Role of CaMKII and sarcolipin in muscle adaptations to strength training with different levels of fatigue in the set

Abstract

Strength training promotes a IIX‐to‐IIA shift in myosin heavy chain (MHC) composition, likely due to changes in sarcoplasmic [Ca2+] which are sensed by CaMKII. Sarcoplasmic [Ca2+] is in part regulated by sarcolipin (SLN), a small protein that when overexpressed in rodents stimulates mitochondrial biogenesis and a fast‐to‐slow fiber type shift. The purpose of this study was to determine whether CaMKII and SLN are involved in muscle phenotype and performance changes elicited by strength training. Twenty‐two men followed an 8‐week velocity‐based resistance training program using the full squat exercise while monitoring repetition velocity. Subjects were randomly assigned to two resistance training programs differing in the repetition velocity loss allowed in each set: 20% (VL20) vs 40% (VL40). Strength training caused muscle hypertrophy, improved 1RM and increased total CaMKII protein expression, particularly of the δD isoform. Phospho‐Thr287‐CaMKII δD expression increased only in VL40 (+89%), which experienced greater muscle hypertrophy, and a reduction in MHC‐IIX percentage. SLN expression was increased in VL20 (+33%) remaining unaltered in VL40. The changes in phospho‐Thr287‐CaMKII δD were positively associated with muscle hypertrophy and the number of repetitions during training, and negatively with the changes in MHC‐IIX and SLN. Most OXPHOS proteins remained unchanged, except for NDUFB8 (Complex I), which was reduced after training (−22%) in both groups. The amount of fatigue allowed in each set critically influences muscle CaMKII and SLN responses and determines muscle phenotype changes. With lower intra‐set fatigue, the IIX‐to‐IIA MHC shift is attenuated.

The effects of different intra-set velocity loss thresholds on lower-limb adaptations to resistance training in young adults: A systematic review and meta-analysis

“…The dissociation between changes in muscle size and muscle function may be related to the molecular events occurring after each RT protocol. High VL thresholds also result in increased skeletal muscle protein expression of total and phosphorylated CaMKII, a predominantly sarcoplasmic protein [32]. In contrast, moderate but not high VL thresholds led to greater elevations in IGF-1 levels [57], which play a major role in the synthesis of important muscle-specific contractile proteins [58].…”

“…and seven [22,23,28,29,32,45,46] included high percentages of VL (≥ 30%). The total number of repetitions during the RT program ranged from ~48 [23] to ~501 [45].…”

“…The pooled number of participants across studies was 309. However, since it was observed that data from the same participants were used in two studies [22,32], the final number of participants included in the retained studies was 287. This represents a mean of ≈ 28 participants per study.…”

“…The intra-set VL magnitude varied from 0% to 45%. Five studies [23,24,29,31,45] included low magnitudes of intraset VL (< 15%), eight [16,[22][23][24]28,32,46,47] included moderate VL magnitudes (≥ 15% and < 30%),…”

“…An expanded and integrated analysis of studies investigating the chronic effects of different intra-set VL thresholds on muscle strength, physical performance, and muscle hypertrophy has important practical implications for managing the level of fatigue during RT and designing training stimuli targeting specific adaptations in a time-efficient manner [24,28,32]. However, there is still no critical review analyzing the results of the literature to derive the practical implications for RT programming.…”