Key pointsr Skeletal muscle hypertrophy is one of the main outcomes from resistance training (RT), but how it is modulated throughout training is still unknown.r We show that changes in myofibrillar protein synthesis (MyoPS) after an initial resistance exercise (RE) bout in the first week of RT (T1) were greater than those seen post-RE at the third (T2) and tenth week (T3) of RT, with values being similar at T2 and T3.r Muscle damage (Z-band streaming) was the highest during post-RE recovery at T1, lower at T2 and minimal at T3.r When muscle damage was the highest, so was the integrated MyoPS (at T1), but neither were related to hypertrophy; however, integrated MyoPS at T2 and T3 were correlated with hypertrophy.r We conclude that muscle hypertrophy is the result of accumulated intermittent increases in MyoPS mainly after a progressive attenuation of muscle damage.Abstract Skeletal muscle hypertrophy is one of the main outcomes of resistance training (RT), but how hypertrophy is modulated and the mechanisms regulating it are still unknown. To investigate how muscle hypertrophy is modulated through RT, we measured day-to-day integrated myofibrillar protein synthesis (MyoPS) using deuterium oxide and assessed muscle damage at the beginning (T1), at 3 weeks (T2) and at 10 weeks of RT (T3). Ten young men (27 (1) years, mean (SEM)) had muscle biopsies (vastus lateralis) taken to measure integrated MyoPS and muscle damage (Z-band streaming and indirect parameters) before, and 24 h and 48 h post resistance exercise (post-RE) at T1, T2 and T3. Fibre cross-sectional area (fCSA) was evaluated using biopsies at T1, T2 and T3. Increases in fCSA were observed only at T3 (P = 0.017). Changes in MyoPS post-RE at T1, T2 and T3 were greater at T1 (P < 0.03) than at T2 and T3 (similar values between T2 and T3). Muscle damage was the highest during post-RE recovery at T1, attenuated at T2 and further attenuated at T3. The change in MyoPS post-RE at both T2 and T3, but not at T1, was strongly correlated (r 0.9, P < 0.04) with muscle hypertrophy. Initial MyoPS response post-RE in an RT programme is not directed to support muscle hypertrophy, coinciding with the greatest muscle damage. However, integrated MyoPS is quickly 'refined' by 3 weeks of RT, and is related to muscle hypertrophy. We conclude that muscle hypertrophy is the result of accumulated intermittent changes in MyoPS post-RE in RT, which coincides with progressive attenuation of muscle damage.

To compare post-resistance exercise hypotension (PREH) and its mechanisms in normotensive and hypertensive individuals, 14 normotensives and 12 hypertensives underwent two experimental sessions: control (rest) and exercise (seven exercises, three sets, 50% of one repetition maximum). Hemodynamic and autonomic clinic measurements were taken before (Pre) and at two moments post-interventions (Post 1: between 30 and 60 min; Post 2: after 7 h). Ambulatory blood pressure (BP) was monitored for 24 h. At Post 1, exercise decreased systolic BP similarly in normotensives and hypertensives (-8 ± 2 vs -13 ± 2 mmHg, P > 0.05), whereas diastolic BP decreased more in hypertensives (-4 ± 1 vs -9 ± 1 mmHg, P < 0.05). Cardiac output and systemic vascular resistance did not change in normotensives and hypertensives (0.0 ± 0.3 vs 0.0 ± 0.3 L/min; -1 ± 1 vs -2 ± 2 U, P > 0.05). After exercise, heart rate (+13 ± 3 vs +13 ± 2 bpm) and its variability (low- to high-frequency components ratio, 1.9 ± 0.4 vs +1.4 ± 0.3) increased whereas stroke volume (-14 ± 5 vs -11 ± 5 mL) decreased similarly in normotensives and hypertensives (all, P > 0.05). At Post 2, all variables returned to pre-intervention, and ambulatory data were similar between sessions. Thus, a session of resistance exercise promoted PREH in normotensives and hypertensives. Although this PREH was greater in hypertensives, it did not last during the ambulatory period, which limits its clinical relevance. In addition, the mechanisms of PREH were similar in hypertensives and normotensives.

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The manipulation of resistance training (RT) variables is used among athletes, recreational exercisers, and compromised populations (e.g., elderly) attempting to potentiate muscle hypertrophy. However, it is unknown whether an individual’s inherent predisposition dictates the RT-induced muscle hypertrophic response. Resistance-trained young [26 (3) y] men ( n = 20) performed 8 wk unilateral RT (2 times/wk), with 1 leg randomly assigned to a standard progressive RT [control (CON)] and the contralateral leg to a variable RT (VAR; modulating exercise load, volume, contraction type, and interset rest interval). The VAR leg completed all 4 RT variations every 2 wk. Bilateral vastus lateralis cross-sectional area (CSA) was measured, pre- and post-RT and acute integrated myofibrillar protein synthesis (MyoPS) rates were assessed at rest and over 48 h following the final RT session. Muscle CSA increase was similar between CON and VAR ( P > 0.05), despite higher total training volume (TTV) in VAR ( P < 0.05). The 0–48-h integrated MyoPS increase postexercise was slightly greater for VAR than CON ( P < 0.05). All participants were considered “responders” to RT, although none benefited to a greater extent from a specific protocol. Between-subjects variability (MyoPS, 3.30%; CSA, 37.8%) was 40-fold greater than the intrasubject (between legs) variability (MyoPS, 0.08%; CSA, 0.9%). The higher TTV and greater MyoPS response in VAR did not translate to a greater muscle hypertrophic response. Manipulating common RT variables elicited similar muscle hypertrophy than a standard progressive RT program in trained young men. Intrinsic individual factors are key determinants of the MyoPS and change in muscle CSA compared with extrinsic manipulation of common RT variables. NEW & NOTEWORTHY Systematically manipulating resistance training (RT) variables during RT augments the stimulation of myofibrillar protein synthesis (MyoPS) and training volume but fails to potentiate muscle hypertrophy compared with a standard progressive RT. Any modest further MyoPS increase and higher training volumes do not reflect in a greater hypertrophic response. Between-subject variability was 40-fold greater than the variability promoted by extrinsic manipulation of RT variables, indicating that individual intrinsic factors are stronger determinants of the hypertrophic response.

Subjects with PD demonstrated blunted metabolic and cardiovascular responses to submaximal and maximal exercise tests, especially at intensities above AT, which are in line with autonomic disturbances present in patients with PD. Future studies need to determine how this affects performance, participation, and responses of these patients to exercise training at different intensities.