The purpose of this study was to evaluate different efficiency indices, i.e., gross (GE: no baseline correction), net (NE: resting metabolism as baseline correction), and work (WE: unloaded exercise as baseline correction), to reveal the effect of endurance training on mechanical efficiency. Nine healthy sedentary women undertook an incremental test and submaximal cycling exercise, at an intensity corresponding to 50% of the pretraining peak oxygen uptake, before and after 6 weeks of endurance training (18 sessions of 45 min). The training effects on efficiency indices were tested by comparisons based on GE, NE, and WE as well as by the differences between the percentage changes of all indices (%GE, %NE, %WE). Endurance training resulted in significantly higher GE (+11.1%; p < 0.001) and NE (+9.1%; p < 0.01). Only minor significant improvement (+2.4%; p < 0.05) was observed with the WE index because the value used for baseline subtraction was significantly reduced by the training sessions, due perhaps to improvement in pedaling skill. As a consequence, %WE was significantly lower than %GE (p < 0.01) and %NE (p < 0.05), while %GE and %NE were not significantly different. We conclude that mechanical efficiency of cycling increases with training in women previously unfamiliar with cycling, and that the WE index is less sensitive to this training effect than GE and NE indices.
A single bout of eccentric exercise confers a long-lasting protective effect against subsequent bouts of the same exercise. This study investigated how the protective effect was lessened when the interval between the initial and secondary exercise bouts was increased from 4 to 12 weeks. Thirty young men performed two bouts of 12 maximal eccentric actions of the elbow flexors of the nondominant arm separated by either 4 (n = 9), 8 (n = 10), or 12 (n = 11) weeks. Maximal isometric strength, flexed and relaxed elbow joint angles, range of motion, upper arm circumference, muscle soreness, plasma creatine kinase (CK), and myoglobin (Mb) were measured before, immediately after, and for 4 days after exercise. Changes in criterion measures were compared between bouts for each group and among groups by two-way repeated-measures ANOVA. There were no significant differences among groups in the changes in all measures following the first bout. Significantly (p < 0.05) smaller responses in all measures were observed after the second bout as compared with first bout for the 4 and 8 weeks, but only in strength, muscle soreness, CK, and Mb for the 12 weeks. It was concluded that some aspects of the protective effect were attenuated after 8 weeks, and the factors responsible for the effect vary among the measures.
The pump-perfused rat hindlimb model, in various forms, has been in use for several decades. There are many applications for this model, owing to the ability to control the content and rate of perfusion. In the context of exercise physiology this model has been put to particularly good use. In this report we summarize some of the central surgical differences between different versions of the pump-perfused rat hindlimb model, including the double hindlimb + trunk, double hindlimb alone, single hindlimb, and distal hindlimb-alone models. We also summarize specific elements of the perfusion medium and measurement of force used in our lab during assessment of muscle metabolic and contractile responses, and illustrate some of the differences from the in vivo condition that merit consideration. We then provide specific examples of how the single pump-perfused hindlimb and distal hindlimb-alone versions of this model have been used to study muscle function and energy metabolism. In this context we show how this model can be used to permit the experimenter to manipulate and control the rate of O(2)delivery and to add specific compounds that inhibit a particular aspect of muscle metabolism, such that in combination with measurements of the flux of specific substances across the muscle and/or fast-freezing of muscle after contractions, more can be understood about the metabolic state of the contracting muscles.
Unilateral, chronic low-frequency electrical stimulation (CLFS) is an experimental model that evokes numerous biochemical and physiological adaptations in skeletal muscle. These occur within a short time frame and are restricted to the stimulated muscle. The humoral effects of whole body exercise are eliminated and the nonstimulated contralateral limb can often be used as a control muscle, if possible effects on the contralateral side are considered. CLFS induces a fast-to-slow transformation of muscle because of alterations in calcium dynamics and myofibrillar proteins, and a white-to-red transformation because of changes in mitochondrial enzymes, myoglobin, and the induction of angiogenesis. These adaptations occur in a coordinated time-dependent manner and result from altered gene expression, including transcriptional and posttranscriptional processes. CLFS techniques have also been applied to myocytes in cell culture, which provide a greater opportunity for the delivery of pharmacological agents or for the application of gene transfer methodologies. Clinical applications of the CLFS technique have been limited, but they have shown potential therapeutic value in patients in whom voluntary muscle contraction is not possible due to debilitating disease and/or injury. Thus the CLFS technique has great value for studying various aspects of muscle adaptation, and its wider scientific application to a variety of neuromuscular-based disorders in humans appears to be warranted.
While the physiological adaptations following endurance training are relatively well understood, in swimming there is a dearth of knowledge regarding the metabolic responses to interval training (IT). The hypothesis tested predicted that two different endurance swimming IT sets would induce differences in the total time the subjects swam at a high percentage of maximal oxygen consumption (VO(2)max). Ten trained triathletes underwent an incremental test to exhaustion in swimming so that the swimming velocity associated with VO(2)max (vVO(2)max) could be determined. This was followed by a maximal 400-m test and two intermittent sets at vVO(2)max: (a) 16 x 50 m with 15-s rest (IT(50)); (b) 8 x 100 m with 30-s rest (IT(100)). The times sustained above 95% VO(2)max (68.50 +/- 62.69 vs. 145.01 +/- 165.91 sec) and 95% HRmax (146.67 +/- 131.99 vs. 169.78 +/- 203.45 sec, p = 0.54) did not differ between IT(50) and IT(100)(values are mean +/- SD). In conclusion, swimming IT sets of equal time duration at vVO(2)max but of differing work-interval durations led to slightly different VO(2)and HR responses. The time spent above 95% of VO(2)max was twice as long in IT(100) as in IT (50), and a large variability between mean VO(2)and HR values was also observed.
Understanding the effects of physiological aging on blood flow to active skeletal muscle and its regulation during exercise has important functional, hemodynamic, and metabolic implications for our rapidly expanding elderly population. During peak exercise involving a large muscle mass, blood flow to the legs is lower in healthy older compared to younger persons; this results from central (reduced cardiac output) and peripheral (reduced leg vascular conductance) limitations. There is considerable variability in the literature concerning age-related changes in leg blood flow during submaximal exercise, with reports of similar or reduced leg blood flow and vascular conductance in older vs. younger subjects depending on the exercise intensity and the gender and training status of the subjects. However, all the studies involving non-endurance-trained subjects are consistent in that older subjects achieve the requisite leg blood flow at higher arterial perfusion pressures than young subjects, suggesting altered local vasoregulatory mechanisms with aging. Although the nature of these age-related alterations is poorly understood, we have preliminary evidence for augmented sympathetic vasoconstrictor responsiveness in the legs of older men during exercise, and blunted leg vasodilator responsiveness in older women. Systematic research will be needed in order to define the central and local mechanisms underlying these age- and gender-specific differences in muscle vascular responsiveness. Such information will be important for designing future interventions aimed at improving muscle blood supply and functional capacity in older persons.
Muscle hypertrophy is an adaptive response to overload that requires increasing gene transcription and synthesis of muscle-specific proteins resulting in increased protein accumulation. Progressive resistance training (P(RT)) is thought to be among the best means for achieving hypertrophy in humans. However, hypertrophy and functional adaptations to P(RT) in the muscles of humans are often difficult to evaluate because adaptations can take weeks, months, or even years before they become evident, and there is a large variability in response to P(RT) among humans. In contrast, various animal models have been developed which quickly result in extensive muscle hypertrophy. Several such models allow precise control of the loading parameters and records of muscle activation and performance throughout overload. Scientists using animal models of muscle hypertrophy should be familiar with the advantages and disadvantages of each and thereby choose the model that best addresses their research question. The purposes of this paper are to review animal models currently being used in basic research laboratories, discuss the hypertrophic and functional outcomes as well as applications of these models to aging, and highlight a few mechanisms involved in regulating hypertrophy as a result of applying these animal models to questions in research on aging.
The purpose of this study was to determine the effects of a 1,500-m swim on energy expenditure during a subsequent cycle task. Eight well-trained male triathletes (age 26.0 +/- 5.0 yrs; height 179.6 +/- 4.5 cm; mass 71.3 +/- 5.8 kg; VO(2)max 71.9 +/- 7.8 ml.kg(-1).min(-1)) underwent two testing sessions in counterbalanced order. The sessions consisted of a 30-min ride on the cycle ergometer at 75% of maximal aerobic power (MAP), and at a pedaling frequency of 95 rev.min(-1), preceded either by a 1,500-m swim at 1.20 m.s(-1) (SC trial) or by a cycling warm-up at 30% of MAP (C trial). Respiratory and metabolic data were collected between the 3rd and the 5th min, and between the 28th and 30th min of cycling. The main results indicated a significantly lower gross efficiency (13.0%) and significantly higher blood lactate concentration (56.4%), VO(2) (5.0%), HR (9.3%), VE (15.7%), and RF (19.9%) in the SC compared to the C trial after 5 min, p < 0.05. After 30 min, only VE (7.9%) and blood lactate concentration (43.9%) were significantly higher in the SC compared to the C trial, p < 0.05. These results confirm the increase in energy cost previously observed during sprint-distance triathlons and point to the importance of the relative intensity of swimming on energy demand during subsequent cycling.