Lifting weights and rowing are a fascinating unknown field. Nobody can assure you that lifting heavyweights will make you faster on the water. Erg test results don’t compare to water speed. To row on the water fast you need to be able to move a boat and to do that you need to be efficient. Bigger muscles go against muscle efficiency and coordination but they are needed to gain power. So how you gain this power and grow these muscles without losing coordination will be a key element of your training.
There is only one thing that is true. Whatever you do that makes you increase water speed is good. If you improve your lifting power, your erg score but don’t increase water speed, you are not really doing it right. If your erg score or how much you can lift had a direct relationship with how fast you can go at 38 strokes a minute during 2000 meters our sport will be too simple, it’s not.
When I coach athletes I like to develop their power using these 4 points listed:
1) Rowing at low rate with maximum power per stroke. I use the small boats and the Rowperfect3.
2) Rowing at low rates with a boungee cord on the water and a heavy drag on the Rowperfect3.
3) Doing lifting with multiple repetitions with very low weight doing parts of the rowing motion like jumpies, bar circuits and body circuits.
4) Doing sets of few strokes at multiple strokes rates with varaiation of drag on boat and Rowperfect3.
With that I achieve huge amounts of rowing efficient coordinated power. With that the athletes I coach can lead the race from the start and low at control rates with plenty of speed.
In this article listed under you can read that lifting lighter weights for a longer time stimulates muscle protein synthesis a lot. This is what i use instead of lifting heavy weights that make the rower to have a bigger chance to injure and destroy their body.
Bigger weights may not beget bigger muscles: evidence from acute muscle protein synthetic responses after resistance exercise
Nicholas A. Burd, Cameron J. Mitchell, Tyler A. Churchward-Venne, and Stuart M. Phillips
Abstract: It is often recommended that heavier training intensities (∼70%–80% of maximal strength) be lifted to maximize muscle growth. However, we have reported that intensities as low as 30% of maximum strength, when lifted to volitional fa- tigue, are equally effective at stimulating muscle protein synthesis rates during resistance exercise recovery. This paper dis- cusses the idea that high-intensity contractions are not the exclusive driver of resistance exercise-induced changes in muscle protein synthesis rates.
The contraction stimulus driving MPS
There are a myriad of resistance exercise variables, beyond intensity, which can be manipulated to produce diverse training mediated hypertrophy; these variables can include volume, muscle action, muscle time under tension, lifting cadence, contraction mode, and inter-set rest interval (American Col- lege of Sports Medicine 2009). Indeed, for each of these variables to have independent effects on muscle protein turnover, and thus hypertrophic adaptation, the skeletal muscle must be able to “gauge” these variables as distinct mechanical stimuli, such as interacting with the metabolic and hormonal milieu, that can subsequently be transformed into intramuscular signals that leads to the stimulation of MPS. Theoretically, each variable would elicit a specific muscle phenotypic response. However, such evidence is, at least in our view, lacking. From a systems perspective, the input into a skeletal motor unit–muscle fibre to lift a weight would come from the neural signals it received, and these signals would determine whether to fire or not fire and at what frequency. The surrounding nutrient milieu would then dictate (to a variable degree) the response of the fibre in terms of MPS (Biolo et al. 1997), which would ulti- mately sum to yield hypertrophy over time. When viewed from this perspective, there is an underlying commonality between many RT variables such that application of any variable in such a way to induce muscle activation ulti- mately serves to activate the same intramuscular signaling pathways necessary to stimulate MPS and potentially training- induced hypertrophy. Indeed, many will argue that the phe- notype of ultimate importance with any program of RT is both strength and hypertrophy and we do not disagree with this. However, a common link between these variables is hypertrophy, and thus we focus on gains in muscle protein mass in this review. Strength gains are, however, a product of neuromuscular and muscular adaptations as reviewed elsewhere (Sale 1988).
Resistance exercise intensities of ∼70%–80% of 1 repeti- tion maximum (1RM) for 8–12 repetitions are the classically prescribed protocols to use to maximize training-induced muscle hypertrophy (American College of Sports Medicine 2009).
What is so intrinsically unique about high-intensity re- sistance exercise in terms of promoting exercise-induced MPS? It may be related to the existence of a positive relationship between greater force development and increased muscle electromyographic activity (Alkner et al. 2000). Accordingly, a greater recruitment of muscle fibres at high exercise intensities may occur to stimulate a robust MPS response. Kumar and colleagues (2009) provide support for the concept of a dose–response relationship between external work-equated exercise intensities and MPS. From this work it appears the relationship reaches a plateau between intensities of ∼60–90% of 1RM (Kumar et al. 2009).
This outcome, we propose, is likely a product of maximal, or at least near max- imal, muscle fibre recruitment at contraction intensities be- yond 60% of 1RM. Thus, there would be little reason to expect a large difference in MPS unless the muscle fibre had an intricately sensitive mechanism to detect a difference be- tween 60% and 90% of 1RM, a concept that appears, at least according to all available data, highly unlikely. It is generally accepted that motor units are recruited in accordance with the size principle during voluntary muscle contraction (Henne- man et al. 1965).
Against this background, it would seem reasonable to assume that lower intensities performed to volitional fatigue (i.e., task failure) could achieve a similar degree of muscle fibre activation to that of high-intensity resistance exercise regimes performed to task failure, and presumably a similar stimulation of MPS during recovery.
Certainly, such a thesis would be dependent on the notion that maximal fibre activation occurs at the moment of fatigue, which is an idea that has support.
Our laboratory has recently tested the thesis that eliciting failure during high- or low-intensity resistance exercise leads to maximal muscle fibre activation, and thus a similar stimu- lation of MPS. It was demonstrated, in resistance-trained young men, that lower intensity (30% of 1RM) and higher volume (24 ± 3 repetitions, means ± SD) resistance exercise performed until failure was equally effective in stimulating myofibrillar protein synthesis rates during 0–4 h recovery as heavy intensity (90% of 1RM) and lower volume (5 ± 1 rep- etitions) resistance exercise (Burd et al. 2010b).
Interestingly, exercise performed at 30% of 1RM induced a longer-lasting effect on MPS at 21–24 h of exercise recovery (Burd et al. 2010b). The observation of a sustained elevation in myofibrillar protein synthesis rates after the low-intensity–higher volume regime corroborates recent data demonstrating that exercise volume is an integral factor for sustaining the myofibrillar protein synthetic response during exercise recovery (Burd et al. 2010a).
Thus, an additional benefit of low-intensity resistance exercise is that it allows for higher total number of repetitions to be performed, which is an important variable to sustain the response, and still eventually results in full motor unit recruitment.
For clarity, the performance of dynamic knee extension exercise at 30% of 1RM to failure, as we did previously (Burd et al. 2010b), induces fatigue in the contracting leg within 24 repetitions. This number of repetitions effectively minimizes the time that loaded muscle is under tension and likely prevents a shift toward the synthesis of non-contractile proteins (Burd et al. 2012). Also, leg extension exercise, even at low intensities, is effective at inducing temporary occlusion of blood flow (Wernbom et al. 2009).
Thus, other types of resistance exercises (e.g., leg press) would require more repetitions to induce fatigue with an intensity at 30% of 1RM (Hoeger et al. 1990). An argument that is commonly put forward is the sustained elevation in postabsorptive MPS observed after the low-intensity–higher volume condition, such as in our previous study (Burd et al. 2010b), simply represents a state of increased muscle protein turnover as compared with the high-intensity condition.
We cannot completely dismiss such an argument as invalid. It is clear the substrates to support MPS, in the fasting state, are the amino acids released from muscle protein breakdown (Phil- lips et al. 1997). However, examining the 24-h responses after feeding 15 g of high-quality protein, and thus decreas- ing muscle protein breakdown (Biolo et al. 1997), demon- strates that myofibrillar protein accretion is occurring in similar magnitude to the high-intensity condition (Burd et al. 2011). Thus, we speculate that low-intensity training would result in a similar amount of training-induced muscle mass as high-intensity resistance training.