- 8.44 N, +/-25.92 N and +/-43.58 N were observed, respectively. These data indicate that young healthy well-familiarized male subjects can reproduce their perceived maximal efforts both within and between days where activation levels of >90% are routinely achieved. Providing activation remains within these limits in the 7 days following an acute bout of exercise, the researcher would be 95% certain that exercise-induced muscle damage is present in individual subjects (taken from similar subject populations) if MVC force falls outside these limits.

Adult↗

PubMed2005

Seasonal rhythms and exercise.

Levels of leisure-time physical activity and physical fitness are generally higher in the summer than in the winter months for most people living away from the equator. The notion that an abrupt increase in physical activity in the spring, after a period of relative inactivity, can trigger sudden cardiac events has not been confirmed. There are seasonal variations in the physiological responses to exercise and the occurrence of injuries during participation in sports, but it is not known whether these changes are explained by fluctuations in activity levels and environmental conditions, or by any endogenous circannual rhythms in the human. There are indications of endogenous control for some physiological processes (eg, the metabolic responses to a given intensity of exercise) that seem to mediate more favorable effects of exercise on body composition in the winter. Well-trained athletes show obvious seasonality in their competitive performances, generally in line with adopted annual periodization strategies, although these strategies can be disrupted by external seasonal factors, such as heat stress or the susceptibility to upper respiratory tract infections. Maximal oxygen consumption and other physiological indicators of exercise performance might not mirror seasonal variation in real performances, which suggests that top-class athletes maintain a good level of general physical conditioning throughout the year.

Climate↗

PubMed2005

The circadian rhythm of core temperature: origin and some implications for exercise performance.

This review first examines reliable and convenient ways of measuring core temperature for studying the circadian rhythm, concluding that measurements of rectal and gut temperature fulfil these requirements, but that insulated axilla temperature does not. The origin of the circadian rhythm of core temperature is mainly due to circadian changes in the rate of loss of heat through the extremities, mediated by vasodilatation of the cutaneous vasculature. Difficulties arise when the rhythm of core temperature is used as a marker of the body clock, since it is also affected by the sleep-wake cycle. This masking effect can be overcome directly by constant routines and indirectly by "purification" methods, several of which are described. Evidence supports the value of purification methods to act as a substitute when constant routines cannot be performed. Since many of the mechanisms that rise to the circadian rhythm of core temperature are the same as those that occur during thermoregulation in exercise, there is an interaction between the two. This interaction is manifest in the initial response to spontaneous activity and to mild exercise, body temperature rising more quickly and thermoregulatory reflexes being recruited less quickly around the trough and rising phase of the resting temperature rhythm, in comparison with the peak and falling phase. There are also implications for athletes, who need to exercise maximally and with minimal risk of muscle injury or heat exhaustion in a variety of ambient temperatures and at different times of the day. Understanding the circadian rhythm of core temperature may reduce potential hazards due to the time of day when exercise is performed.

Activity Cycles↗

PubMed2005

Effects of melatonin on the thermoregulatory responses to intermittent exercise.

We examined the effects of a single 2.5-mg dose of melatonin on the thermoregulatory and circulatory responses to intermittent exercise at a room temperature of 27.2+/-0.4 degrees C (mean+/-S.D.), a relative humidity of 55+/-3% (mean+/-S.D.), and a light intensity of 200-300 lux. In a double-blind cross-over study, six male participants ingested either melatonin or placebo at 11:45 hr. Participants then rested in a semi-supine position for 75 min and completed an intermittent running protocol for 66 min at alternating intensities of 40, 60 and 80% of maximal oxygen uptake. Rectal and mean skin temperature, heart rate, blood pressure, skin blood flow, subjective alertness and sleepiness, ratings of perceived exertion (RPE) and thermal strain were recorded. No effects of melatonin were found on these variables measured during the resting period (P>0.10). During exercise, melatonin was found to moderate the increase in rectal temperature by approximately 0.25 degrees C (P=0.050) and magnify the increase in skin blood flow (P=0.047). Postexercise systolic blood pressure was 7.8+/-2.5 mmHg (mean+/-S.D.) lower than before the exercise in the melatonin trial; a change which differed significantly to that in the placebo trial (P=0.018). Melatonin did not influence subjective alertness and sleepiness before or after exercise and did not change the responses of mean skin temperature, RPE and thermal strain during the exercise (P>0.10). In summary it is apparent that a 2.5-mg dose of melatonin has hypothermic, but not soporific, effects during 66 min of intermittent exercise performed under moderate heat stress. Whether such effects improve endurance athletic performance in hot conditions remains to be confirmed. Our data also suggest that postexercise systolic hypotension is more marked after ingestion of melatonin.

Adult↗

PubMed2003

The relevance of melatonin to sports medicine and science.

The pineal hormone, melatonin, has widespread effects on the body. The aim of this review is to consider the specific interactions between melatonin and human physiological functions associated with sport and exercise medicine. Separate researchers have reported that melatonin concentrations increase, decrease and remain unaffected by bouts of exercise. Such conflicting findings may be explained by inter-study differences in lighting conditions and the time of day the study participants have exercised. Age and fitness status have also been identified as intervening factors in exercise-mediated changes in melatonin concentration. The administration of exogenous melatonin leads to hypnotic and hypothermic responses in humans, which can be linked to immediate reductions in short-term mental and physical performance. Depending on the dose of melatonin, these effects may still be apparent 3-5 hours after administration for some types of cognitive performance, but effects on physical performance seem more short-lived. The hypothesis that the hypothermic effects of melatonin lead to improved endurance performance in hot environments is not supported by evidence from studies involving military recruits who exercised at relatively low intensities. Nevertheless, no research group has examined such a hypothesis with athletes as study participants and with the associated more intense levels of exercise. The fact that melatonin has also been found to preserve muscle and liver glycogen in exercised rats adds weight to the notion that melatonin might affect endurance exercise in humans. Melatonin has been successfully used to alleviate jet lag symptoms of travellers and there is also a smaller amount of evidence that the hormone helps shiftworkers adjust to nocturnal regimens. Nevertheless, the symptoms of jet lag and shiftwork problems have primarily included sleep characteristics rather than performance variables. The few studies that have involved athletes and performance-related symptoms have produced equivocal results. Melatonin has also been found to be useful for treating some sleeping disorders, but interactions between sleep, melatonin and exercise have not been studied extensively with trained study participants. It is unknown whether melatonin plays a role in some exercise training-related problems such as amenorrhoea and over-training syndrome.

Aging↗