Exercise training had beneficial effects on cardiopulmonary function and QOL in postmenopausal breast cancer survivors.

The purpose of this study was to investigate the effect of concurrent strength and endurance training on strength, endurance, endocrine status and muscle fibre properties. A total of 45 male and female subjects were randomly assigned to one of four groups; strength training only (S), endurance training only (E), concurrent strength and endurance training (SE), or a control group (C). Groups S and E trained 3 days a week and the SE group trained 6 days a week for 12 weeks. Tests were made before and after 6 and 12 weeks of training. There was a similar increase in maximal oxygen consumption (VO2max) in both groups E and SE (P < 0.05). Leg press and knee extension one repetition maximum (1 RM) was increased in groups S and SE (P < 0.05) but the gains in knee extension 1 RM were greater for group S compared to all other groups (P < 0.05). Types I and II muscle fibre area increased after 6 and 12 weeks of strength training and after 12 weeks of combined training in type II fibres only (P < 0.05). Groups SE and E had an increase in succinate dehydrogenase activity and group E had a decrease in adenosine triphosphatase after 12 weeks of training (P < 0.05). A significant increase in capillary per fibre ratio was noted after 12 weeks of training in group SE. No changes were observed in testosterone, human growth hormone or sex hormone binding globulin concentrations for any group but there was a greater urinary cortisol concentration in the women of group SE and decrease in the men of group E after 12 weeks of training (P < 0.05). These findings would support the contention that combined strength and endurance training can suppress some of the adaptations to strength training and augment some aspects of capillarization in skeletal muscle.

This review has grouped many studies on different populations with different protocols to show the interactive effects of intensity, frequency and duration of training as well as the effects of initial fitness levels and programme length on cardiorespiratory fitness as reflected by aerobic power (VO2max). Within each level of exercise duration, frequency, programme length or initial fitness level, the greatest improvements in aerobic power occur when the greatest challenge to aerobic power occurs i.e., when intensity is from 90 to 100% of VO2max. The pattern of improvement where different intensities are compared with different durations suggests that when exercise exceeds 35 minutes, a lower intensity of training results in the same effect as those achieved at higher intensities for shorter durations. Frequencies of as low as 2 per week can result in improvements in less fit subjects but when aerobic power exceeds 50 ml/kg/min, exercise frequency of at least 3 times per week is required. As the levels of initial fitness improve, the changes in aerobic power decreases regardless of the intensity, frequency or duration of exercise. Although these pooled data suggest that maximal gains in aerobic power are elicited with intensities between 90 to 100% VO2max, 4 times per week with exercise durations of 35 to 45 minutes, it is important to note that lower intensities still produce effective changes and reduce the risks of injury in non-athletic groups.

Biopsies from the vastus lateralis muscle were obtained from three astronauts before and after two 5-day flights and from five astronauts before and after one 11-day flight (space shuttle flights: STS-32, -33, and -34). Muscle fibers from two separate samples from each biopsy were classified as type I and II or as type I, IIA, and IIB by using qualitative myofibrillar adenosinetriphosphatase (ATPase) staining. Cross-sectional area (CSA), number of capillaries per fiber, and the activities of succinate dehydrogenase (SDH), alpha-glycerophosphate dehydrogenase (GPD), and myofibrillar ATPase were determined from one sample of fibers of each myofibrillar ATPase type. Postflight biopsies had 6-8% fewer type I fibers than preflight. Mean fiber CSAs were 16-36% smaller after the 11-day flight with the relative effect being type IIB > IIA > I. Mean fiber CSAs were 11 and 24% smaller in type I and II fibers after 5 days of flight. Myofibrillar ATPase activities increased in type II but not in type I fibers after flight, whereas SDH activity was unaffected in either fast or slow fibers. GPD activity in type I fibers was approximately 80% higher (P > 0.05) postflight compared with preflight. Myofibrillar ATPase/SDH ratios in type II fibers were higher after than before flight, suggesting that some fast fibers were more susceptible to fatigue after flight. The GPD/SDH ratios were elevated in some type I fibers after spaceflight. The number of capillaries per fiber was 24% lower after than before flight, whereas the number of capillaries per unit CSA of muscle tissue was unchanged. These data suggest that adaptations in the size, metabolic properties, and vascularity of muscle fibers can occur rapidly in the space environment. These adaptations were qualitatively similar to those observed in animals after actual or simulated spaceflight conditions for short periods.

Following spinal cord injury (SCI), upper motor neuron paralysed muscles lose the normal type I (slow) and II (fast) ®bre mosaic pattern and become predominantly composed of type II (fast glycolytic) ®bres). The majority of the research demonstrating this ®bre type shift was based on pH sensitive myo®brillar ATPase staining techniques on muscle from longstanding paraplegics and quadriplegics. The purpose of this study was to describe muscle ®bre type changes over a wide time spectrum post SCI using immuno¯uorescent techniques which may be more sensitive to change. A total of 19 vastus lateralis muscle biopsy specimens were obtained from 12 SCI subjects representing time points of 0.5 ± 219 months post SCI. Fast and slow myosin heavy chain isoform distribution was determined on single muscle ®bres for each of the biopsy specimens. Early post SCI (51 month) myosin heavy chain (MCH) isoform composition remained relatively stable. A transitional period was seen between 1 and 20 months post SCI wherein there was a progressive drop in the proportion of slow MHC isoform ®bres and a rise in the proportion that co-expressed both the fast and slow MHC isoform. By approximately 70 months post SCI a new steady state had been reached characterized by almost exclusively fast MHC isoform expression. This research has demonstrated that post SCI muscle type II transformation occurs in stages and commences earlier than previously appreciated. Interventions aimed at preventing or minimizing the transformation would need to be instituted within weeks post SCI.