Santorio Santorio (1561-1636), a physician from Koper trained in the exacting environment of Vesalius and a man used to exchanging ideas in the brilliant circle of people meeting in the drawing room of Morosini Palace (among whom were Paolo Sarpi, Galileo Galilei, Fabrizio d’Acquapendente, Giovambattista della Porta and Prospero Alpini), used the power of the experimental method to unseat a model of metabolic balance. Santorio embodied the role of a modern physician- scientist directly experimenting on patients, who after measuring the deviation from the norm of their functions (metabolism, temperature and pulse) offers a reasoned therapy. He was the model of a charismatic physician for the thousands of medical students who trained in Padua, benefiting from the tolerant atmosphere of the Republic of Venice. They, returning to their homelands, granted a continuous discussion and success to Santorio’s teachings and works. He introduced quantitative medicine by measuring physical activity, foods, drinkables, urine, feces and calculating perspiration. He also developed – inspired by Galileo’s experiments – a clinical thermometer and the rules to measure temperature in humans (on the skin, in the mouth and in expired air), and a stop clock to measure the pulse, by developing the pulsilogium (pulsometer) based on the Galilean principle of oscillation. The present study gives a start to presenting Santorio’s contributions to nephrology, by discussing aphorisms related to kidney function and body fluid balance.
COBISS.SI-ID: 1536281540
Costameres are mechano-sensory sites of focal adhesion in the sarcolemma that provide a structural anchor for myofibrils. Their turnover is regulated by integrin-associated focal adhesion kinase (FAK). We hypothesized that changes in content of costamere components (beta 1 integrin, FAK, meta-vinculin, gamma-vinculin) with increased and reduced loading of human anti-gravity muscle would: (i) relate to changes in muscle size and molecular parameters of muscle size regulation [p70S6K, myosin heavy chain (MHC)1 and MHCIIA]; (ii) correspond to adjustments in activity and expression of FAK, and its negative regulator, FRNK; and (iii) reflect the temporal response to reduced and increased loading. Unloading induced a progressive decline in thickness of human vastus lateralis muscle after 8 and 34 days of bedrest (−4% and −14%, respectively; n = 9), contrasting the increase in muscle thickness after 10 and 27 days of resistance training (+5% and +13%; n = 6). Changes in muscle thickness were correlated with changes in cross-sectional area of type I muscle fibers (r = 0.66) and beta 1 integrin content (r = 0.76) at the mid-point of altered loading. Changes in meta-vinculin and FAK-pY397 content were correlated (r = 0.85) and differed, together with the changes of beta 1 integrin, MHCI, MHCII and p70S6K, between the mid- and end-point of resistance training. By contrast, costamere protein level changes did not differ between time points of bedrest. The findings emphasize the role of FAK-regulated costamere turnover in the load-dependent addition and removal of myofibrils, and argue for two phases of muscle remodeling with resistance training, which do not manifest at the macroscopic level.
COBISS.SI-ID: 2432723
Oxidative function during exercise was evaluated in 11 young athletes with marked skeletal muscle hypertrophy induced by long-term resistance training (RTA, body mass 102.67.3 kg, meanSD) and 11 controls (CTRL, body mass 77.86.0). Pulmonary O2 uptake (V'O2) and vastus lateralis muscle fractional O2 extraction (by near-infrared spectroscopy) were determined during an incremental cycle ergometer (CE) and one-leg knee-extension (KE) exercise. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibers obtained by biopsy. Quadriceps femoris muscle cross sectional area, volume (determined by magnetic resonance imaging) and strength were greater in RTA vs. CTRL (by ~40%, ~33% and ~20%, respectively). V'O2peak during CE was higher in RTA vs. CTRL (4.050.64 L min-1 vs. 3.560.30); no difference between groups was observed during KE. The O2 cost of CE exercise was not different between groups. When divided per muscle mass (for CE) or quadriceps muscle mass (for KE) V'O2peak was lower (by 15-20%) in RTA vs. CTRL. Vastus lateralis fractional O2 extraction was lower in RTA vs. CTRL at all work rates, both during CE and KE. RTA had higher ADP-stimulated mitochondrial respiration (56.723.7 pmolO2s-1mg-1 ww) vs. CTRL (35.710.2), and a tighter coupling of oxidative phosphorylation. In RTA the greater muscle mass and maximal force, and the enhanced mitochondrial respiration seem to compensate for the hypertrophy-induced impaired peripheral O2 diffusion. The net results are an enhanced whole body oxidative function at peak exercise, and unchanged efficiency and O2 cost at submaximal exercise, despite a much greater body mass
COBISS.SI-ID: 2371027
During the reambulation procedure after 35-day head-down tilt bed rest (HDTBR) for 9 men, we recorded for the first time heart rate (HR; with electrocardiogram) and arterial pressure profiles (fingertip plethysmography) for 5 min in HDTBR and horizontal (SUP) positions, followed by 12 min in standing position, during which 4 subjects fainted (intolerant, INT) and were laid horizontal again (Recovery). We computed: mean arterial pressure (P; pressure profiles integral mean), stroke volume (SV; obtained with Modelflow method), and cardiac output (Q; SV HR). All cardiovascular data remained stable in HDTBR and SUP for both groups (EXP). Taking the upright posture, EXP showed a decrease in SV and an increase in HR, becoming significantly different from SUP within 1 min. Further evolution of these parameters kept Q stable in both groups until the second minute of standing. Afterward, in INT, P precipitated without further HR increases: SV stopped being corrected and Q reached 2.9 0.4 Lmin(-1) at the last 15 s of standing. Sudden drop in P allowed identification of a low-pressure threshold in INT (70.7 12.9 mm Hg), after which syncope occurred within 80 s. During Recovery, baroreflex curves showed a flat phase (P increase, HR stable), followed by a steep phase (P increased, HR decreased, starting when P was 84.5 12.5 mm Hg and Q was 9.6 1.5 Lmin(-1)). INT, in contrast with tolerant subjects, did not sustain standing because HR was unable to correct for the P drop. These results indicate a major role for impaired arterial baroreflexes in the onset of orthostatic intolerance
COBISS.SI-ID: 2396627
The aim of this study was to determine the effect of prolonged intensive cycling and postexercise recovery in the heat on brain sources of altered brain oscillations. After a max test and familiarization trial, nine trained male subjects (23 ± 3 yr; maximal oxygen uptake = 62.1 ± 5.3 ml•min(-1)•kg(-1)) performed three experimental trials in the heat (30°C; relative humidity 43.7 ± 5.6%). Each trial consisted of two exercise tasks separated by 1 h. The first was a 60-min constant-load trial, followed by a 30-min simulated time trial (TT1). The second comprised a 12-min simulated time trial (TT2). After TT1, active recovery (AR), passive rest (PR), or cold water immersion (CWI) was applied for 15 min. Electroencephalography was measured at baseline and during postexercise recovery. Standardized low-resolution brain electromagnetic tomography was applied to accurately pinpoint and localize altered electrical neuronal activity. After CWI, PR and AR subjects completed TT2 in 761 ± 42, 791 ± 76, and 794 ± 62 s, respectively. A prolonged intensive cycling performance in the heat decreased β activity across the whole brain. Postexercise AR and PR elicited no significant electrocortical differences, whereas CWI induced significantly increased β3 activity in Brodmann areas (BA) 13 (posterior margin of insular cortex) and BA 40 (supramarginal gyrus). Self-paced prolonged exercise in the heat seems to decrease β activity, hence representing decreased arousal. Postexercise CWI increased β3 activity at BA 13 and 40, brain areas involved in somatosensory information processing.
COBISS.SI-ID: 2451411