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Biomedical subjects

J Rittweger

Publications and source records attributed to J Rittweger.

27 records · Page 2Linked to original sources
PubMed1999

Muscle and bone-aging and space.

One of the major concerns of aging, but also during and after spaceflight, is loss of muscle and bone mass. In aging, this is associated with an increasing risk of fractures. Recently, the possibility of aged and aging astronauts has been arisen. Thus considering the perspectives of aging and space we want to discuss, in how far the adaptations during spaceflight and during aging interfere. In other words: does spaceflight push the astronauts along the irreversible axis of aging? And which of the spaceflight effects will be reversible? Bones adapt to their mechanical function. For convenience, a simple model has been proposed: Bone, as a 'mechanostat', keeps the strains within certain thresholds, namely one threshold for modeling, i.e. formation of new bone, and one for remodeling, i.e. repair and removal. These thresholds are usually expressed as strains. A crucial role in physiological strain detection is obviously played by the osteocytes. The largest forces in the musculo-skeletal systems arise from muscle contractions. The reason for this are the poor levers, against which the muscles pull. For example: during a one-leg vertical jump, a young subject (body weight 70 kg) exerts a vertical ground reaction force of 2500 N. Due to the lever ratio of os calcis and forefoot around the tibio-talar joint, the calf muscles must exert a force 3 times greater, so that together with the body weight the bones of the lower leg are loaded with 10000 N, i.e. 14 times the body weight. Accordingly, good correlations can be observed between muscle strength and bone strength, or muscle mass and bone mass. It is therefore reasonable to discuss the accumulated knowledge about loss of muscle and bone in a combined approach. In this respect, two points must be considered: (i) for structural adaptation of bone, the muscular variable of interest arc force and rate of force development, but not power, and (ii) women before menopause have a greater bone to muscle ratio than men.

Adaptation, Physiological↗
PubMed1998

Respiratory-like periodicities in slow eye movements during sleep onset.

Slow eye movements (SEMs) during sleep onset and their relationship to vegetative rhythms were investigated in six healthy, sleep-deprived subjects, yielding 143-289 SEMs in an epoch of 31.5-56 min per experiment. Exclusively, sleep in stages I and II was recorded. From the bandpass-filtered electro-oculogram (EOG) signal (cut-off frequencies 0.05 and 1 Hz), turning points of the gaze were detected and compared with the start of inspiration, which was discriminated from the abdominal respiratory excursions. SEM cycle times varied considerably more than respiratory cycle times (P < 0.05 in Levene's test). Both were preferentially of equal length, or, in some subjects, in 2:1 co-ordination. Cross-correlation histograms yielded that inspiration and SEMs were also temporally co-ordinated. Thus, there is a temporal coherence regarding the occurrence, the cycle time and the phase between SEMs and a respiratory-like rhythm. Our findings show that it is not exactly the respiratory rhythm that is mirrored in the SEMs. Rather, we favour the interpretation of an autorhythmicity that is temporarily connected to the common brainstem system in the reticular formation of the brainstem.

Adult↗
PubMed1997

Influences of mandatory breathing on rhythmical components of electrodermal activity.

We investigated whether rhythmical components of electrodermal activity (EDA) can be influenced by voluntary modification of the respiratory frequency. Fifty-five volunteers participated in an experiment with nine mandatory sections of cycle times between 3.1 s and 12.2 s. The cycle time of the rhythmical EDA components often differed considerably from respiratory cycle time. ANOVA yielded that both cycle time and position within the section had an effect on the EDA power of the mandatory cycles (P < 0.05). No significant interaction between effects of section and of position was discovered (P > 0.1). A separate analysis of the cycle times of the rhythmical EDA components revealed integer relationship with the respiratory cycle times. Thus, voluntary changes in the respiratory frequency can influence occurrence and cycle time of rhythmical EDA components in a way similar to sliding coordination in the sense of E. von Holst.

Adult↗
PubMed1996

Electrodermal activity reveals respiratory and slower rhythms of the autonomic nervous system.

Electrodermal Activity (EDA) was measured in 55 subjects during (1) an alarm reaction, (2) mental load, and (3) physical load. In 34 subjects, not only was a transient response observed, but also, oscillatory patterns characterizing short term variations of EDA. The durations of these oscillations varied between 3-16 s. Most commonly, they were approximately within the frequency range of respiration, or lower, at about 0.1 Hz. The EDA-rhythms were also related to the arterial blood pressure. They were, however, not strictly synchronized with respiration or with the blood pressure waves. We conclude that assessment of EDA in combination with fluctuations of the heart rate, and also, if possible, arterial blood pressure, may turn out to be a useful tool in the evaluation of the interaction between different regulatory processes that are realized by the common brainstem system.

Acoustic Stimulation↗
PubMed1992

Different modes of dampening influence from baroreceptors are determined by the functional organization of the NTS neuronal network.

Simultaneous recordings of several neurones of the first relay station of baroreceptor afferents show that its general activity-dampening influence is realized via the common brainstem system (CBS) which itself controls the processing on the neurones of the nucleus of the solitary tract (NTS). This feedback system maintains the degree of activity which is necessary for the ongoing behaviour as long as it fits to the environmental situation. The output of the NTS is determined partly by the CBS, partly by the properties of the peripheral afferent input, partly by the dynamic functional organization of the local circuits and partly by influences from other brain areas.

Action Potentials↗
PubMedDate not supplied

Adaptive processes in skeletal muscle: molecular regulators and genetic influences.

Skeletal muscle is a highly adaptable tissue. It responds to environmental and physiological challenges by changes in size, fibre type and metabolism. All of these responses are underpinned by our genes and it is therefore generally assumed that genetic variation between individuals may account for the differences in musculature and athletic capabilities between people. Research into the genetic influences of our muscle is at an embryonic stage, but some early insight into potential regulators has recently emerged, which is reflected in this review. Broad heritability, which appears to affect muscle size and strength more than metabolism has been assessed in twin and sibling studies. It appears to account for more inter-individual variation in the young as opposed to older people. However, the studies reported to date do demonstrate a large degree of diversity, which is probably predominantly due to different methodological approaches being adopted as well as distinct populations being studied. At a molecular level, there has been enormous progress in identifying regulators of atrophy and hypertrophy though the study of knock-out and transgenic animals and also through the utilisation of cell culture models. Among others, the insulin-like growth factors, calcineurin, desmin, myf5, mrf4, MyoD and myogenin have been identified as positive regulators of muscle size, while TNF-alpha, myostatin and components of the ubiquitin pathway have been recognized as regulators of muscle wasting. However, given the ethical and mechanistic constraints of performing similar studies in humans, difficulties have arisen when attempting to translate the animal and cell culture findings to humans. However, the current search for target "exercise genes" in humans has yielded the first successful results. Variations in the genes encoding for: the angiotensin converting enzyme, alpha-actinin 3, bradykinin, ciliary neurotrophic factor, interleukin-15, insulin-like growth factor II, myostatin and the vitamin D-receptor have all been found to account for some of the inter-subject variability in muscle strength or size. However, the influences of these genetic variations are somewhat weak, and not always reproducible and furthermore they are predominantly based in young healthy people. Hence, a key topic, namely the molecular mechanisms of muscle frailty in the elderly still remains to be elucidated.

Animals↗
PubMedDate not supplied

Can exercise prevent osteoporosis?

Commonly used definitions of osteoporosis rely upon the measurement of bone mass or bone mineral density and regard the difference between osteopenia and osteoporosis as gradual. An alternative definition has been proposed by Harold Frost, suggesting that osteopenia is the bone's physiological response to disuse. On the contrary, true osteoporoses imply the bone's inability to adapt to the loads imposed on them by their habitual mechanical usage. As a consequence, fractures occur with no or very little trauma in osteoporotic, but not in osteopenic bones. There is now ample evidence that mechanical stimuli can increase strength. Accordingly, exercise, in particular some new forms of it that involve high strain rates, seems to be preventing bone loss and possibly also induces increases in bone mass even at older ages. Hence, exercise may ameliorate osteopenia in the sense of Frost's definition. However, exercise must be feared to facilitate rather than to ameliorate the occurrence of true osteoporoses, e.g., due to microdamage accumulation. This is in sharp contrast to the general 'understanding'.

Adolescent↗
PubMedDate not supplied

Bone adaptation to altered loading after spinal cord injury: a study of bone and muscle strength.

Bone loss from the paralysed limbs after spinal cord injury (SCI) is well documented. Under physiological conditions, bones are adapted to forces which mainly emerge from muscle pull. After spinal cord injury (SCI), muscles can no longer contract voluntarily and are merely activated during spasms. Based on the Ashworth scale, previous research has suggested that these spasms may mitigate bone losses. We therefore wished to assess muscle forces after SCI with a more direct measure and compare it to measures of bone strength. We hypothesized that the bones in SCI patients would be in relation to the loss of muscle forces. Six male patients with SCI 6.4 (SD 4.3) years earlier and 6 age-matched, able-bodied control subjects were investigated. Bone scans from the right knee were obtained by pQCT. The knee extensor muscles were electrically stimulated via the femoral nerve, isometric knee extension torque was measured and patellar tendon force was estimated. Tendon force upon electrical stimulation in the SCI group was 75% lower than in the control subjects (p<0.01). Volumetric bone mineral density of the patella and of the proximal tibia epiphysis were 50% lower in the SCI group than in the control subjects (p<0.01). Cortical area was lower by 43% in the SCI patients at the proximal tibia metaphysis, and by 33% at the distal femur metaphysis. No group differences were found in volumetric cortical density. Close curvilinear relationships were found between stress and volumetric density for the tibia epiphysis (r(2)=0.90) and for the patella (r(2)=0.91). A weaker correlation with the tendon force was found for the cortical area of the proximal tibia metaphysis (r(2)=0.63), and none for the distal femur metaphysis. These data suggest that, under steady state conditions after SCI, epiphyseal bones are well adapted to the muscular forces. For the metaphysis of the long bones, such an adaptation appears to be less evident. The reason for this remains unclear.

Adult↗