Exercise training is associated with peripheral-cellular and central-cerebral processes, hormonal-neuronal regulation and transmission mechanisms. During the acute training response, peripheral cellular mechanisms are mainly metabolostatic to achieve energy supply and involve associated cytokine and hormonal reactions. Glycogen deficiency is associated with increased expression of local cytokines (interleukin-6, IL-6), decreased expression of glucose transporters, increased cortisol and decreased insulin secretion and beta-adrenergic stimulation. A nutrient-sensing signal of adipose tissue may be represented by leptin which, as for insulin, IL-6 and insulin-like growth-factor I (IGF-I), has profound effects on the hypothalamus and is involved in the metabolic hormonal regulation of exercise and training. Muscle damage and repair processes may involve the expression of inflammatory cytokines (e.g. tumour necrosis factor-alpha, TNF-alpha) and of stress proteins (e.g. heat shock protein 72). During overreaching and overtraining, a myopathy-like state is observed in skeletal muscle with depressed turnover of contractile proteins (e.g. in fast-type glycolytic fibres with a concomitant increase in slow type myosins). These alterations are influenced by exercise-induced hypercortisolism, and by decreased somatotropic hormones (e.g. IGF-I). The hypothalamus integrates various error signals (metabolic, hormonal, sensory afferents and central stimuli) and therefore pituitary releasing hormones represent the functional status of an athlete and long-term hypothalamic hormonal and sympathoadrenal downregulation are some of the prominent hormonal signs of prolonged overtraining and performance incompetence syndrome.

Heat shock protein, e.g. HSP70, can be induced in human skeletal muscle undergoing exercise training, and plays important role in adaptation to stress. This study was designed to investigate the effects of high-intensity strength training and low-intensity endurance training on the HSP70 response to exercise, bearing in mind whether HSP70 is induced in the well-trained muscle during low-intensity endurance training. Six well-trained rowers (male, aged 18 years) underwent a training program which consisted of 3 weeks high-intensity training (HIT) and 3 weeks low-intensity endurance training (ET), followed by 1 week of recovery each (R1 and R2, respectively). HSP70 (2.5 microg total protein loaded) was determined by Western blot with reference to a series of known amount of standard HSP70. HSP70 mRNA was analyzed by RT-PCR, and the relative percentage change was referred to the baseline level (before training). HSP70 increased significantly at the end of HIT (from 51 to 73 ng), decreased at the end of R1(66 ng), and remained unchanged throughout ET and R2. HSP70 mRNA increased significantly after HIT (257%) and decreased gradually afterwards (194%, 166%, and 119% for R1, ET, and R2, respectively). It can be concluded that: (1) HSP70 was induced by high-intensity training, but not by endurance training at low intensity, and (2) there was a discrepancy in terms of HSP70 regulation between the protein and mRNA levels, suggesting that posttranscriptional regulation may play a role in HSP70 expression in human skeletal muscle in response to exercise.

No abstract

The use of the acetylene rebreathing method to estimate cardiac output (CO) during high-intensity exercise, which may be influenced by recirculation of acetylene, has not been validated. This study was designed to validate the acetylene rebreathing method to measure CO during high-intensity exercise using the direct Fick method. CO was measured at rest and during exercise at 25%, 50%, 75% and 90% of the nine subjects' maximum oxygen uptake (VO2max) by the direct Fick and acetylene rebreathing method. CO measured by the acetylene rebreathing method correlated with work rate (r = 0.90, P < 0.01) and with oxygen uptake (r = 0.94, P < 0.01). The correlation coefficient of CO between both methods was r = 0.91 (P < 0.01). There was no significant difference in CO measured by each method at rest as well as at each work rate. The difference in CO between each method was greater at lower CO than at higher CO. At 90% of VO2max, the CO measured by acetylene rebreathing was nearly identical to that measured by the Fick method. It can be concluded that acetylene rebreathing for measurement of CO is valid not only at rest but also during exercise, especially during high-intensity exercise.

An important mechanism of muscle adaptation to exercise is the alteration of myosin heavy chain (MHC) isoform expression. This study investigated the effect of a high intensity resistance training (HIRT) and a low intensity endurance rowing (LIER) on MHC isoform expression in highly trained human muscle. Six well-trained male rowers underwent a training program consisting of a 3-week HIRT and a 3-week LIER, each followed by one-week of recovery. Muscle samples were taken from vastus lateralis before and at the end of each training and recovery phase. MHC isoform was analyzed by SDS-PAGE using silver stain and MHC isoform mRNA by RT-PCR. The maximum oxygen uptake and power output did not change after the training. MHC isoform composition did not change over HIRT or LIER, and there was a decrease in MHC I with concomitant increase in MHC IIa after recovery following HIRT. HIRT led to mRNA upregulation of MHC Ialpha, Ibeta and IIx (127 %, 148 % and 117 %, respectively, p < 0.05), but not MHC I protein (60 % vs 62 %, NS), and LIER led merely to MHC Ibeta mRNA upregulation (131 %, p < 0.05). Thus, different responses of MHC isoform expression to HIRT and LIER occurred in the highly trained muscle, and a "ceiling effect" in terms of MHC I expression could be observed. The upregulation of MHC Ialpha mRNA in human skeletal muscle documented in this study may encourage further observations in this field.