Needle biopsy samples were taken from vastus lateralis muscle (VL) of five male body builders (BB, age 27.4 ± 0.93 years; mean ±s.e.m.), who had being performing hypertrophic heavy resistance exercise (HHRE) for at least 2 years, and from five male active, but untrained control subjects (CTRL, age 29.9 ± 2.01 years). The following determinations were performed: anatomical cross‐sectional area and volume of the quadriceps and VL muscles in vivo by magnetic resonance imaging (MRI); myosin heavy chain isoform (MHC) distribution of the whole biopsy samples by SDS‐PAGE; cross‐sectional area (CSA), force (P_o), specific force (P_o/CSA) and maximum shortening velocity (V_o) of a large population (n= 524) of single skinned muscle fibres classified on the basis of MHC isoform composition by SDS‐PAGE; actin sliding velocity (V_f) on pure myosin isoforms by in vitro motility assays. In BB a preferential hypertrophy of fast and especially type 2X fibres was observed. The very large hypertrophy of VL in vivo could not be fully accounted for by single muscle fibre hypertrophy. CSA of VL in vivo was, in fact, 54% larger in BB than in CTRL, whereas mean fibre area was only 14% larger in BB than in CTRL. MHC isoform distribution was shifted towards 2X fibres in BB. P_o/CSA was significantly lower in type 1 fibres from BB than in type 1 fibres from CTRL whereas both type 2A and type 2X fibres were significantly stronger in BB than in CTRL. V_o of type 1 fibres and V_f of myosin 1 were significantly lower in BB than in CTRL, whereas no difference was observed among fast fibres and myosin 2A. The findings indicate that skeletal muscle of BB was markedly adapted to HHRE through extreme hypertrophy, a shift towards the stronger and more powerful fibre types and an increase in specific force of muscle fibres. Such adaptations could not be fully accounted for by well known mechanisms of muscle plasticity, i.e. by the hypertrophy of single muscle fibre (quantitative mechanism) and by a regulation of contractile properties of muscle fibres based on MHC isoform content (qualitative mechanism). Two BB subjects took anabolic steroids and three BB subjects did not. The former BB differed from the latter BB mostly for the size of their muscles and muscle fibres.

“Central” and “peripheral” limitations to oxidative metabolism during exercise were evaluated in 10 young males following a 35-day horizontal bed rest (BR). Incremental exercise (IE) and moderate- and heavy-intensity constant-load exercises (CLE) were carried out on a cycloergometer before and 1–2 days after BR. Pulmonary gas exchange, cardiac output (Q̇; by impedance cardiography), skeletal muscle (vastus lateralis), and brain (frontal cortex) oxygenation (by near-infrared spectroscopy) were determined. After BR, “peak” (values at exhaustion during IE) workload, peak O₂ uptake (V̇o_2peak), peak stroke volume, Q̇_peak, and peak skeletal muscle O₂ extraction were decreased (−18, −18, −22, −19, and −33%, respectively). The gas exchange threshold was ∼60% of V̇o_2peak both before and after BR. At the highest workloads, brain oxygenation data suggest an increased O₂ extraction, which was unaffected by BR. V̇o₂ kinetics during CLE (same percentage of peak workload before and after BR) were slower (time constant of the “fundamental” component: 31.1 ± 2.0 s before vs. 40.0 ± 2.2 s after BR); the amplitude of the “slow component” was unaffected by BR, thus it would be greater, after BR, at the same absolute workload. A more pronounced “overshoot” of skeletal muscle O₂ extraction during CLE was observed after BR, suggesting an impaired adjustment of skeletal muscle O₂ delivery. The role of skeletal muscles in the impairment of oxidative metabolism during submaximal and maximal exercise after BR was identified. The reduced capacity of peak cardiovascular O₂ delivery did not determine a “competition” for the available O₂ between skeletal muscles and brain.

S to constant-load moderate-intensity cycle ergometer exercise were determined on 15 MM, 8 McA, 21 patients with signs and/or symptoms of metabolic myopathy but a negative biopsy ("patient controls"; P-CTRL), and 22 healthy untrained controls (CTRL). Results: V˙O2 kinetics were slower in MM and in McA versus P-CTRL and CTRL, slower in McA versus MM, and not significantly different between P-CTRL and CTRL. The time constants (τ) of the monoexponential function describing the V˙O2 kinetics were (X¯ ± SE) 59.2 ± 8.5 s in MM, 87.6 ± 16.4 s in McA, 36.9 ± 3.1 s in P-CTRL, and 35.4 ± 1.9 s in CTRL. In a subgroup of the patients (eight MM and seven McA), τ of V˙O2 kinetics were negatively correlated with two variables determined in a previous study (Grassi B, Marzorati M, Lanfranconi F, et al. Impaired oxygen extraction in metabolic myopathies: detection and quantification by near-infrared spectroscopy. Muscle Nerve. 2007;35:510-20): a) a muscle oxygenation index, obtained by near-infrared spectroscopy, estimating the peak capacity of skeletal muscle fractional O2 extraction; and b) V˙O2 peak. Conclusions: In MM and McA patients, analysis of pulmonary V˙O2 kinetics during moderate-intensity exercise allows to identify and to quantify, noninvasively, the impairment of skeletal muscle oxidative metabolism. In these patients, the slower V˙O2 kinetics can be considered a marker of the impaired exercise tolerance. The present data could be useful for clinicians who need an objective, quantitative, and longitudinal evaluation of the impairment to be used in the follow-up of these patients as well as in the assessment of therapeutic interventions....

Al exercise (IE) and a series of constant-load (CLE) moderate-intensity exercise tests on a cycloergometer. The following variables were determined: heart rate (HR); breath-by-breath pulmonary O2 uptake (V̇O2); and skeletal muscle (vastus lateralis) oxygenation indices by continuous-wave near-infrared spectroscopy. Changes in concentration of deoxygenated hemoglobin (Hb) and myoglobin (Mb) (Δ[deoxy(Hb + Mb)]), expressed as a fraction of values obtained during a transient limb ischemia, were taken as an index of skeletal muscle O2 extraction. "Peak" values were determined at exhaustion during IE. Kinetics of adjustment of variables were determined during CLE. Results: V̇O2peak, HRpeak, and Δ[deoxy(Hb + Mb)] peak were significantly lower in HTR than in CTRL (17.1 ± 0.7 vs 34.0 ± 1.9 mL·kg−1·min−1, 133.8 ± 3.8 vs 173.0 ± 4.8 bpm, and 0.42 ± 0.03 vs 0.58 ± 0.04, respectively). In HTR, Δ[deoxy(Hb + Mb)] increase at submaximal workloads was steeper than in CTRL, suggesting an impaired O2 delivery to skeletal muscles, whereas the lower Δ[deoxy(Hb + Mb)] peak values suggest an impaired capacity of O2 extraction at peak exercise. V̇O2 and HR kinetics during CLE were significantly slower in HTR than in CTRL, whereas, unexpectedly, no significant differences were found for Δ[deoxy(Hb+Mb)] kinetics (mean response time: 21.3 ± 1.1 vs 20.2 ± 1.2 s). Conclusion: The findings confirm the presence of both "central" (cardiovascular) and "peripheral" (at the skeletal muscle level) impairments to oxidative metabolism in HTR. The noninvasiveness of the measurements will allow for serial evaluation of the patients, in the presence and/or absence of rehabilitation programs....

Separating out the effects of cancer and treatment between central and peripheral components of the O₂ delivery chain should be of interest to clinicians for longitudinal evaluation of potential functional impairment in order to set appropriate individually tailored training/rehabilitation programmes. We propose a non-invasive method (NIRS, near infrared spectroscopy) to be used in routine clinical practice to evaluate a potential impairment of skeletal muscle oxidative capacity during exercise in children previously diagnosed with acute lymphoblastic leukaemia (ALL). The purpose of this study was to evaluate the capacity of skeletal muscle to extract O₂ in 10 children diagnosed with ALL, 1 year after the end of malignancy treatment, compared to a control group matched for gender and age (mean±SD = 7.8±1.5 and 7.3±1.4 years, respectively). Participants underwent an incremental exercise test on a treadmill until exhaustion. Oxygen uptake ( ), heart rate (HR), and tissue oxygenation status (Δ[HHb]) of the vastus lateralis muscle evaluated by NIRS, were measured. The results showed that, in children with ALL, a significant linear regression was found by plotting vs Δ[HHb] both measured at peak of exercise. In children with ALL, the slope of the HR vs linear response (during sub-maximal and peak work rates) was negatively correlated with the peak value of Δ[HHb]. The present study proves that the NIRS technique allows us to identify large inter-individual differences in levels of impairment in muscle O₂ extraction in children with ALL. The outcome of these findings is variable and may reflect either muscle atrophy due to lack of use or, in the most severe cases, an undiagnosed myopathy.